Saturday, 29 December 2018
The death of privacy? II
Never mind the police state,thanks to technology,your next door neighbour could be as big a threat.
How
long will it be before common criminals are walking around with drones
in their pockets.What will become of our privacy then.
Darwin's tree vs. the real world's forest.
Nature's Dis-Continuum: Why Structural Explanations Win Hands Down:
Michael Denton February 22, 2016 3:26 AM
Editor's note: In his new book Evolution: Still a Theory in Crisis, Michael Denton not only updates the argument from his groundbreaking Evolution: A Theory in Crisis (1985) but also presents a powerful new critique of Darwinian evolution. This article is one in a series in which Dr. Denton summarizes some of the most important points of the new book. For the full story, get your copy of Evolution: Still a Theory in Crisis. For a limited time, you'll enjoy a 30 percent discount at CreateSpace by using the discount code QBDHMYJH.
There is no evidence to support the Darwinian claim that the biological world is a functional continuum where it is possible to move from the base of the trunk to all the most peripheral branches in tiny incremental adaptive steps.
On the contrary, all of the evidence as reviewed in the first six chapters of Evolution: Still a Theory in Crisis implies that nature is a discontinuum. The tree is a discontinuous system of distinct Types characterized by sudden and saltational transitions and sudden origins of taxa-defining novelties and homologs, exactly as I claimed in Evolution thirty years ago. The claim has weathered well!
The grand river of life that has flowed on earth over the past four billion years has not meandered slowly and steadily across some flat and featureless landscape, but tumbled constantly through a rugged landscape over endless cataracts and rapids. No matter how unfashionable, no matter how at odds with current thinking in evolutionary biology, there is no empirical evidence for believing that organic nature is any less discontinuous than the inorganic realm. There is not the slightest reason for believing that the major homologs were achieved gradually via functional continuums. It is only the a priori demands of Darwinian causation that have imposed continuity on a basically discontinuous reality.
No matter how "unacceptable," the notion that the organic world consists of a finite set of distinct Types, which have been successively actualized during the evolutionary history of life on earth, satisfies the facts far better that its Darwinian rival.
Firstly, the absence of transitional sequences leading from antecedent structures to the each of the thousands of Type-defining homologs actualized during phylogeny is far more consonant with typology than Darwinism. The Darwinian claim that all the homologs were gradually achieved over millions of generations by incremental functionalism -- the genetic code, human language, the flower, the feather, the diaphragm, etc. -- is a phantasm. The near-universal absence of intermediates leading from antecedent structures to the homologs speaks volumes.
Secondly, on any Darwinian account, one must assume that previously plastic forms, "the homologs in the making," became fixed for some absolutely mysterious reason at specific points in phylogeny and thereafter remained invariant. This is a curiously non-adaptive picture, and highly incongruous in the context of a biology wedded to pan-adaptationism and a biological worldview that posits all living forms as part of an ever-mutating continuum.
Thirdly, and perhaps most importantly, in the case of many of the homologous patterns -- and particularly the Bauplans like the tetrapod limb -- there is no evidence that they are basically adaptive forms. Certainly in the vast majority of cases, they have never been shown to serve some functional end. Self-evidently, in accounting for the evolutionary emergence of homologs that serve no specific adaptive function, structural explanations win hands down.
Michael Denton February 22, 2016 3:26 AM
Editor's note: In his new book Evolution: Still a Theory in Crisis, Michael Denton not only updates the argument from his groundbreaking Evolution: A Theory in Crisis (1985) but also presents a powerful new critique of Darwinian evolution. This article is one in a series in which Dr. Denton summarizes some of the most important points of the new book. For the full story, get your copy of Evolution: Still a Theory in Crisis. For a limited time, you'll enjoy a 30 percent discount at CreateSpace by using the discount code QBDHMYJH.
There is no evidence to support the Darwinian claim that the biological world is a functional continuum where it is possible to move from the base of the trunk to all the most peripheral branches in tiny incremental adaptive steps.
On the contrary, all of the evidence as reviewed in the first six chapters of Evolution: Still a Theory in Crisis implies that nature is a discontinuum. The tree is a discontinuous system of distinct Types characterized by sudden and saltational transitions and sudden origins of taxa-defining novelties and homologs, exactly as I claimed in Evolution thirty years ago. The claim has weathered well!
The grand river of life that has flowed on earth over the past four billion years has not meandered slowly and steadily across some flat and featureless landscape, but tumbled constantly through a rugged landscape over endless cataracts and rapids. No matter how unfashionable, no matter how at odds with current thinking in evolutionary biology, there is no empirical evidence for believing that organic nature is any less discontinuous than the inorganic realm. There is not the slightest reason for believing that the major homologs were achieved gradually via functional continuums. It is only the a priori demands of Darwinian causation that have imposed continuity on a basically discontinuous reality.
No matter how "unacceptable," the notion that the organic world consists of a finite set of distinct Types, which have been successively actualized during the evolutionary history of life on earth, satisfies the facts far better that its Darwinian rival.
Firstly, the absence of transitional sequences leading from antecedent structures to the each of the thousands of Type-defining homologs actualized during phylogeny is far more consonant with typology than Darwinism. The Darwinian claim that all the homologs were gradually achieved over millions of generations by incremental functionalism -- the genetic code, human language, the flower, the feather, the diaphragm, etc. -- is a phantasm. The near-universal absence of intermediates leading from antecedent structures to the homologs speaks volumes.
Secondly, on any Darwinian account, one must assume that previously plastic forms, "the homologs in the making," became fixed for some absolutely mysterious reason at specific points in phylogeny and thereafter remained invariant. This is a curiously non-adaptive picture, and highly incongruous in the context of a biology wedded to pan-adaptationism and a biological worldview that posits all living forms as part of an ever-mutating continuum.
Thirdly, and perhaps most importantly, in the case of many of the homologous patterns -- and particularly the Bauplans like the tetrapod limb -- there is no evidence that they are basically adaptive forms. Certainly in the vast majority of cases, they have never been shown to serve some functional end. Self-evidently, in accounting for the evolutionary emergence of homologs that serve no specific adaptive function, structural explanations win hands down.
Matthew Henry's commentary on Michael the Great Prince of Jehovah's people.
It
is usual with the prophets, when they foretel the grievances of the
church, to furnish it at the same time with proper antidotes, a remedy
for every malady. And no relief is so sovereign, of such general
application, so easily accommodated to every case, and of such powerful
efficacy, as those that are fetched from Christ and the future state;
thence the comforts here are fetched.
I. Jesus Christ shall appear his church’s patron and protector: At that time, when the persecution is at the hottest, Michael shall stand up, Dan. 12:1. The angel had told Daniel what a firm friend Michael was to the church, Dan. 10:21. He all along showed this friendship in the upper world; the angels knew it; but now Michael shall stand up in his providence, and work deliverance for the Jews, when he sees that their power is gone, Deut. 32:3. 6. Christ is that great prince, for he is the prince of the kings of the earth, Rev. 1:5. And, if he stand up for his church, who can be against it? But this is not all: At that time (that
is, soon after) Michael shall stand up for the working out of our
eternal salvation; the Son of God shall be incarnate, shall be manifested to destroy the works of the devil. Christ stood for the children of our people when
he was made sin and a curse for them, stood in their stead as a
sacrifice, bore the cure for them, to bear it from them. He stands for
them in the intercession he ever lives to make within the veil, stands
up for them, and stands their friend. And after the destruction of
antichrist, of whom Antiochus was a type, Christ shall stand at the latter day upon the earth, shall appear for the complete redemption of all his.
II. When Christ appears he will recompense tribulation to those that trouble his people. There shall be a time of trouble, threatening to all, but ruining to all the implacable enemies of God’s kingdom among men, such trouble as never was since there was a nation. This is applicable. 1. To the destruction of Jerusalem, which Christ calls (perhaps with an eye to this prediction) such a great tribulation as was not since the beginning of the world to this time, Matt. 24:21. This the angel had spoken much of (Dan. 9:26, 27); and it happened about the same time that Christ set up the gospel-kingdom in the world, that Michael our prince stands up. Or, 2. To the judgment of the great day, that day that shall burn as an oven, and consume the proud and all that do wickedly; that will be such a day of trouble as never was to all those whom Michael our prince stands against.
Ps.here is John Wesley's take on Michael in Daniel 12:1
For the children - The meaning seems to be, as after the death of Antiochus the Jews had some deliverance, so there will be yet a greater deliverance to the people of God, when Michael your prince, the Messiah shall appear for your salvation. A time of trouble - A the siege of Jerusalem, before the final judgment. The phrase at that time, probably includes all the time of Christ, from his first, to his last coming.
Ps.here is John Wesley's take on Michael in Daniel 12:1
For the children - The meaning seems to be, as after the death of Antiochus the Jews had some deliverance, so there will be yet a greater deliverance to the people of God, when Michael your prince, the Messiah shall appear for your salvation. A time of trouble - A the siege of Jerusalem, before the final judgment. The phrase at that time, probably includes all the time of Christ, from his first, to his last coming.
MicroRNAs = Macro-problems for Darwinism.
MicroRNAs Don’t Fit the Evolution Model
Cornelius Hunter
MicroRNAs are small RNA gene products, typically consisting of 20-24 nucleotides, which help to regulate protein synthesis, for example by pausing or halting the ribosome translation process. Like the small drill bit that is inserted into the much larger drill tool, the small microRNAs are attached to a much larger molecular machine that performs the regulation. The microRNA role is to help the molecular machine recognize the correct RNA target.
In other words, instead of the cell having to construct a large quantity of different molecular machines to perform the regulatory role on a large quantity of RNA targets, the cell can construct a more generic type of molecular machine, and then simply attach the instructions — the microRNA — as needed.
This design approach requires the existence of these two entities: the big molecular machine and its little instruction set. Remove either entity, and this particular regulatory process isn’t going to happen.
That does not fit the evolutionary narrative. According to evolution you need a slow, gradual buildup of designs, not all-or-nothing scenarios. But not surprisingly biology is chocked full of the latter. And so with evolution we must say that the different parts just happened to arise, perhaps serving some other roles, and then just luckily they worked fantastically together to achieve a new function.
MicroRNAs are yet another finding that must be force-fit into evolutionary theory. But this irreducible complexity is only the beginning of the problem. With microRNAs, it only gets worse.
A completely different problem that microRNAs pose for evolutionary “theory” is that microRNAs do not fit the common descent pattern. As a recent paper in Genome Biology and Evolution admitted:
There is no evidence of conservation of miRNAs between the phylogenetic groups, indicating that miRNA systems evolved independently in each lineage
Evolved independently?
In other words, microRNAs do not fit the evolution model. The evidence contradicts the theory. Of course one can always make up an explanation. In this case, we say that the microRNAs “evolved independently.”
There you go, problem solved.
But let’s be honest — this is not indicated by the evidence. When the paper states that there is no evidence of conservation of miRNAs between the phylogenetic groups, thus “indicating” that miRNA systems evolved independently, it is simply misrepresenting the science.
There is precisely zero scientific evidence that microRNAs “evolved independently.” Zero. That is not my opinion. That is not conjecture. That is scientific fact.
Evolutionists talk a lot about scientific “fact.” They insist evolution is such a “fact.” But let’s just be honest. What is a scientific fact here is not evolution, but rather the exact opposite. The “fact” is the microRNAs show “no evidence of conservation.”
That fact does not “indicate” evolution, it contradicts evolution. Let’s just be honest. For once.
