Saturday, 11 June 2016
File under "Well said" XXIX
Education begins the gentleman, but reading, good company and reflection must finish him. John Locke
The simian stone age?
Monkeys Do Not Have a "Stone Age" Culture
Wesley J. Smith
It is amazing how some in the sciences are so desperate to knock humans off the pedestal of exceptionalism. Ironically, a primary manner in which they seek to do this is by demonstrating how animals are like us -- indirectly admitting our special status.
Latest example? Monkeys supposedly have a "stone age culture" because some have used tools made of durable natural materials. From "Monkey 'Archeology' Reveals Macaque's Own Stone Age Culture," in New Scientist:
The world's first archaeology dig of an old world monkey culture has uncovered the tools used by previous generations of wild macaques -- a group of primates separated from humans by some 25 million years of evolution. The discovery means humans aren't unique in leaving a record of our past culture that can be pried open through archaeology.
Only a few decades ago scientists thought that humans were the only species to have worked out how to turn objects in their environment into useful tools. We now know all sorts of animals can do the same - but the tools of choice are usually perishable materials like leafs and twigs. This makes the origin of these behaviours difficult to study, especially when you consider that the record of hominin stone tool use stretches back more than 3 million years.
Burmese long-tailed macaques are a rare exception. They are renowned for their use of stone tools to crack open shellfish, crabs and nuts, making them one of the very few primates that have followed hominins into the Stone Age.
Please. Using stones does not make a culture.
Here are the "Seven Elements of Culture":
Customs: Are the written and unwritten rules of society. They can refer to a culture's laws, but also its moral and ethical expectations.
Religion: Unites people under a common belief system and values. Religion is the most important aspect of many people's lives, and is a major bonding factor within communities.
Government: Offers protection and order, and defines power and responsibility within a culture.
Language: Can act to join people of the same culture, but can also distinguish people of different sub-groups within a common culture.
Communication: Vital to the spread of culture, so you can see how having the same language is important in cultural terms.
Arts: Art and literature is one of the most powerful ways of spreading cultural knowledge and beliefs.
Economy: A culture's economy regulates what it needs to survive in terms of resources.
Using stones in the manner of tools? Nope.
And was anything really new learned in this dig? Not much.
We know from eyewitness accounts that these monkeys have been using tools for at least 120 years, so the study doesn't push the age of the behaviour back. But Haslam sees it as a first step towards digging deeper into the origins of the behaviour.
In other words, this is a big nothing burger.
The real human stone age culture included all seven elements, for example, explicit creativity (the incredible beauty seen in the cave paintings), the emergence of moral agency, the coming together of clans and tribes with governing rules, inventing, burying the dead (implying a spiritual belief), an aesthetic sense, evidenced by the making of jewelry, and on and on and on.
Monkeys using stones for tools? That's not culture, at least, not in the sense that humans create, mold, and shape it. Nice try fellas, but no cigar.
Wesley J. Smith
It is amazing how some in the sciences are so desperate to knock humans off the pedestal of exceptionalism. Ironically, a primary manner in which they seek to do this is by demonstrating how animals are like us -- indirectly admitting our special status.
Latest example? Monkeys supposedly have a "stone age culture" because some have used tools made of durable natural materials. From "Monkey 'Archeology' Reveals Macaque's Own Stone Age Culture," in New Scientist:
The world's first archaeology dig of an old world monkey culture has uncovered the tools used by previous generations of wild macaques -- a group of primates separated from humans by some 25 million years of evolution. The discovery means humans aren't unique in leaving a record of our past culture that can be pried open through archaeology.
Only a few decades ago scientists thought that humans were the only species to have worked out how to turn objects in their environment into useful tools. We now know all sorts of animals can do the same - but the tools of choice are usually perishable materials like leafs and twigs. This makes the origin of these behaviours difficult to study, especially when you consider that the record of hominin stone tool use stretches back more than 3 million years.
Burmese long-tailed macaques are a rare exception. They are renowned for their use of stone tools to crack open shellfish, crabs and nuts, making them one of the very few primates that have followed hominins into the Stone Age.
Please. Using stones does not make a culture.
Here are the "Seven Elements of Culture":
Customs: Are the written and unwritten rules of society. They can refer to a culture's laws, but also its moral and ethical expectations.
Religion: Unites people under a common belief system and values. Religion is the most important aspect of many people's lives, and is a major bonding factor within communities.
Government: Offers protection and order, and defines power and responsibility within a culture.
Language: Can act to join people of the same culture, but can also distinguish people of different sub-groups within a common culture.
Communication: Vital to the spread of culture, so you can see how having the same language is important in cultural terms.
Arts: Art and literature is one of the most powerful ways of spreading cultural knowledge and beliefs.
Economy: A culture's economy regulates what it needs to survive in terms of resources.