The paper finds yet another example of this failure in the microRNAs in brown algae. The study investigated the microRNAs in the species Saccharina japonica and compared them to previously investigated microRNAs, including those in a different brown algae species. Their findings were, as usual, “surprising.” The microRNAs in the two brown algae species were different. Completely different.
There was not a single pair of microRNAs, between the two species, that showed any sign of statistically significant sequence similarity.
Interestingly, the microRNAs in the two species did generally share some structural and genomic features. So the evolutionists had to conclude that the microRNAs in the two species evolved from a common ancestor, but then their respective sequences evolved like crazy, leaving zero trace of sequence similarity.
This. Makes. No. Sense.
Here how the paper spun the results:
Surprisingly, none of the S. japonica miRNAs share significant sequence similarity with the Ectocarpus sp. miRNAs. However, the miRNA repertoires of the two species share a number of structural and genomic features indicating that they were generated by similar evolutionary processes and therefore probably evolved within the context of a common, ancestral miRNA system. This lack of sequence similarity suggests that miRNAs evolve rapidly in the brown algae (the two species are separated by ∼95 Myr of evolution). The sets of predicted targets of miRNAs in the two species were also very different suggesting that the divergence of the miRNAs may have had significant consequences for miRNA function.
“Probably evolved within the context of a common, ancestral miRNA system”? So what does “within the context” mean?
The answer is this is a meaningless cover phrase that masks the fact that the evidence contradicts the theory. It is evo-speak for “We don’t know what we’re talking about.” A more polite description is “hand-waving.” A less polite, but more accurate description won’t be repeated here.
I will now consider the elephant in the room: Why is evolution being used to interpret the results in the first place? The theory is superfluous. It is redundant. It is vacuous. It is non-parsimonious. It is meaningless.
The theory does nothing to help us understand, interpret, elucidate, guide, or formulate meaningful predictions. Its only justification is itself. We use the theory of evolution to interpret the results because the theory is true. And how do we know it is true? Because it is true?
The theory is self-referential. It is circular. It is famous for being famous. It is a hold-over from the Epicureans of antiquity, the schoolmen of the Middle Ages, the rationalists of the 17th century, and the Darwinists today, and it has made a mockery of science.
Cornelius Hunter
MicroRNAs are small RNA gene products, typically consisting of 20-24 nucleotides, which help to regulate protein synthesis, for example by pausing or halting the ribosome translation process. Like the small drill bit that is inserted into the much larger drill tool, the small microRNAs are attached to a much larger molecular machine that performs the regulation. The microRNA role is to help the molecular machine recognize the correct RNA target.
In other words, instead of the cell having to construct a large quantity of different molecular machines to perform the regulatory role on a large quantity of RNA targets, the cell can construct a more generic type of molecular machine, and then simply attach the instructions — the microRNA — as needed.
This design approach requires the existence of these two entities: the big molecular machine and its little instruction set. Remove either entity, and this particular regulatory process isn’t going to happen.
That does not fit the evolutionary narrative. According to evolution you need a slow, gradual buildup of designs, not all-or-nothing scenarios. But not surprisingly biology is chocked full of the latter. And so with evolution we must say that the different parts just happened to arise, perhaps serving some other roles, and then just luckily they worked fantastically together to achieve a new function.
MicroRNAs are yet another finding that must be force-fit into evolutionary theory. But this irreducible complexity is only the beginning of the problem. With microRNAs, it only gets worse.
A completely different problem that microRNAs pose for evolutionary “theory” is that microRNAs do not fit the common descent pattern. As a recent paper in Genome Biology and Evolution admitted:
There is no evidence of conservation of miRNAs between the phylogenetic groups, indicating that miRNA systems evolved independently in each lineage
Evolved independently?
In other words, microRNAs do not fit the evolution model. The evidence contradicts the theory. Of course one can always make up an explanation. In this case, we say that the microRNAs “evolved independently.”
There you go, problem solved.
But let’s be honest — this is not indicated by the evidence. When the paper states that there is no evidence of conservation of miRNAs between the phylogenetic groups, thus “indicating” that miRNA systems evolved independently, it is simply misrepresenting the science.
There is precisely zero scientific evidence that microRNAs “evolved independently.” Zero. That is not my opinion. That is not conjecture. That is scientific fact.
Evolutionists talk a lot about scientific “fact.” They insist evolution is such a “fact.” But let’s just be honest. What is a scientific fact here is not evolution, but rather the exact opposite. The “fact” is the microRNAs show “no evidence of conservation.”
That fact does not “indicate” evolution, it contradicts evolution. Let’s just be honest. For once.
The paper finds yet another example of this failure in the microRNAs in brown algae. The study investigated the microRNAs in the species Saccharina japonica and compared them to previously investigated microRNAs, including those in a different brown algae species. Their findings were, as usual, “surprising.” The microRNAs in the two brown algae species were different. Completely different.
There was not a single pair of microRNAs, between the two species, that showed any sign of statistically significant sequence similarity.
Interestingly, the microRNAs in the two species did generally share some structural and genomic features. So the evolutionists had to conclude that the microRNAs in the two species evolved from a common ancestor, but then their respective sequences evolved like crazy, leaving zero trace of sequence similarity.
This. Makes. No. Sense.
Here how the paper spun the results:
Surprisingly, none of the S. japonica miRNAs share significant sequence similarity with the Ectocarpus sp. miRNAs. However, the miRNA repertoires of the two species share a number of structural and genomic features indicating that they were generated by similar evolutionary processes and therefore probably evolved within the context of a common, ancestral miRNA system. This lack of sequence similarity suggests that miRNAs evolve rapidly in the brown algae (the two species are separated by ∼95 Myr of evolution). The sets of predicted targets of miRNAs in the two species were also very different suggesting that the divergence of the miRNAs may have had significant consequences for miRNA function.
“Probably evolved within the context of a common, ancestral miRNA system”? So what does “within the context” mean?
The answer is this is a meaningless cover phrase that masks the fact that the evidence contradicts the theory. It is evo-speak for “We don’t know what we’re talking about.” A more polite description is “hand-waving.” A less polite, but more accurate description won’t be repeated here.
I will now consider the elephant in the room: Why is evolution being used to interpret the results in the first place? The theory is superfluous. It is redundant. It is vacuous. It is non-parsimonious. It is meaningless.
The theory does nothing to help us understand, interpret, elucidate, guide, or formulate meaningful predictions. Its only justification is itself. We use the theory of evolution to interpret the results because the theory is true. And how do we know it is true? Because it is true?
The theory is self-referential. It is circular. It is famous for being famous. It is a hold-over from the Epicureans of antiquity, the schoolmen of the Middle Ages, the rationalists of the 17th century, and the Darwinists today, and it has made a mockery of science.
Why the talking ape is undeniably exceptional.
I and Thou — Roger Scruton on What Makes Human Beings Unique -
Wesley J. Smith
Writing in the New York Times, philosopher Roger Scruton denies the divine spark argument that supports human exceptionalism — which I agree is not required to support HE — and focuses instead on our unique moral natures. He cites the “astonishing moral equipment of the human being — including rights and duties, personal obligations, justice, resentment, judgment, forgiveness,” which Scruton believes arises solely out of evolution.
Yes, I note before going on, this appeared in the New York Times, a newspaper that publishes articles denying or attacking human exceptionalism so often that when it publishes a piece supportive of our uniqueness, fairness requires that notice be taken.
Whatever its cause, our moral natures do indeed distinguish us from fauna. But Scruton adds our ability to relate to each other — and use language consistent with — all of us being subjects rather than objects. From“If We Are Not Just Animals, What Are We ?“:
We human beings do not see one another as animals see one another, as fellow members of a species. We relate to one another not as objects but as subjects, as creatures who address one another “I” to “you” — a point made central to the human condition by Martin Buber, in his celebrated mystical meditation “I and Thou.”
Yes. And this is a distinction between us and animals that extends beyond mere biology to the moral realm. Scruton concludes:
By speaking in the first person we can make statements about ourselves, answer questions, and engage in reasoning and advice in ways that bypass all the normal methods of discovery. As a result, we can participate in dialogues founded on the assurance that, when you and I both speak sincerely, what we say is trustworthy: Hence as persons we inhabit a lifeworld that is not reducible to the world of nature, any more than the life in a painting is reducible to the lines and pigments from which it is composed.
If that is true, then there is something left for philosophy to do, by way of making sense of the human condition. Philosophy has the task of describing the world in which we live — not the world as science describes it, but the world as it is represented in our mutual dealings, a world organized by language, in which we meet one another I to I.
This is not a matter of pins and angels. Accepting human exceptionalism is a crucial predicate to attaining and philosophically defending universal human rights.
Because if human interactions are not always subject-to-subject — as Roger Scruton contends correctly — but, in some cases, can be reduced to subject interacting with human object, those denigrated as the latter will be vulnerable to oppression, exploitation, and destruction.
Wesley J. Smith
Writing in the New York Times, philosopher Roger Scruton denies the divine spark argument that supports human exceptionalism — which I agree is not required to support HE — and focuses instead on our unique moral natures. He cites the “astonishing moral equipment of the human being — including rights and duties, personal obligations, justice, resentment, judgment, forgiveness,” which Scruton believes arises solely out of evolution.
Yes, I note before going on, this appeared in the New York Times, a newspaper that publishes articles denying or attacking human exceptionalism so often that when it publishes a piece supportive of our uniqueness, fairness requires that notice be taken.
Whatever its cause, our moral natures do indeed distinguish us from fauna. But Scruton adds our ability to relate to each other — and use language consistent with — all of us being subjects rather than objects. From“If We Are Not Just Animals, What Are We ?“:
We human beings do not see one another as animals see one another, as fellow members of a species. We relate to one another not as objects but as subjects, as creatures who address one another “I” to “you” — a point made central to the human condition by Martin Buber, in his celebrated mystical meditation “I and Thou.”
Yes. And this is a distinction between us and animals that extends beyond mere biology to the moral realm. Scruton concludes:
By speaking in the first person we can make statements about ourselves, answer questions, and engage in reasoning and advice in ways that bypass all the normal methods of discovery. As a result, we can participate in dialogues founded on the assurance that, when you and I both speak sincerely, what we say is trustworthy: Hence as persons we inhabit a lifeworld that is not reducible to the world of nature, any more than the life in a painting is reducible to the lines and pigments from which it is composed.
If that is true, then there is something left for philosophy to do, by way of making sense of the human condition. Philosophy has the task of describing the world in which we live — not the world as science describes it, but the world as it is represented in our mutual dealings, a world organized by language, in which we meet one another I to I.
This is not a matter of pins and angels. Accepting human exceptionalism is a crucial predicate to attaining and philosophically defending universal human rights.
Because if human interactions are not always subject-to-subject — as Roger Scruton contends correctly — but, in some cases, can be reduced to subject interacting with human object, those denigrated as the latter will be vulnerable to oppression, exploitation, and destruction.
Saturday, 22 December 2018
On science and magic in the new millenium.
Unbelievable: Science Fiction, Science Fact, and How to Tell the Difference
Mike Keas
Editor’s note: Unbelievable: 7 Myths About the History and Future of Science and Religion is currently available at a 50 percent pre-order holiday discount from the publisher, ISI Books.
Mike Keas
Editor’s note: Unbelievable: 7 Myths About the History and Future of Science and Religion is currently available at a 50 percent pre-order holiday discount from the publisher, ISI Books.
My box of books just arrived. Now you know what all of my family and best local friends are getting for Christmas this year. In Unbelievable: 7 Myths about the History and Future of Science and Religion I show how science fiction shapes science, especially speculative scientific inquiry into the likelihood and cultural impact of superhuman AI and the arrival of super-intelligent extraterrestrials. The publication date is January 7, 2019.