Using stones in the manner of tools? Nope.
And was anything really new learned in this dig? Not much.
We know from eyewitness accounts that these monkeys have been using tools for at least 120 years, so the study doesn't push the age of the behaviour back. But Haslam sees it as a first step towards digging deeper into the origins of the behaviour.
In other words, this is a big nothing burger.
The real human stone age culture included all seven elements, for example, explicit creativity (the incredible beauty seen in the cave paintings), the emergence of moral agency, the coming together of clans and tribes with governing rules, inventing, burying the dead (implying a spiritual belief), an aesthetic sense, evidenced by the making of jewelry, and on and on and on.
Monkeys using stones for tools? That's not culture, at least, not in the sense that humans create, mold, and shape it. Nice try fellas, but no cigar.
Universal common ancestry in the hot seat V
Vincent Torley Thinks I Have Egg on My Face
Ann Gauger
Well, I must say I didn't expect to be honored by a 7500-word broadside by philosopher Dr. Vincent Torley, assisted by Dr. Josh Swamidass, Assistant Professor at Washington University. I guess they must have a lot of spare time. The reason for the post at Uncommon Descent? Both hold common descent to be absolutely, incontrovertibly, obviously true, and they apparently wish I would fall into line and stop embarrassing them by doubting common descent. They wish I would give up my "peculiar kind of intellectual obstinacy."
The argument is in the end all about common descent. (There are a few accusations of poor reasoning, obscuring the issue, and even a little bad faith along the way.) Look, intelligent design is not wedded to common descent. Neither is it wedded to a denial of common descent. Intelligent design states that there is evidence of design in the universe. I think we are in agreement on this point. In terms of biology, how the designer instantiated that design is still subject to debate, based on the strength of the evidence for each position.
As a biologist, I see evidence on both sides of the debate. The evidence is equivocal -- hence the fact that ID advocates take different positions on the subject. Yet common descent -- the idea that organisms descend from one or a few common ancestors -- is treated like a sacred cow by many scientists, and even, it appears, by some philosophers. Indignation arises that anyone would doubt it, would even have questions. Scientists take common descent as axiomatic, and accept evidence that is itself interpreted through a lens of common descent as proof of common descent. As a consequence, any evidence against common descent meets opposition and is explained away.
So when I see weak evidence for common descent I say so, as I did in a post here, "The Vitellogenin Pseudogene Story: Unequally Yolked." (Apparently Dr. Torley caught the reference but missed the yolk, as he repeatedly misstates my post's subtitle as "Unequally Yoked.") I wrote the aforementioned post because of weak evidence, and even an overstatement of the evidence by some.
The controversy began with the post on vitellogenin synteny, "Vitellogenin and Common Ancestry: Reading Tomkins," by Professor Dennis Venema at Trinity Western University, where I read some interesting arguments regarding cross-species synteny in the region of the chicken vitellogenin genes. Synteny is the term for the shared arrangement of genes along chromosomes from different organisms, and its existence is taken as evidence for common descent. Vitellogenins are egg yolk proteins, present and used in egg-laying organisms.
I followed up by reading the paper "Loss of Egg Yolk Genes in Mammals and the Origin of Lactation and Placentation," by David Brawand, Walter Wahli, and Henrik Kaessmann, on which Venema's post was based. (It's free access. You can verify all this yourself.) It's always a good idea to read the original material and evaluate the evidence for yourself. What I saw in Brawand et al. is what prompted me to write my post.
My dispute with Torley (and Venema) is at bottom a dispute about the scientific interpretation of data, or should be. Therefore I am going to go through the data in some detail, to show why I reached the conclusions I did with regard to the human "VIT1" pseudogene, and where we differ in interpretations. This essentially covers Torley's points 1 and 2. I will address the points 3-7 in later posts, so as not to burden the reader with excess length.
There are three chicken egg yolk genes, VIT1, VIT2, and VIT3, all expressed and made into protein because chickens lay eggs. The Brawand paper set out to see if there was any evidence for a vitellogenin presence in the human genome, with the idea that we are descended from an egg-laying animal. They looked in the region of our chromosome that is analogous to the chicken genome, and aligned the two against each other. A dotplot from the Brawand paper (see below) shows where the human (Y axis) and chicken (X axis) DNA sequences align. A perfect alignment (for example if human sequence was aligned against human) should show a diagonal solid line.
All figures taken from Brawand, D., Wali, W., and Kaessmann, H. 2008. Loss of Egg Yolk Genes in Mammals and the Origin of Lactation and Placentation. PLoS Biology (6) 507-517. Creative Commons license.