The topics I discuss are timely. Last year, in response to political fears, George Orwell’s 1984 became a bestseller on Amazon. The full scenario of this dystopian novel, written in 1949, did not actually come to pass in 1984, or in 2017. But some of its plot elements are becoming increasingly feasible. One of the hottest Christmas gifts this season is pocket-size drones with HD cameras that enable even Little Brother to watch over you. Big Brother has even more sophisticated toys by which human privacy is invaded, especially if you live in China.
A Game of Catch-up
Science is playing catch-up with science fiction, and this is nothing new. For example, some of Johannes Kepler’s (1571-1630) imaginative story of space travel, Dream or Astronomy of the Moon (posthumous, 1634) , became reality in my lifetime. But some sci-fi scenarios, such as the one where artificial intelligence comes to exceed human intelligence and achieves self-awareness, are just impossible. My book Unbelievable helps you sort the possible from the impossible. Kepler and H.G. Wells figure in my survey of the history of science fiction and how this history has influenced futuristic mythology. I show how anti-religious ideology has shaped the picture of the future found in textbooks, on TV, and elsewhere in our culture.
Here is a test of your ability to distinguish plausible scientific technology from stuff that is implausible given the limits of natural law. Do you think it is possible to buy a device that would project your cell phone’s GPS mapping software into the space above your dashboard, so you can see it and the road at the same time? Answer: yes, and this is another popular gift this Christmas season. Of course military and airline pilots have had similar heads-up displays for quite a while, but now this technology is available to any automobile user with a smartphone.
How about a device that allows you to upload your mind to a computer so you can have conditional immortality after your body dies? I’ll leave that one for homework.
Horror and Euphoria
Arthur C. Clarke, the influential writer of science fact and and science fiction, commented in a prophetic manner that “Any sufficiently advanced technology is indistinguishable from magic.” He cowrote the screenplay for Stanley Kubrick’s film 2001: A Space Odyssey (1968), which depicts the horror and euphoria of an encounter with techno-magical AI and ET.
The movie ends with a vision of the starchild, a human fetus floating serenely in space. This appears to be the new humanity after ET enlightenment. For those disenchanted with traditional religion, 2001 sketched a space-age faith. Clarke’s imagination has shaped some of the mythic elements of futuristic AI-ET storytelling. But much of what he wrote is simply unbelievable.
Futuristic myths of this sort come into better focus in my book Unbelievable, which, I don’t mind repeating, would make a fine gift, at Christmas or anytime!
On "The only true God" II
1.
Some of the many trinitarian sources which admit that the Bible actually describes men who represent God (judges, Israelite kings, etc.) and God's angels as gods include:
1. Young's Analytical Concordance of the Bible, "Hints and Helps...," Eerdmans, 1978 reprint;
2. Strong's Exhaustive Concordance of the Bible, #430, Hebrew and Chaldee Dict., Abingdon, 1974;
3. New Bible Dictionary, p. 1133, Tyndale House Publ., 1984;
4. Today's Dictionary of the Bible, p. 208, Bethany House Publ., 1982;
5. Hastings' A Dictionary of the Bible, p. 217, Vol. 2;
6. The New Brown-Driver-Briggs-Gesenius Hebrew-English Lexicon, p. 43, Hendrickson publ.,1979;
7. Greek-English Lexicon of the New Testament, #2316 (4.), Thayer, Baker Book House, 1984 printing;
8. The International Standard Bible Encyclopaedia, p. 132, Vol. 1; and p. 1265, Vol. 2, Eerdmans, 1984;
9. The NIV Study Bible, footnotes for Ps. 45:6; Ps. 82:1, 6; and Jn 10:34; Zondervan, 1985;
10. New American Bible, St. Joseph ed., footnote for Ps. 45:7, 1970 ed.;
11. A. T. Robertson, Word Pictures, Vol. 5, pp. 188-189;
12. William G. T. Shedd, Dogmatic Theology, Vol. 1, pp. 317, 324, Nelson Publ., 1980 printing;
13. Murray J. Harris, Jesus As God, p. 202, Baker Book House, 1992;
14. William Barclay, The Gospel of John, V. 2, Daily Study Bible Series, pp. 77, 78, Westminster Press, 1975;
15. The New John Gill Exposition of the Entire Bible (John 10:34 and Ps. 82:6);
16. The Fourfold Gospel (Note for John 10:35);
17. Commentary Critical and Explanatory on the Whole Bible - Jamieson, Fausset, Brown
(John 10:34-36);
18. Matthew Henry Complete Commentary on the Whole Bible (Ps. 82:6-8 and John 10:35);
19. John Wesley's Explanatory Notes on the Whole Bible (Ps. 82:1).
20. Theological Dictionary of the New Testament ('Little Kittel'), - p. 328, Eerdmans Publishing Co., 1985.
21. The Expositor's Greek Testament, pp. 794-795, Vol. 1, Eerdmans Publishing Co.
22. The Amplified Bible, Ps. 82:1, 6 and John 10:34, 35, Zondervan Publ., 1965.
23. Barnes' Notes on the New Testament, John 10:34, 35.
24. B. W. Johnson's People's New Testament, John 10:34-36.
(also John 10:34, 35 - CEV: TEV; GodsWord; The Message; NLT; NIRV; David Guzik -
http://www.blueletterbible.org/commentaries/comm_view.cfm?AuthorID=2&contentID=7942&commInfo=31&topic=John; Pastor Jon Courson, The Gospel According to John.)
And, of course the highly respected and highly popular Jewish writer, Philo, had the same understanding for "God"/"a god" about the same time the NT was written.
And many of the earliest Christians like the highly respected NT scholar Origen (and others including Tertullian; Justin Martyr; Hippolytus; Clement of Alexandria; Theophilus; the writer of "The Epistle to Diognetus" - Staniforth, p. 181; and even super-trinitarians Athanasius and St. Augustine) also had this understanding for "a god." And, as we saw above, many highly respected NT scholars of this century agree. (For example, Ernst Haenchen tells us in his commentary on the Gospel of John:
"It was quite possible in Jewish and Christian monotheism to speak of divine beings that existed alongside and under God but were not identical with him. Phil 2:6-10 proves that. In that passage Paul depicts just such a divine being, who later became man in Jesus Christ". - John 1, translated by R. W. Funk, 1984, pp. 109, 110, Fortress Press.)
2.
"I say, 'You [human judges representing God] are gods, sons of the Most High, all of you'" - Ps. 82:6, RSV. Footnotes in NIVSB for Ps. 82:1, 6 say: "In the language of the OT ... rulers, and judges, as deputies [representatives] of the heavenly King, could be given the honorific title 'god' ... or be called 'son of God'...." God Himself (as Jesus noted in Jn 10:34) said these representatives of Him were gods!
"Jesus, Son of the Most High God" - Lk 8:28, RSV.
"you [Jesus' disciples] will be sons of the Most High" - Luke 6:35, RSV.
Just these three scriptures alone show who the "only true God" and "most high God" is and that other persons may be called "a god" and "son of God" or "son of the most high" in a subordinate but still proper (not "false") sense.
3.
"5:20 him who is true. God the Father." And next, the same footnote admits: "He is the true God. [This] Could refer to EITHER God the Father OR God the Son." [Emphasis added - as usual]
4.Commentators who Professor Harris says support Jesus not being called "true God":
Huther, Alford, Haupt, Westcott, Holtzmann, Law, Brooke, Dodd, Preisker, Stott, Smalley, Grayston.
Authors of general studies who Dr. Harris says support Jesus not being called "true God": Findlay, Harnack, Dupont, W.F. Howeard, Wainwright, Taylor, Segond
Grammarians who Professor Harris says support Jesus not being called "true God":
Winer, Buttman, Schmiedel, A.T. Robertson, N. Turner, Zerwick, Grosvenor, see also BADG37a, 340c
....................................................
"...it is more likely that the word 'this' has a wider and vaguer reference. The writer is gathering together in his mind all that he has been saying about God- how He is light and love, how He is revealed as the Father through his Son Jesus Christ, and 'this', he adds, 'is the real God' ... For illustration of this we need only recall John 17:3." C. H. Dodd, Moffatt New Testament Commentary.
"[1 John] 5.20-21. Knowing the true God;... The Greek of 5:20 has only the true (one) and reads literally: we know that the Son of God has come and has given us understanding 'so that we know the true(one) and we are in the true (one)', in his Son Jesus Christ. 'This (one) is the true God and eternal life.' It is clear from this that 'the true (one)' is God throughout. Christ is his Son. In the final sentence this (one) most naturally refers still to God, not to Christ, as some have suggested. It is not unknown for Christ to be given God's name(Phil. 2:9-11) or even to be called 'God' (Heb. 1:8-9; John 1:1), but that would run contrary to the theme here, which is contrasting true and false understandings of God for which Christ's revelation is the criterion. 5:20 reminds us of Jesus' prayer according to John 17:3: 'This is eternal life: to know you the only true God and Jesus Christ whom you have sent...."- William Loader, The Johannine Epistles, Epworth Commentaries, 1992, p.79.(This commentary uses the Revised English Bible (1989) for it's quotations.)
"The final sentence of verse 20 runs: This is the true God, and eternal life. To whom does this refer? Grammatically speaking, it would normally refer to the nearest preceding subject, namely his Son Jesus Christ. If so, this would be the most unequivocal statement of the deity of Jesus Christ in the New Testament, which the champions of orthodoxy were quick to exploit against the heresy of Arius. Luther and Calvin adopted this view. Certainly it is by no means an impossible interpretation. Nevertheless, 'the most natural reference'(Westcott) is to him that is true. In this way the three references to 'the true' are to the same Person, the Father, and the additional points made in the apparent final repetition are that this is this One, namely the God made known by Jesus Christ, who is the true God, and that, besides this, He is eternal life...."-The Epistles of John, An Introduction and Commentary by The Rev. J. R.W. Stott, Tyndale New Testament Commentaries, Tyndale Press, London, 1st edition, July 1964, p.195, 196.
"Him that is true (ton alethinon). That is, God. Cf. 1:8. In him that is true (en to alethino). In God in contrast with the world 'in the evil one' (verse 19). See John 17:3. Even in his Son Jesus Christ (en to huio autou Iesou Christo). The autou refers clearly to en to alethino (God). Hence this clause is not in apposition with the preceding, but an explanation as to how we are 'in the True One' by being 'in his Son Jesus Christ.' This (houtos). Grammatically houtos [or outos] may refer to Jesus Christ or to 'the True One.' It is a bit tautological to refer it to God, but that is probably correct, God in Christ, at any rate. God is eternal life (John 5:26) and he gives it to us through Christ."-Robertson, A.T., p. 245, Vol. 6, Robertson's Word Pictures of the New Testament.
"As far as the grammatical construction of the sentence is concerned the pronoun [houtos, 'this one'] may refer to 'Him that is true' or to 'Jesus Christ'. The most natural reference however is to the subject not locally nearest but dominant in the mind of the apostle. (compare 1 John 2:22; 2 John 7; Acts 4:11; 7:19) This is obviously 'He that is true', further described by the addition of 'His Son.' Thus the pronoun gathers up the revelation indicated in the words which proceed."-Brooke Foss Westcott, The Epistles of St. John: The Greek Text with Notes and Essays, London, Macmillan and Co, 1883, p. 187.
"The KJV by adding here the word 'even,' implies that him that is true now refers to Christ...But the natural sense of the passage and the charecteristic thought of the epistle and the Gospels preclude this interpretation. It is through Christ that we are in God. This God so known is the true God. The thought centers in God from Vs. 18 on, and the contrast with the idols in the last verse confirms it."-The Interpreter's Bible, Vol. XII, p. 301.
"houtos ["this one"] in the Gospel and Epistles is not used merely to avoid the repetition of a name. It seems often to refer to the previous subject as previously described.Here (verses 18-20) God has been described as truly made known in Jesus Christ. The God who completely fulfills the highest conception of the Godhead is the God who has been revealed in Jesus Christ as contrasted with all false conceptions of God, against which the readers are warned in the next verse...Holtzman aptly quotes 2 John 7 as proof that in the Johannine writings houtos ["this one"] may refer to the subject of the preceeding sentence rather than to the name which has immediately preceded."- A. E. Brooke, The International Crititcal Commentary: A Critical and Exegetical Commentary on the Johannine Epsistles, p 152-153.
On asking the right questions re:the origin of biological information.
Asking the Right Questions about the Evolutionary Origin of New Biological Information
Casey Luskin
As we've seen, it's easy to duplicate a gene, but the key missing ingredient in many neo-Darwinian explanations of the origin of new genetic information is how a gene duplicate then acquires some new optimized function. Evolutionists have not demonstrated, except in rare cases, that step-wise paths to new function for duplicate genes exist.
As we saw in an earlier post, Austin Hughes cautions against making "statistically based claim[s] of evidence for positive selection divorced from any biological mechanism."26 In other words, natural selection is invoked to explain the evolution of genes where we do not even know the functional effect of the mutations being asserted. In this regard, Hughes observes that even in one of the more sophisticated studies, "there was no direct evidence that natural selection was actually involved in fixing adaptive changes."27
Hughes also acknowledges a problem inherent in many appeals to natural selection, namely that required mutations may not give any selective advantage when they first arise. He thus writes regarding one study:
For example, a rhodopsin from the Japanese conger eel with λmax ≈ 480 nm achieved this sensitivity through the interaction of three different amino acid replacements (at sites 195, 195, and 292). There does not seem to be any way that natural selection could favor an amino acid replacement that would be of adaptive value only if two other replacements were to occur as well.28
In this case, there was no stepwise advantage gained with each successive mutation. Because no advantage could have been gained until all three mutations were present, Hughes finds it more "plausible" to believe that the first two mutations were "selectively neutral" and became fixed due to random, non-adaptive processes such as genetic drift. Once the third mutation arose it might have provided an advantage, but to paraphrase Scott Gilbert, at best this really only explains the survival of the fittest, not the arrival of the fittest.29
But Hughes' explanation has deep deficiencies: it requires that two mutations become fixed before any selective advantage for the third mutation is gained. This implies that there must be three specific mutations to gain any selective advantage. A key question is thus, Are multiple specific mutational changes likely to appear in the same individual through unguided chance mutations given known mutation rates and population sizes? Even Hughes, despite his exhortations to fellow evolutionary biologists to employ more rigor in their studies, does not address this fundamental question.
A similar example is found when leading paleoanthropologist Bernard Wood critiqued a simplistic model of human cranial evolution on the grounds that too many mutations would be required to gain any functional advantage:
The mutation would have reduced the Darwinian fitness of those individuals. . . . It only would've become fixed if it coincided with mutations that reduced tooth size, jaw size and increased brain size. What are the chances of that? 30
Similarly, Jerry Coyne writes that "It is indeed true that natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism."31 This highlights a key deficiency in many neo-Darwinian accounts of the evolution of genes. Namely, they fail to demonstrate that the processes necessary to generate new functionally advantageous genetic information are plausible. As with Hughes's or Wood's examples above, multiple mutations might be necessary to gain any functional advantage. Any account invoking blind, unguided, random mutations to evolve a gene from Function A to Function B must address at least these three questions:
Question 1: Is there a step-wise adaptive pathway to mutate from A to B, with a selective advantage gained at each small step of the pathway?
Question 2: If not, are multiple specific mutations ever necessary to gain or improve function?
Question 3: If so, are such multi-mutation events likely to occur given the available probabilistic resources?
Mathematician David Berlinski considers such questions when critiquing evolutionary accounts of eye evolution. Darwinian processes fail because multiple changes are required for a new function to appear:
If these changes come about simultaneously, it makes no sense to talk of a gradual ascent of Mount Improbable. If they do not come about simultaneously, it is not clear why they should come about at all. 32
Again, the key question is therefore, how hard is it for new functional biological information to arise? Answering this question requires assessing the ability of random mutation and natural selection to generate new functional biological information. But when most evolutionary biologists play the Gene Evolution Game, they do not make such assessments and rarely consider these questions. Instead they typically invoke processes such as gene duplication, natural selection, and rearrangement, without demonstrating that random and unguided mutations are sufficient to produce the information needed. Any explanation that at base is little more complicated than "duplication, rearrangement, and natural selection" is not a demonstration that new functional genes can arise by unguided processes.
Thankfully, some scientists are willing to consider these key questions. They have performed research providing data that offers strong reasons to be skeptical of the ability of mutation and selection to form new functional genetic sequences.
A. Asking Questions 1 and 2:
Molecular biologist Doug Axe has performed mutational sensitivity tests on enzymes and found that functional protein folds may be as rare as 1 in 1077.33 His research shows that the fitness landscape for many enzymes looks like this, making it very unlikely that neo-Darwinian processes will find the specific amino acid sequences that yield functional protein folds:
To put the matter in perspective, these results indicate that the odds of Darwinian processes generating a functional protein fold are less than the odds of someone closing his eyes and firing an arrow into the Milky Way galaxy, and hitting one pre-selected atom.34 To say the least, this exhausts the probabilistic resources available. Such data help us answer the first question: it's not likely that there will be a functional stepwise mutational pathway leading from Function A to Function B.
Douglas Axe is by no means the only biologist to make this observation. A leading college-level biology textbook, Campbell's Biology, observes that "Even a slight change in primary structure can affect a protein's conformation and ability to function."35 Likewise, David S. Goodsell, an evolutionist biologist, writes:
As you might imagine, only a small fraction of the possible combinations of amino acids will fold spontaneously into a stable structure. If you make a protein with a random sequence of amino acids, chances are that it will only form a gooey tangle when placed in water. Cells have perfected the sequences of amino acids over many years of evolutionary selection...36
What Goodsell does not mention is that if "perfected" amino acid sequences and functional protein folds are rare and slight changes can disrupt function, then selection will be highly unlikely to take proteins from one functional fold to the next without traversing some non-functional stage. So how do new functional protein folds evolve? This effectively answers question two, implying that many specific mutations would be necessary for evolving genes to pass through non-functional stages while evolving some new function. Question 3 assesses whether this is likely to happen.
B. Asking Question 3:
In 2004, Michael Behe and physicist David Snoke published a paper in the journal Protein Science reporting results of computer simulations and theoretical calculations. They showed that the Darwinian evolution of a simple functional bond between two proteins would be highly unlikely to occur in populations of multicellular organisms. The reason, simply put, is because too many amino acids would have to be fixed by non-adaptive mutations before gaining any functional binding interaction. They found:
The fact that very large population sizes--109 or greater--are required to build even a minimal [multi-residue] feature requiring two nucleotide alterations within 108 generations by the processes described in our model, and that enormous population sizes are required for more complex features or shorter times, seems to indicate that the mechanism of gene duplication and point mutation alone would be ineffective, at least for multicellular diploid species, because few multicellular species reach the required population sizes.37
According to this data, chance mutations are unlikely to produce even two required non-adaptive mutations in multicellular diploid species within any reasonable timescale. This answers the third question: getting multiple specific non-adaptive mutations in one individual is extremely difficult, and more than two required but non-adaptive mutations are likely beyond the reach of multi-cellular organisms. Studies like this show that the actual ability of random mutation and unguided selection to produce even modestly complex new genetic functions is insufficient.
In 2008, Behe and Snoke's would-be critics tried to refute them in the journal Genetics, but found that to obtain only two specific mutations via Darwinian evolution "for humans with a much smaller effective population size, this type of change would take > 100 million years." The critics admitted this was "very unlikely to occur on a reasonable timescale." 38 In other words, there is too much complex and specified information in many proteins and enzymes to be generated in humans by Darwinian processes on a reasonable evolutionary timescale.
As noted in the comments on the Gene Evolution Game, when neo-Darwinists try to explain the evolution of genes, mere point mutations often are insufficient to account for the gene's sequence. They must therefore appeal to genetic rearrangements such as insertions, deletions, or an alleged process called "domain shuffling" where segments of proteins become shuffled to new positions in the genome. In his book The Edge of Evolution, Michael Behe reviews research that engineered new protein function by swapping domains to change protein function, and found that the intelligently engineered changes required multiple modifications that, in nature, would require too many simultaneous mutational events to yield functional changes:
[Protein engineering research] does not mimic random mutation. It is the exact opposite of random mutation. ... What do the lab results tell us about whether random-yet-productive shuffling of domains "occurs with significant frequency under conditions that are likely to occur in nature"? About whether that is biologically reasonable? Nothing at all. When a scientist intentionally arranges fragments of genes in order to maximize the chances of their interacting productively, he has left Darwin far, far behind. ... [Experiments that engineered proteins by shuffling domains] didn't just splice two genes together in a single step; they took several additional steps as well. ... Remember the more steps that have to occur between beneficial states, the much less plausible are Darwinian explanations. ... Domain shuffling would be an instance of the "natural genetic engineering" championed by James Shapiro where evolution by big random changes is hoped to do what evolution by small random changes can't. But random is random. No matter if a monkey is rearranging single letters or whole chapters, incoherence plagues every step. ... One step might luckily be helpful on occasion, maybe rarely a second step might build on it. But Darwinian processes in particular and unintelligent ones in general don't build coherent systems. So it is biologically most reasonable to conclude that, like multiple brand new protein-protein binding sites, the arrangement of multiple genetic elements into sophisticated logic circuits similar to those of computers is also well beyond the edge of Darwinian evolution. 39
As Behe observes, "No matter if a monkey is rearranging single letters or whole chapters, incoherence plagues every step." Thus, when multiple mutational events--whether point mutations, "domain shuffling," or other types of rearrangements--are required to gain some functional advantage, it seems unlikely that blind neo-Darwinian processes can produce the new biological function.
Unfortunately, few if any advocates of the neo-Darwinian just-so stories investigate whether mutation and natural selection are sufficient to produce new functional genetic information. Instead they believe that finding similarities and differences between genes demonstrates that neo-Darwinian evolution has occurred, and they assume that "positive selection" is a sufficient explanation.
As Hughes cautions, they engage in "use of certain poorly conceived statistical methods to test for positive selection," causing "the literature of evolutionary biology [to become] glutted with extravagant claims of positive selection" resulting in a "vast outpouring of pseudo-Darwinian hype [that] has been genuinely harmful to the credibility of evolutionary biology as a science." 40 Or, as Michael Behe cautions, they confuse mere sequence similarity with evidence of neo-Darwinian evolution. Finally, Michael Lynch warns his colleagues that "Evolutionary biology is not a story-telling exercise, and the goal of population genetics is not to be inspiring, but to be explanatory." 41
With these principles in mind, in the next installment we will assess about a dozen of the just-so stories concerning the origin of genes offered in studies cited by the NCSE.
References Cited:
[26.] Austin L. Hughes, "Looking for Darwin in all the wrong places: the misguided quest for positive selection at the nucleotide sequence level," Heredity, Vol. 99:364--373 (2007).