The top panel illustrates the VIT1 alignment between the two sequences, chicken and human, and the bottom panel VIT2 and VIT3. Black dots show where sequence similarity exists. The colored stripes indicate coding sequences (exons) for each "gene." In between in the white regions are the non-coding introns and intergenic spaces (sequences between genes). ELDT1, FP, SSX2IP, and CTBS are functional genes in both human and chicken and show sequence similarity and synteny in all coding sequences (the yellow stripes). Even some intergenic spaces show evidence of synteny. Where the synteny disappears is where the VIT1, VIT2, and VIT3 coding sequences should be.
I found the VIT1, VIT2, and VIT3 alignments to be ambiguous at best. However, in the supplemental materials for the Brawand paper is another representation of the syntenic regions where the human VIT1, VIT2, and VIT3 remnants should be. That makes things clearer. It is reproduced below, but click on the image to see the figure properly:
The bars colored red and black represent the chicken VIT genes, showing only their exons (the parts of the gene that contribute to making protein), alternating as red and black segments along the VIT sequences. (There are 35 exons in VIT1 and 2, 36 exons in VIT3.) Above each bar and running parallel to it are thin red lines, indicating where similarity has been detected, with insertions, deletions and stop codons necessary to make the sequence line up also indicated. To find this alignment they used "highly sensitive similarity search algorithms," and ran repeated trials. From the paper:
The best scoring alignment chain was determined from the 2,000 best local alignments for each VIT region using dynamic programming. Importantly, the combined alignments of VIT coding sequences of the best chain for each of the opossum VIT1-VIT3 regions (aligned to chicken) showed significantly higher alignment scores than the genomic background (introns and intergenic regions) in the chain, as assessed by a Mann-Whitney U test (P < 0.05). This suggests that the obtained (pseudogenic) VIT remnants from opossum are nonrandom sequence matches and represent true VIT sequences. In the eutherian [human and dog] comparison, VIT1 coding sequences showed significantly higher scores than the genomic background [reported as P < 0.05 elsewhere] (the alignable regions for the other two VIT genes may be too short to provide statistical significance -- VIT3 -- or represent spurious matches -- VIT2). [Emphasis added.]
There was very little actual sequence alignment data given for the human syntenic regions, just the 150 base sequence from exon 3 that I mentioned in my post. Since I was asked to provide the source of my analysis, here is it, as obtained in the paper in a supplementary figure; again, click on the image to see it better:
Full disclosure: this is the best-reported evidence they have for human synteny. The rest is unconvincing to me, though it may be convincing to others. Surely if they had a better or more extensive alignment they would have reported it. This by the way, I would assume is the stretch of DNA used by Jeff Tomkins in his analysis of the region.
Now for a general comment regarding the accusation of faulty statistics made against me by Torley and Swamidass. Here is the segment from Torley's post:
Professor Swamidass has two comments which are germane here. First, he points out that as a matter of standard practice, the data relating to similarity in the paper by Brawand et al. should be considered correct, unless proven otherwise. If Dr. Gauger thinks that the authors' claims of similarity are doubtful, then I would invite her to show the exact DNA sequence she used, so that interested readers can perform a BLAST by themselves (there is a website for this), to verify both the match to the vitellogenin chicken gene and to the human sequence. This doesn't resolve the issue of picking the right DNA sequence, but it is a start. Selecting the right parameters is important, too: if you use the wrong gapped parameter (a mistake Tomkins is notorious for making), then there will be discrepancies. [Emphasis added.]
I do not question the authors' data, but I do question their interpretation that it proves there is a VIT1 pseudogene in humans. Actually to be fair, they merely suggest it as evidence. They do not go much further than what I have quoted above: they point out a few deletions held in common by dogs, humans, and armadillo in the 150 base sequence I show above, arguing that they all share common ancestry. The bulk of the paper is about the remnants of opossum and platypus vitellogenin genes, perhaps because they recognize that the evidence is weak for dogs (for which they report no analysis I could find) and humans.
About the data being correct and my questioning it: All scientists are (or should be) taught in graduate school to critically evaluate conclusions. That is not the same as questioning original data, which I do not do. Questioning conclusions, evaluating them carefully to see if they are warranted, is something all scientists should do.
Again, I based my analysis on the data reported in the paper; I did not question the underlying data. The 150 base sequence I talked about was available as a supplementary figure in the paper itself, and I have already shown it to you. Careful reading of Brawand et al. would have revealed it -- it is the only sequence reported for human alignments. But since I am asked to provide the sequence I used, here it is. The 50 percent identity that is so disputed was simply calculated based on the percent identical positions for this 150 base alignment. I used the authors' own data. By the way, nowhere do they report a sequence identity for the region, probably because with poor alignment elsewhere, the percent identity would be considerably lower than 50 percent.