[27.] Id.
[28.] Id.
[29.] "The modern synthesis is good at modeling the survival of the fittest, but not the arrival of the fittest." Scott Gilbert, quoted in John Whitfield, "Biological Theory: Postmodern evolution?," Nature, Vol. 455:281-284 (2008).
[30.] Bernard Wood, quoted in Joseph B. Verrengia, "Gene Mutation Said Linked to Evolution," Associated Press, found in San Diego Union Tribune, March 24, 2004.
[31.] Jerry Coyne, "The Great Mutator," The New Republic (June 14, 2007). Coyne asserts he knows of no example where this is the case.
[32.] David Berlinski, "Keeping an Eye on Evolution: Richard Dawkins, a relentless Darwinian spear carrier, trips over Mount Improbable. Review of Climbing Mount Improbable by Richard Dawkins (W. H. Norton & Company, Inc. 1996)," in The Globe & Mail (November 2, 1996) at http://www.discovery.org/a/132
[33.] Douglas D. Axe, "Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds," Journal of Molecular Biology, Vol. 341: 1295-1315 (2004); Douglas D. Axe, "Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors," Journal of Molecular Biology, Vol. 301: 585-595 (2000).
[34.] See Stephen C. Meyer, Signature in the Cell: DNA and the Evidence for Intelligent Design, pg. 211 (Harper One, 2009).
[35.] Neil A. Campbell and Jane B. Reece, Biology, pg. 84 (7th ed, 2005).
[36.] David S. Goodsell, The Machinery of Life, pg. 17, 19 (2nd ed, Springer, 2009).
[37.] Michael J. Behe & David W. Snoke, "Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues," Protein Science, Vol 13:2651-2664 (2004).
[38.] Rick Durrett and Deena Schmidt, "Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution," Genetics, Vol. 180: 1501--1509 (November 2008).
[39.] Michael Behe, The Edge of Evolution: The Search for the Limits of Darwinism, Appendix D, pgs. 272-275 (Free Press, 2007) (emphasis added).
[40.] Austin L. Hughes, "The origin of adaptive phenotypes," Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193--13194 (Sept. 9, 2008) (internal citations removed).
[41.] Michael Lynch, "The frailty of adaptive hypotheses for the origins of organismal complexity," Proceedings of the National Academy of Sciences, Vol. 104:8597--8604 (May 15, 2007).
Casey Luskin
As we've seen, it's easy to duplicate a gene, but the key missing ingredient in many neo-Darwinian explanations of the origin of new genetic information is how a gene duplicate then acquires some new optimized function. Evolutionists have not demonstrated, except in rare cases, that step-wise paths to new function for duplicate genes exist.
As we saw in an earlier post, Austin Hughes cautions against making "statistically based claim[s] of evidence for positive selection divorced from any biological mechanism."26 In other words, natural selection is invoked to explain the evolution of genes where we do not even know the functional effect of the mutations being asserted. In this regard, Hughes observes that even in one of the more sophisticated studies, "there was no direct evidence that natural selection was actually involved in fixing adaptive changes."27
Hughes also acknowledges a problem inherent in many appeals to natural selection, namely that required mutations may not give any selective advantage when they first arise. He thus writes regarding one study:
For example, a rhodopsin from the Japanese conger eel with λmax ≈ 480 nm achieved this sensitivity through the interaction of three different amino acid replacements (at sites 195, 195, and 292). There does not seem to be any way that natural selection could favor an amino acid replacement that would be of adaptive value only if two other replacements were to occur as well.28
In this case, there was no stepwise advantage gained with each successive mutation. Because no advantage could have been gained until all three mutations were present, Hughes finds it more "plausible" to believe that the first two mutations were "selectively neutral" and became fixed due to random, non-adaptive processes such as genetic drift. Once the third mutation arose it might have provided an advantage, but to paraphrase Scott Gilbert, at best this really only explains the survival of the fittest, not the arrival of the fittest.29
But Hughes' explanation has deep deficiencies: it requires that two mutations become fixed before any selective advantage for the third mutation is gained. This implies that there must be three specific mutations to gain any selective advantage. A key question is thus, Are multiple specific mutational changes likely to appear in the same individual through unguided chance mutations given known mutation rates and population sizes? Even Hughes, despite his exhortations to fellow evolutionary biologists to employ more rigor in their studies, does not address this fundamental question.
A similar example is found when leading paleoanthropologist Bernard Wood critiqued a simplistic model of human cranial evolution on the grounds that too many mutations would be required to gain any functional advantage:
The mutation would have reduced the Darwinian fitness of those individuals. . . . It only would've become fixed if it coincided with mutations that reduced tooth size, jaw size and increased brain size. What are the chances of that? 30
Similarly, Jerry Coyne writes that "It is indeed true that natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism."31 This highlights a key deficiency in many neo-Darwinian accounts of the evolution of genes. Namely, they fail to demonstrate that the processes necessary to generate new functionally advantageous genetic information are plausible. As with Hughes's or Wood's examples above, multiple mutations might be necessary to gain any functional advantage. Any account invoking blind, unguided, random mutations to evolve a gene from Function A to Function B must address at least these three questions:
Question 1: Is there a step-wise adaptive pathway to mutate from A to B, with a selective advantage gained at each small step of the pathway?
Question 2: If not, are multiple specific mutations ever necessary to gain or improve function?
Question 3: If so, are such multi-mutation events likely to occur given the available probabilistic resources?
Mathematician David Berlinski considers such questions when critiquing evolutionary accounts of eye evolution. Darwinian processes fail because multiple changes are required for a new function to appear:
If these changes come about simultaneously, it makes no sense to talk of a gradual ascent of Mount Improbable. If they do not come about simultaneously, it is not clear why they should come about at all. 32
Again, the key question is therefore, how hard is it for new functional biological information to arise? Answering this question requires assessing the ability of random mutation and natural selection to generate new functional biological information. But when most evolutionary biologists play the Gene Evolution Game, they do not make such assessments and rarely consider these questions. Instead they typically invoke processes such as gene duplication, natural selection, and rearrangement, without demonstrating that random and unguided mutations are sufficient to produce the information needed. Any explanation that at base is little more complicated than "duplication, rearrangement, and natural selection" is not a demonstration that new functional genes can arise by unguided processes.
Thankfully, some scientists are willing to consider these key questions. They have performed research providing data that offers strong reasons to be skeptical of the ability of mutation and selection to form new functional genetic sequences.
A. Asking Questions 1 and 2:
Molecular biologist Doug Axe has performed mutational sensitivity tests on enzymes and found that functional protein folds may be as rare as 1 in 1077.33 His research shows that the fitness landscape for many enzymes looks like this, making it very unlikely that neo-Darwinian processes will find the specific amino acid sequences that yield functional protein folds:
To put the matter in perspective, these results indicate that the odds of Darwinian processes generating a functional protein fold are less than the odds of someone closing his eyes and firing an arrow into the Milky Way galaxy, and hitting one pre-selected atom.34 To say the least, this exhausts the probabilistic resources available. Such data help us answer the first question: it's not likely that there will be a functional stepwise mutational pathway leading from Function A to Function B.
Douglas Axe is by no means the only biologist to make this observation. A leading college-level biology textbook, Campbell's Biology, observes that "Even a slight change in primary structure can affect a protein's conformation and ability to function."35 Likewise, David S. Goodsell, an evolutionist biologist, writes:
As you might imagine, only a small fraction of the possible combinations of amino acids will fold spontaneously into a stable structure. If you make a protein with a random sequence of amino acids, chances are that it will only form a gooey tangle when placed in water. Cells have perfected the sequences of amino acids over many years of evolutionary selection...36
What Goodsell does not mention is that if "perfected" amino acid sequences and functional protein folds are rare and slight changes can disrupt function, then selection will be highly unlikely to take proteins from one functional fold to the next without traversing some non-functional stage. So how do new functional protein folds evolve? This effectively answers question two, implying that many specific mutations would be necessary for evolving genes to pass through non-functional stages while evolving some new function. Question 3 assesses whether this is likely to happen.
B. Asking Question 3:
In 2004, Michael Behe and physicist David Snoke published a paper in the journal Protein Science reporting results of computer simulations and theoretical calculations. They showed that the Darwinian evolution of a simple functional bond between two proteins would be highly unlikely to occur in populations of multicellular organisms. The reason, simply put, is because too many amino acids would have to be fixed by non-adaptive mutations before gaining any functional binding interaction. They found:
The fact that very large population sizes--109 or greater--are required to build even a minimal [multi-residue] feature requiring two nucleotide alterations within 108 generations by the processes described in our model, and that enormous population sizes are required for more complex features or shorter times, seems to indicate that the mechanism of gene duplication and point mutation alone would be ineffective, at least for multicellular diploid species, because few multicellular species reach the required population sizes.37
According to this data, chance mutations are unlikely to produce even two required non-adaptive mutations in multicellular diploid species within any reasonable timescale. This answers the third question: getting multiple specific non-adaptive mutations in one individual is extremely difficult, and more than two required but non-adaptive mutations are likely beyond the reach of multi-cellular organisms. Studies like this show that the actual ability of random mutation and unguided selection to produce even modestly complex new genetic functions is insufficient.
In 2008, Behe and Snoke's would-be critics tried to refute them in the journal Genetics, but found that to obtain only two specific mutations via Darwinian evolution "for humans with a much smaller effective population size, this type of change would take > 100 million years." The critics admitted this was "very unlikely to occur on a reasonable timescale." 38 In other words, there is too much complex and specified information in many proteins and enzymes to be generated in humans by Darwinian processes on a reasonable evolutionary timescale.
As noted in the comments on the Gene Evolution Game, when neo-Darwinists try to explain the evolution of genes, mere point mutations often are insufficient to account for the gene's sequence. They must therefore appeal to genetic rearrangements such as insertions, deletions, or an alleged process called "domain shuffling" where segments of proteins become shuffled to new positions in the genome. In his book The Edge of Evolution, Michael Behe reviews research that engineered new protein function by swapping domains to change protein function, and found that the intelligently engineered changes required multiple modifications that, in nature, would require too many simultaneous mutational events to yield functional changes:
[Protein engineering research] does not mimic random mutation. It is the exact opposite of random mutation. ... What do the lab results tell us about whether random-yet-productive shuffling of domains "occurs with significant frequency under conditions that are likely to occur in nature"? About whether that is biologically reasonable? Nothing at all. When a scientist intentionally arranges fragments of genes in order to maximize the chances of their interacting productively, he has left Darwin far, far behind. ... [Experiments that engineered proteins by shuffling domains] didn't just splice two genes together in a single step; they took several additional steps as well. ... Remember the more steps that have to occur between beneficial states, the much less plausible are Darwinian explanations. ... Domain shuffling would be an instance of the "natural genetic engineering" championed by James Shapiro where evolution by big random changes is hoped to do what evolution by small random changes can't. But random is random. No matter if a monkey is rearranging single letters or whole chapters, incoherence plagues every step. ... One step might luckily be helpful on occasion, maybe rarely a second step might build on it. But Darwinian processes in particular and unintelligent ones in general don't build coherent systems. So it is biologically most reasonable to conclude that, like multiple brand new protein-protein binding sites, the arrangement of multiple genetic elements into sophisticated logic circuits similar to those of computers is also well beyond the edge of Darwinian evolution. 39
As Behe observes, "No matter if a monkey is rearranging single letters or whole chapters, incoherence plagues every step." Thus, when multiple mutational events--whether point mutations, "domain shuffling," or other types of rearrangements--are required to gain some functional advantage, it seems unlikely that blind neo-Darwinian processes can produce the new biological function.
Unfortunately, few if any advocates of the neo-Darwinian just-so stories investigate whether mutation and natural selection are sufficient to produce new functional genetic information. Instead they believe that finding similarities and differences between genes demonstrates that neo-Darwinian evolution has occurred, and they assume that "positive selection" is a sufficient explanation.
As Hughes cautions, they engage in "use of certain poorly conceived statistical methods to test for positive selection," causing "the literature of evolutionary biology [to become] glutted with extravagant claims of positive selection" resulting in a "vast outpouring of pseudo-Darwinian hype [that] has been genuinely harmful to the credibility of evolutionary biology as a science." 40 Or, as Michael Behe cautions, they confuse mere sequence similarity with evidence of neo-Darwinian evolution. Finally, Michael Lynch warns his colleagues that "Evolutionary biology is not a story-telling exercise, and the goal of population genetics is not to be inspiring, but to be explanatory." 41
With these principles in mind, in the next installment we will assess about a dozen of the just-so stories concerning the origin of genes offered in studies cited by the NCSE.
References Cited:
[26.] Austin L. Hughes, "Looking for Darwin in all the wrong places: the misguided quest for positive selection at the nucleotide sequence level," Heredity, Vol. 99:364--373 (2007).
[27.] Id.
[28.] Id.
[29.] "The modern synthesis is good at modeling the survival of the fittest, but not the arrival of the fittest." Scott Gilbert, quoted in John Whitfield, "Biological Theory: Postmodern evolution?," Nature, Vol. 455:281-284 (2008).
[30.] Bernard Wood, quoted in Joseph B. Verrengia, "Gene Mutation Said Linked to Evolution," Associated Press, found in San Diego Union Tribune, March 24, 2004.
[31.] Jerry Coyne, "The Great Mutator," The New Republic (June 14, 2007). Coyne asserts he knows of no example where this is the case.
[32.] David Berlinski, "Keeping an Eye on Evolution: Richard Dawkins, a relentless Darwinian spear carrier, trips over Mount Improbable. Review of Climbing Mount Improbable by Richard Dawkins (W. H. Norton & Company, Inc. 1996)," in The Globe & Mail (November 2, 1996) at http://www.discovery.org/a/132
[33.] Douglas D. Axe, "Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds," Journal of Molecular Biology, Vol. 341: 1295-1315 (2004); Douglas D. Axe, "Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors," Journal of Molecular Biology, Vol. 301: 585-595 (2000).
[34.] See Stephen C. Meyer, Signature in the Cell: DNA and the Evidence for Intelligent Design, pg. 211 (Harper One, 2009).
[35.] Neil A. Campbell and Jane B. Reece, Biology, pg. 84 (7th ed, 2005).
[36.] David S. Goodsell, The Machinery of Life, pg. 17, 19 (2nd ed, Springer, 2009).
[37.] Michael J. Behe & David W. Snoke, "Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues," Protein Science, Vol 13:2651-2664 (2004).
[38.] Rick Durrett and Deena Schmidt, "Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution," Genetics, Vol. 180: 1501--1509 (November 2008).
[39.] Michael Behe, The Edge of Evolution: The Search for the Limits of Darwinism, Appendix D, pgs. 272-275 (Free Press, 2007) (emphasis added).
[40.] Austin L. Hughes, "The origin of adaptive phenotypes," Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193--13194 (Sept. 9, 2008) (internal citations removed).
[41.] Michael Lynch, "The frailty of adaptive hypotheses for the origins of organismal complexity," Proceedings of the National Academy of Sciences, Vol. 104:8597--8604 (May 15, 2007).
Who're you calling primitive?
Even Sponges Are Complex Enough to Inspire Architects
Evolution News & Views September 21, 2015 3:22 AM
Sponges are outliers in biology's big bang, the Cambrian explosion. Their embryos appear in Precambrian strata, leading some to consider them primitive. That's an illusion. New studies of how they construct their skeletons with silica "spicules" have revealed design principles remarkable enough to inspire biomimicry.
The punch line first -- here's how a news item from Cell Press concludes:
"This work not only sheds new light on skeleton formation of animals, but also might inspire interdisciplinary studies in fields such as theoretical biology, bioengineering, robotics, and architectural engineering, utilizing mechanisms of self-constructing architectures that self-adjust to their environments, including remote environments such as the deep sea or space," the researchers write.
Goodness! What are these simple animals doing to arouse such commotion? Just watch the video clip in the article of sponge cells at work. Then, look at the Graphical Abstract in the paper in Current Biology and see the steps diagrammed in well-organized stages: (1) spicules are manufactured in specialized cells, then transported to the construction site; (2) the silica spicules pierce the epithelial tissue; (3) they are then raised up into position; (4) the bases are cemented by collagen provided by basal epithelial cells.
This simple animal knows, in short, how to build a house with pole-and-beam architecture in a way that self-adjusts to its environment. That's pretty impressive.
Sponge skeletons, with their unique spicules, have been studied for a long time, but the manner of construction has been a mystery till now. What's new, according to the Japanese researchers, is the identification of specialized "transport cells" that carry and finally push the spicules through the epithelia, and cementer cells that fasten them in place like poles. The process reveals division of labor and an overall plan.
Here we report a newly discovered mode of skeleton formation: assembly of sponges' mineralized skeletal elements (spicules) in locations distant from where they were produced. Although it was known that internal skeletons of sponges consist of spicules assembled into large pole-and-beam structures with a variety of morphologies, the spicule assembly process (i.e., how spicules become held up and connected basically in staggered tandem) and what types of cells act in this process remained unexplored. Here we found that mature spicules are dynamically transported from where they were produced and then pierce through outer epithelia, and their basal ends become fixed to substrate or connected with such fixed spicules. Newly discovered "transport cells" mediate spicule movement and the "pierce" step, and collagen-secreting basal-epithelial cells fix spicules to the substratum, suggesting that the processes of spiculous skeleton construction are mediated separately by specialized cells. Division of labor by manufacturer, transporter, and cementer cells, and iteration of the sequential mechanical reactions of "transport," "pierce," "raise up," and "cementation," allows construction of the spiculous skeleton spicule by spicule as a self-organized biological structure, with the great plasticity in size and shape required for indeterminate growth, and generating the great morphological diversity of individual sponges.
This method of skeleton construction differs greatly from arthropods and vertebrates. It doesn't appear to follow a set of rules or a preordained pattern, but it is very effective for sponges, "whose growth is plastic (i.e. largely depends on their microenvironment) and indeterminate, with great morphological variations among individuals." Nevertheless, design and coordination is evident in the division of labor, the specialization of cells, and the end result that is good enough to inspire architects. If it were so simple, the authors would not have left many questions unanswered:
Many precise cellular and molecular mechanisms still remain to be elucidated, such as how transport cells can carry spicules, or how one end of pierced spicules is raised up. Additionally, one of the further questions that need to be answered is how sponges fine-tune their skeleton construction according to conditions of their microenvironment, such as water flow or stiffness of the substratum, since it is reported that the growth form of marine sponges changes according to the water movement of their environment.
Design is also evident in the self-organizational principles encoded in sponge DNA that make these results successful. Human intelligent designers would like to benefit from this knowledge. The authors conclude, repeating the "punch line":
Intriguingly, our study revealed that the spiculous skeleton of sponges is a self-organized biological structure constructed by collective behaviors of individual cells. A chain of simple and mechanical reactions, "transport-pierce (by transport cells)-raise up (by yet unknown cells and/or mechanisms)-cementation (using collagenous matrix secreted by basopinacocytes and possibly by spicule-coating cells)," adds a spicule to the skeleton, and as a result of the iteration of these sequential behaviors of cells, the spiculous skeleton expands. As far as we know, this is the first report of collective behaviors of individual cells building a self-organized biological structure using non-cellular materials, like the collective behaviors of individual termites building mounds. Thus, our work not only sheds new light on skeleton formation in animals but also might inspire interdisciplinary studies in fields such as theoretical biology, bioengineering, robotics, and architectural engineering, utilizing mechanisms of self-constructing architectures that self-adjust to their environments, including remote environments such as the deep sea or space.
The reference to termite mounds is apt. Science Magazine recently described how these mounds, built by hundreds of individual termites, are able to "breathe" like an "external lung":
Here's how it works: Inside the hill is a large central chimney connected to a system of conduits located in the mound's thin, flutelike buttresses. During the day, the air in the thin buttresses warms more quickly than the air in the insulated chimney. As a result, the warm air rises, whereas the cooler, chimney air sinks -- creating a closed convection cell that drives circulation, not external pressure from wind as had been hypothesized. At night, however, the ventilation system reverses, as the air in the buttresses cools quickly, falling to a temperature below that of the central chimney. The reversal in air flow, in turn, expels the carbon dioxide-rich air -- a result of the termites' metabolism -- that builds up in the subterranean nest over the course of the day, the researchers report online this week in the Proceedings of the National Academy of Sciences.
We know that some caves "breathe" as the temperature changes, but this is different. Termites construct their mounds for a purpose: to control the temperature and remove carbon dioxide for their health. It's a bit like active transport in cells that draws in what the cell needs and removes what it doesn't need, using machines that work against natural concentration gradients.
Intelligent Self-Organization
We all know that some beautiful things can self-organize without programming (snowflakes are a prime example). What we see here, though, are systems working from genetic programs for a purpose. In the case of sponges, its specialized cells cooperate in a plan to build a skeleton that adapts to the environment. In the case of termites, each individual insect's genetic program makes it behave in a cooperative enterprise to build an air-conditioned mound. Such things do not arise by unguided natural forces.
If functional self-organization were simple, why are five European countries taking years "working to design the European Union's first autonomously deployed space and terrestrial habitat"? (see Space.com). The effort, called the "Self-deployable Habitat for Extreme Environments" (SHEE) project, has a goal of programming elements for "autonomous construction" of housing for astronauts on Mars or other hostile locales. It's requiring years of work in design, prototyping, construction, and optimization to get these buildings to "self-deploy" with no humans in the loop.
So when a sponge can do it, we should see intelligent design behind the scenes -- not the sponge's intelligence, which admittedly is miniscule, but intelligence as a cause for the genetic information that allows the sponge to run a program that leads to a functional result.
Those of us who appreciate the spectacular genetic programs that built the Cambrian animals should take note of the level of complex specified information in the lowly sponge. We can also notice that the sponge's mode of construction bears no evolutionary ancestry with the diverse, complex body plans that exploded into existence in the Cambrian strata. Sponges did well. They're still with us.
Evolution News & Views September 21, 2015 3:22 AM
Sponges are outliers in biology's big bang, the Cambrian explosion. Their embryos appear in Precambrian strata, leading some to consider them primitive. That's an illusion. New studies of how they construct their skeletons with silica "spicules" have revealed design principles remarkable enough to inspire biomimicry.
The punch line first -- here's how a news item from Cell Press concludes:
"This work not only sheds new light on skeleton formation of animals, but also might inspire interdisciplinary studies in fields such as theoretical biology, bioengineering, robotics, and architectural engineering, utilizing mechanisms of self-constructing architectures that self-adjust to their environments, including remote environments such as the deep sea or space," the researchers write.
Goodness! What are these simple animals doing to arouse such commotion? Just watch the video clip in the article of sponge cells at work. Then, look at the Graphical Abstract in the paper in Current Biology and see the steps diagrammed in well-organized stages: (1) spicules are manufactured in specialized cells, then transported to the construction site; (2) the silica spicules pierce the epithelial tissue; (3) they are then raised up into position; (4) the bases are cemented by collagen provided by basal epithelial cells.
This simple animal knows, in short, how to build a house with pole-and-beam architecture in a way that self-adjusts to its environment. That's pretty impressive.
Sponge skeletons, with their unique spicules, have been studied for a long time, but the manner of construction has been a mystery till now. What's new, according to the Japanese researchers, is the identification of specialized "transport cells" that carry and finally push the spicules through the epithelia, and cementer cells that fasten them in place like poles. The process reveals division of labor and an overall plan.
Here we report a newly discovered mode of skeleton formation: assembly of sponges' mineralized skeletal elements (spicules) in locations distant from where they were produced. Although it was known that internal skeletons of sponges consist of spicules assembled into large pole-and-beam structures with a variety of morphologies, the spicule assembly process (i.e., how spicules become held up and connected basically in staggered tandem) and what types of cells act in this process remained unexplored. Here we found that mature spicules are dynamically transported from where they were produced and then pierce through outer epithelia, and their basal ends become fixed to substrate or connected with such fixed spicules. Newly discovered "transport cells" mediate spicule movement and the "pierce" step, and collagen-secreting basal-epithelial cells fix spicules to the substratum, suggesting that the processes of spiculous skeleton construction are mediated separately by specialized cells. Division of labor by manufacturer, transporter, and cementer cells, and iteration of the sequential mechanical reactions of "transport," "pierce," "raise up," and "cementation," allows construction of the spiculous skeleton spicule by spicule as a self-organized biological structure, with the great plasticity in size and shape required for indeterminate growth, and generating the great morphological diversity of individual sponges.
This method of skeleton construction differs greatly from arthropods and vertebrates. It doesn't appear to follow a set of rules or a preordained pattern, but it is very effective for sponges, "whose growth is plastic (i.e. largely depends on their microenvironment) and indeterminate, with great morphological variations among individuals." Nevertheless, design and coordination is evident in the division of labor, the specialization of cells, and the end result that is good enough to inspire architects. If it were so simple, the authors would not have left many questions unanswered:
Many precise cellular and molecular mechanisms still remain to be elucidated, such as how transport cells can carry spicules, or how one end of pierced spicules is raised up. Additionally, one of the further questions that need to be answered is how sponges fine-tune their skeleton construction according to conditions of their microenvironment, such as water flow or stiffness of the substratum, since it is reported that the growth form of marine sponges changes according to the water movement of their environment.
Design is also evident in the self-organizational principles encoded in sponge DNA that make these results successful. Human intelligent designers would like to benefit from this knowledge. The authors conclude, repeating the "punch line":
Intriguingly, our study revealed that the spiculous skeleton of sponges is a self-organized biological structure constructed by collective behaviors of individual cells. A chain of simple and mechanical reactions, "transport-pierce (by transport cells)-raise up (by yet unknown cells and/or mechanisms)-cementation (using collagenous matrix secreted by basopinacocytes and possibly by spicule-coating cells)," adds a spicule to the skeleton, and as a result of the iteration of these sequential behaviors of cells, the spiculous skeleton expands. As far as we know, this is the first report of collective behaviors of individual cells building a self-organized biological structure using non-cellular materials, like the collective behaviors of individual termites building mounds. Thus, our work not only sheds new light on skeleton formation in animals but also might inspire interdisciplinary studies in fields such as theoretical biology, bioengineering, robotics, and architectural engineering, utilizing mechanisms of self-constructing architectures that self-adjust to their environments, including remote environments such as the deep sea or space.
The reference to termite mounds is apt. Science Magazine recently described how these mounds, built by hundreds of individual termites, are able to "breathe" like an "external lung":
Here's how it works: Inside the hill is a large central chimney connected to a system of conduits located in the mound's thin, flutelike buttresses. During the day, the air in the thin buttresses warms more quickly than the air in the insulated chimney. As a result, the warm air rises, whereas the cooler, chimney air sinks -- creating a closed convection cell that drives circulation, not external pressure from wind as had been hypothesized. At night, however, the ventilation system reverses, as the air in the buttresses cools quickly, falling to a temperature below that of the central chimney. The reversal in air flow, in turn, expels the carbon dioxide-rich air -- a result of the termites' metabolism -- that builds up in the subterranean nest over the course of the day, the researchers report online this week in the Proceedings of the National Academy of Sciences.
We know that some caves "breathe" as the temperature changes, but this is different. Termites construct their mounds for a purpose: to control the temperature and remove carbon dioxide for their health. It's a bit like active transport in cells that draws in what the cell needs and removes what it doesn't need, using machines that work against natural concentration gradients.
Intelligent Self-Organization
We all know that some beautiful things can self-organize without programming (snowflakes are a prime example). What we see here, though, are systems working from genetic programs for a purpose. In the case of sponges, its specialized cells cooperate in a plan to build a skeleton that adapts to the environment. In the case of termites, each individual insect's genetic program makes it behave in a cooperative enterprise to build an air-conditioned mound. Such things do not arise by unguided natural forces.
If functional self-organization were simple, why are five European countries taking years "working to design the European Union's first autonomously deployed space and terrestrial habitat"? (see Space.com). The effort, called the "Self-deployable Habitat for Extreme Environments" (SHEE) project, has a goal of programming elements for "autonomous construction" of housing for astronauts on Mars or other hostile locales. It's requiring years of work in design, prototyping, construction, and optimization to get these buildings to "self-deploy" with no humans in the loop.
So when a sponge can do it, we should see intelligent design behind the scenes -- not the sponge's intelligence, which admittedly is miniscule, but intelligence as a cause for the genetic information that allows the sponge to run a program that leads to a functional result.
Those of us who appreciate the spectacular genetic programs that built the Cambrian animals should take note of the level of complex specified information in the lowly sponge. We can also notice that the sponge's mode of construction bears no evolutionary ancestry with the diverse, complex body plans that exploded into existence in the Cambrian strata. Sponges did well. They're still with us.
Saturday, 15 December 2018
Looking for magical beasts? Just ask your nearest Darwinian apologist.
Prehoda's Goof: Mutational Fitness Effects Cannot Be Predicted
Evolution News & Views
Last February when we looked into the claims of University of Oregon biochemist Kenneth Prehoda, we saw him pounding Darwin's pulpit with righteous fervor. He practically shouted that you could get instant animals by chance. His team's discovery of a mutation that seemed to allow proteins to interact more easily in a choanoflagellate became the springboard for a sermon envisioning all the marvels of multicellularity without intelligent design.
Indeed, a breathless reporter from the Washington Post gave him credit for explaining human beings with that one random accident: "Every example of cells collaborating that has arisen since -- from the trilobites of 500 million years ago to the dinosaurs, woolly mammoths and you -- probably relied on it or some other similar mutation."
He has toned down the rhetoric a bit in the latest news from his lab. Maybe he didn't want to face another Twitter storm by engaging "the ire of anti-evolutionists" the way he did last time. "We've witnessed evolution," he had said. "Evolution is just a fact, hands down." Even his reviewers had gotten on his case for overstating the implications of his findings. We showed that there were plenty of empirical and logical reasons, not religious reasons, for doubting the significance of his instant-animal mutation.
This time, the news item makes more modest claims:
Just as the course of a drift boat can be irreversibly altered by a log in its path, a single mutation can send life in an entirely new direction.
That scenario, says UO biochemist Ken Prehoda, provides a window on how one mutation sparked a huge jump in the evolutionary course of a protein important for the evolution of animals.
Earlier this year, Prehoda was on a team that found that a random mutation 600 million years ago in a single-celled organism created a new family of proteins that are important for multicellular life. In a new paper, now online ahead of print in the Journal of the American Chemical Society, Prehoda and colleagues describe what the mutation did to the original protein family.
Mutations happen randomly. Most are bad news. But occasionally a mutation is good, helping an organism adapt to environmental changes or advancing overall fitness. Understanding such changes better, Prehoda said, could potentially point to new treatments for human diseases such as cancer.
Ah, yes; evolutionists can score extra points for claiming their otherwise esoteric research "could potentially" lead to cures for cancer. But we don't need to deduct those points; there are enough other vulnerable points at risk of lowering Darwin's score.
Prehoda's basic claim was that a point mutation in an enzyme called guanylate kinase gave it a new protein-interacting domain (PID), launching the GKPID family of enzymes used by all animals. And coincidentally, this mutation happened right when multicellular organisms were first appearing 600 million years ago. Could human beings be far behind?
Prehoda now reveals that all he found was that the mutation "stiffened" the GK enzyme a bit. One might think this to be a disadvantage, but he weaves a story that the stiffening of the enzyme's backbone actually was a good thing.
The mutation, which researchers labeled s36P, set off a cascade of events in which protein interactions took new routes and evolved into more complex multicellular organisms, Prehoda said. The mutation is still conserved in all animals today, he added.
"A lot of the proteins that do the work in our bodies can be thought of as molecular machines," Prehoda said. "They move in a way that is coordinated with function. Each protein spins in a circle or motors along filaments. Our protein, before the mutation, was an enzyme that had certain flexible movements related to its function. This one mutation fixed the protein's backbone, locking the molecule into a shape that is important for its new function."
Incidentally, the spinning machine is ATP synthase, and the motor is most likely kinesin. We find that out in the new paper, published this time not in eLife but in the Journal of the American Chemical Society, which does not include reviewer's comments. For obvious reasons, Prehoda does not try to evolve ATP synthase by single point mutations.
In the paper, Whitney, Volkman and Prehoda mere "suggest" that the mutation that stiffened the GK enzyme "might have been important" for instigating new functions by "tuning" its "conformational flexibility" in some way. Even so, they retain some epistemic modesty in this less audacious hypothesis: "Furthermore, even if flexibility was important in the functional transition from enzyme to PID, we do not know how it was altered or how doing so could lead to such a dramatic change in function."
Unfortunately, a new paper just appeared in the Proceedings of the National Academy of Sciences that undercuts their premise. Prehoda's team assumes that random mutations can be ranked as "good" and "bad" -- as if you can sort them like marbles into green jars and red jars. In this view, good things add up, and bad things get tossed out by natural selection. That was Darwin's view, too:
It may be said that natural selection is daily and hourly scrutinising, throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good; silently and insensibly working, whenever and wherever opportunity offers, at the improvement of each organic being in relation to its organic and in organic conditions of life.
The new PNAS paper by Bank et al., "On the (un)predictability of a large intragenic fitness landscape," takes a serious look at the effects of mutational interactions. Mutations aren't like isolated red and green marbles. They interact in complex ways. "Epistasis" is a term referring to the combinatorial effects of mutations. For instance, two neutral mutations might interact to produce a benefit; that would be a case of positive epistasis. On the other hand, a seemingly beneficial mutation could have negative effects elsewhere in the organism; that's called negative epistasis. It won't improve an organism's fitness, for example, if a mutation for stronger muscles also produces heart attacks.
The point of the study is that epistatic interactions are profoundly unpredictable. By performing one of the largest-ever surveys of epistasis on engineered mutations to Hsp90, a well-known protein, they concluded that it is extremely difficult to predict what will happen. Because their conclusion has far-reaching implications for all evolutionary predictions, it bears quoting in full:
Originally introduced as a metaphor to describe adaptive evolution, fitness landscapes promise to become a powerful tool in biology to address complex questions regarding the predictability of evolution and the prevalence of epistasis within and between genomic regions. Due to the high-dimensional nature of fitness landscapes, however, the ability to extrapolate will be paramount to progress in this area, and the optimal quantitative and qualitative approaches to achieve this goal are yet to be determined.
Here, we have taken an important step toward addressing this question via the creation and analysis of a landscape comprising 640 engineered mutants of the Hsp90 protein in yeast. The unprecedented size of the fitness landscape, along with the multiallelic nature, allows us to test whether global features could be extrapolated from subsets of the data. Although the global pattern indicates a rather homogeneous landscape, smaller sublandscapes are a poor predictor of the overall global pattern because of "epistatic hotspots."
In combination, our results highlight the inherent difficulty imposed by the duality of epistasis for predicting evolution. In the absence of epistasis (i.e., in a purely additive landscape), evolution is globally highly predictable because the population will eventually reach the single-fitness optimum, but the path taken is locally entirely unpredictable. Conversely, in the presence of (sign and reciprocal sign) epistasis evolution is globally unpredictable, because there are multiple optima and the probability to reach any one of them depends strongly on the starting genotype. At the same time, evolution may become locally predictable with the population following obligatory adaptive paths that are a direct result of the creation of fitness valleys owing to epistatic interactions.
The empirical fitness landscape studied here appears to be intermediate between these extremes. Although the global peak is within reach from almost any starting point, there is a local optimum that will be reached with appreciable probability, particular when starting from the parental genotype. From a practical standpoint, these results thus highlight the danger inherent to the common practice of constructing fitness landscapes from ascertained mutational combinations. However, this work also suggests that one promising way forward for increasing predictive power will be the utilization of multiple small landscapes used to gather information about the properties of individual mutations, combined with the integration of site-specific biophysical properties.
From this, we can see that Prehoda's team has taken a leap to think that one mutation in one enzyme would start a path to animals. He has not taken into account the effects of epistasis. Bank et al. say that local fitness peaks would be more likely to strand the animal there, rather than let it progress. Walking right past the "danger" sign, Prehoda engaged in the "common practice of constructing fitness landscapes from ascertained mutational combinations." At best, he should only investigate a "small landscape" around the mutation to see what might happen. Maybe it would help a certain choanoflagellate. Beyond that, he is on dangerous ground making predictions.
Prehoda might have this comeback argument. He could say that his work on "ancestral protein reconstruction" shows that the mutation occurred right at the time multicellularity took off. It's a postdiction, therefore, not a prediction. This argument, however, commits the fallacy of "affirming the consequent" -- i.e., "If P, then Q. Q occurs. Therefore, P." You can't say P caused Q. That overlooks multiple other possibilities for Q. In fact, there could be an infinite number of causes for Q besides P. Prehoda could only argue Q if and only if P: specifically, that the emergence of animals required a specific mutation to guanylate kinase. That would be unwarranted even within neo-Darwinian theory. The best he can say is that the mutation is "consistent with" a scenario in which a stiffer enzyme contributed to new functions useful to multicellular organisms, assuming it avoided negative epistasis in the process.
Such clarification, however, would be unlikely to yield headlines in the Washington Post. Empirically speaking, Bank et al.'s yeast remain yeast, and Prehoda et al.'s choanoflagellates remain choanoflagellates.
Evolution News & Views
Last February when we looked into the claims of University of Oregon biochemist Kenneth Prehoda, we saw him pounding Darwin's pulpit with righteous fervor. He practically shouted that you could get instant animals by chance. His team's discovery of a mutation that seemed to allow proteins to interact more easily in a choanoflagellate became the springboard for a sermon envisioning all the marvels of multicellularity without intelligent design.
Indeed, a breathless reporter from the Washington Post gave him credit for explaining human beings with that one random accident: "Every example of cells collaborating that has arisen since -- from the trilobites of 500 million years ago to the dinosaurs, woolly mammoths and you -- probably relied on it or some other similar mutation."
He has toned down the rhetoric a bit in the latest news from his lab. Maybe he didn't want to face another Twitter storm by engaging "the ire of anti-evolutionists" the way he did last time. "We've witnessed evolution," he had said. "Evolution is just a fact, hands down." Even his reviewers had gotten on his case for overstating the implications of his findings. We showed that there were plenty of empirical and logical reasons, not religious reasons, for doubting the significance of his instant-animal mutation.
This time, the news item makes more modest claims:
Just as the course of a drift boat can be irreversibly altered by a log in its path, a single mutation can send life in an entirely new direction.
That scenario, says UO biochemist Ken Prehoda, provides a window on how one mutation sparked a huge jump in the evolutionary course of a protein important for the evolution of animals.
Earlier this year, Prehoda was on a team that found that a random mutation 600 million years ago in a single-celled organism created a new family of proteins that are important for multicellular life. In a new paper, now online ahead of print in the Journal of the American Chemical Society, Prehoda and colleagues describe what the mutation did to the original protein family.
Mutations happen randomly. Most are bad news. But occasionally a mutation is good, helping an organism adapt to environmental changes or advancing overall fitness. Understanding such changes better, Prehoda said, could potentially point to new treatments for human diseases such as cancer.
Ah, yes; evolutionists can score extra points for claiming their otherwise esoteric research "could potentially" lead to cures for cancer. But we don't need to deduct those points; there are enough other vulnerable points at risk of lowering Darwin's score.
Prehoda's basic claim was that a point mutation in an enzyme called guanylate kinase gave it a new protein-interacting domain (PID), launching the GKPID family of enzymes used by all animals. And coincidentally, this mutation happened right when multicellular organisms were first appearing 600 million years ago. Could human beings be far behind?
Prehoda now reveals that all he found was that the mutation "stiffened" the GK enzyme a bit. One might think this to be a disadvantage, but he weaves a story that the stiffening of the enzyme's backbone actually was a good thing.
The mutation, which researchers labeled s36P, set off a cascade of events in which protein interactions took new routes and evolved into more complex multicellular organisms, Prehoda said. The mutation is still conserved in all animals today, he added.
"A lot of the proteins that do the work in our bodies can be thought of as molecular machines," Prehoda said. "They move in a way that is coordinated with function. Each protein spins in a circle or motors along filaments. Our protein, before the mutation, was an enzyme that had certain flexible movements related to its function. This one mutation fixed the protein's backbone, locking the molecule into a shape that is important for its new function."
Incidentally, the spinning machine is ATP synthase, and the motor is most likely kinesin. We find that out in the new paper, published this time not in eLife but in the Journal of the American Chemical Society, which does not include reviewer's comments. For obvious reasons, Prehoda does not try to evolve ATP synthase by single point mutations.
In the paper, Whitney, Volkman and Prehoda mere "suggest" that the mutation that stiffened the GK enzyme "might have been important" for instigating new functions by "tuning" its "conformational flexibility" in some way. Even so, they retain some epistemic modesty in this less audacious hypothesis: "Furthermore, even if flexibility was important in the functional transition from enzyme to PID, we do not know how it was altered or how doing so could lead to such a dramatic change in function."
Unfortunately, a new paper just appeared in the Proceedings of the National Academy of Sciences that undercuts their premise. Prehoda's team assumes that random mutations can be ranked as "good" and "bad" -- as if you can sort them like marbles into green jars and red jars. In this view, good things add up, and bad things get tossed out by natural selection. That was Darwin's view, too:
It may be said that natural selection is daily and hourly scrutinising, throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good; silently and insensibly working, whenever and wherever opportunity offers, at the improvement of each organic being in relation to its organic and in organic conditions of life.
The new PNAS paper by Bank et al., "On the (un)predictability of a large intragenic fitness landscape," takes a serious look at the effects of mutational interactions. Mutations aren't like isolated red and green marbles. They interact in complex ways. "Epistasis" is a term referring to the combinatorial effects of mutations. For instance, two neutral mutations might interact to produce a benefit; that would be a case of positive epistasis. On the other hand, a seemingly beneficial mutation could have negative effects elsewhere in the organism; that's called negative epistasis. It won't improve an organism's fitness, for example, if a mutation for stronger muscles also produces heart attacks.
The point of the study is that epistatic interactions are profoundly unpredictable. By performing one of the largest-ever surveys of epistasis on engineered mutations to Hsp90, a well-known protein, they concluded that it is extremely difficult to predict what will happen. Because their conclusion has far-reaching implications for all evolutionary predictions, it bears quoting in full:
Originally introduced as a metaphor to describe adaptive evolution, fitness landscapes promise to become a powerful tool in biology to address complex questions regarding the predictability of evolution and the prevalence of epistasis within and between genomic regions. Due to the high-dimensional nature of fitness landscapes, however, the ability to extrapolate will be paramount to progress in this area, and the optimal quantitative and qualitative approaches to achieve this goal are yet to be determined.
Here, we have taken an important step toward addressing this question via the creation and analysis of a landscape comprising 640 engineered mutants of the Hsp90 protein in yeast. The unprecedented size of the fitness landscape, along with the multiallelic nature, allows us to test whether global features could be extrapolated from subsets of the data. Although the global pattern indicates a rather homogeneous landscape, smaller sublandscapes are a poor predictor of the overall global pattern because of "epistatic hotspots."
In combination, our results highlight the inherent difficulty imposed by the duality of epistasis for predicting evolution. In the absence of epistasis (i.e., in a purely additive landscape), evolution is globally highly predictable because the population will eventually reach the single-fitness optimum, but the path taken is locally entirely unpredictable. Conversely, in the presence of (sign and reciprocal sign) epistasis evolution is globally unpredictable, because there are multiple optima and the probability to reach any one of them depends strongly on the starting genotype. At the same time, evolution may become locally predictable with the population following obligatory adaptive paths that are a direct result of the creation of fitness valleys owing to epistatic interactions.
The empirical fitness landscape studied here appears to be intermediate between these extremes. Although the global peak is within reach from almost any starting point, there is a local optimum that will be reached with appreciable probability, particular when starting from the parental genotype. From a practical standpoint, these results thus highlight the danger inherent to the common practice of constructing fitness landscapes from ascertained mutational combinations. However, this work also suggests that one promising way forward for increasing predictive power will be the utilization of multiple small landscapes used to gather information about the properties of individual mutations, combined with the integration of site-specific biophysical properties.
From this, we can see that Prehoda's team has taken a leap to think that one mutation in one enzyme would start a path to animals. He has not taken into account the effects of epistasis. Bank et al. say that local fitness peaks would be more likely to strand the animal there, rather than let it progress. Walking right past the "danger" sign, Prehoda engaged in the "common practice of constructing fitness landscapes from ascertained mutational combinations." At best, he should only investigate a "small landscape" around the mutation to see what might happen. Maybe it would help a certain choanoflagellate. Beyond that, he is on dangerous ground making predictions.
Prehoda might have this comeback argument. He could say that his work on "ancestral protein reconstruction" shows that the mutation occurred right at the time multicellularity took off. It's a postdiction, therefore, not a prediction. This argument, however, commits the fallacy of "affirming the consequent" -- i.e., "If P, then Q. Q occurs. Therefore, P." You can't say P caused Q. That overlooks multiple other possibilities for Q. In fact, there could be an infinite number of causes for Q besides P. Prehoda could only argue Q if and only if P: specifically, that the emergence of animals required a specific mutation to guanylate kinase. That would be unwarranted even within neo-Darwinian theory. The best he can say is that the mutation is "consistent with" a scenario in which a stiffer enzyme contributed to new functions useful to multicellular organisms, assuming it avoided negative epistasis in the process.
Such clarification, however, would be unlikely to yield headlines in the Washington Post. Empirically speaking, Bank et al.'s yeast remain yeast, and Prehoda et al.'s choanoflagellates remain choanoflagellates.
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