Lastly, I don't know where Torley's computer scientist friend Glenn Williamson got his figures, but they do not match the data reported in the paper. Says Williamson:
About 1,500 base pairs can be aligned with around 73% identity. That's much more than the 150 base pairs that Tomkins chose to focus on. Readers will recall that Tomkins claimed only a 62% identity, even for this short segment. [Emphasis in the original.]
If the alignment was as high as Williamson said over such a long stretch, surely it would have been reported by the authors. It certainly doesn't agree with the figures I have shown from the original paper itself. (See Figure S1 and S2.) The 150 base alignment shown in figure S2, with its 50 percent identity, is the little segment on the left side of VIT1, directly over exon 3 in Figure S1. There is no other alignment around it, let alone 1500 bases with 73 percent identity. I'll leave readers to judge whether Williamson's alignments are valid. But as Torley says, "if you use the wrong gapped parameter then there will be discrepancies."
Now for why I wrote the post. For this you will have to go to Dr. Dennis Venema's post that started it all, and which was mentioned earlier. (I do not think it is under the Creative Commons license so I won't reproduce his figure here.) I want you to compare his "redrawings" of the synteny between humans and chickens in the VIT1, VIT2, and VIT3 genes to the actual data reported in Brawand et al.'s paper. Does Venema's redrawing strike you as an exaggeration of the synteny for VIT1, as it did me? Compare it to the figures I have shown here from the original paper.
If all people did was to read Venema's post, the synteny would look pretty convincing. That's unfortunate. Those not trained in science will take his post at face value, and be convinced of VIT1 synteny and its status as a former vitellogenin gene. When the original data is examined, it's not nearly as convincing. Scientists have a duty to represent data accurately, even other people's data. Now I may not have access to information Dennis Venema has, so I will give him the benefit of the doubt. But I would be happier if he changed his figures, or revealed his source for any data that didn't come from the paper he cited.
Finally, Torley makes a point about my having commented that the opossum alignment might show synteny better than the human or dog sequence. I didn't discuss it in my post beyond that comment because it wasn't the focus of my argument. I will turn to the discussion of the alignment between opossum and other genomes with the chicken, and the evidence for pseudogenes in another post. I will also answer Torley's question about logical inferences, and offer him my own logical puzzle.
I will deal with his other accusations along the way.
Thanks for sticking with the nitty-gritty analysis, dear readers. It's up to you to decide what you think about human synteny with VIT genes, whether it is strongly or weakly supported by the evidence, and whether we are justified in considering alternate explanations.
Ann Gauger
Well, I must say I didn't expect to be honored by a 7500-word broadside by philosopher Dr. Vincent Torley, assisted by Dr. Josh Swamidass, Assistant Professor at Washington University. I guess they must have a lot of spare time. The reason for the post at Uncommon Descent? Both hold common descent to be absolutely, incontrovertibly, obviously true, and they apparently wish I would fall into line and stop embarrassing them by doubting common descent. They wish I would give up my "peculiar kind of intellectual obstinacy."
The argument is in the end all about common descent. (There are a few accusations of poor reasoning, obscuring the issue, and even a little bad faith along the way.) Look, intelligent design is not wedded to common descent. Neither is it wedded to a denial of common descent. Intelligent design states that there is evidence of design in the universe. I think we are in agreement on this point. In terms of biology, how the designer instantiated that design is still subject to debate, based on the strength of the evidence for each position.
As a biologist, I see evidence on both sides of the debate. The evidence is equivocal -- hence the fact that ID advocates take different positions on the subject. Yet common descent -- the idea that organisms descend from one or a few common ancestors -- is treated like a sacred cow by many scientists, and even, it appears, by some philosophers. Indignation arises that anyone would doubt it, would even have questions. Scientists take common descent as axiomatic, and accept evidence that is itself interpreted through a lens of common descent as proof of common descent. As a consequence, any evidence against common descent meets opposition and is explained away.
So when I see weak evidence for common descent I say so, as I did in a post here, "The Vitellogenin Pseudogene Story: Unequally Yolked." (Apparently Dr. Torley caught the reference but missed the yolk, as he repeatedly misstates my post's subtitle as "Unequally Yoked.") I wrote the aforementioned post because of weak evidence, and even an overstatement of the evidence by some.
The controversy began with the post on vitellogenin synteny, "Vitellogenin and Common Ancestry: Reading Tomkins," by Professor Dennis Venema at Trinity Western University, where I read some interesting arguments regarding cross-species synteny in the region of the chicken vitellogenin genes. Synteny is the term for the shared arrangement of genes along chromosomes from different organisms, and its existence is taken as evidence for common descent. Vitellogenins are egg yolk proteins, present and used in egg-laying organisms.
I followed up by reading the paper "Loss of Egg Yolk Genes in Mammals and the Origin of Lactation and Placentation," by David Brawand, Walter Wahli, and Henrik Kaessmann, on which Venema's post was based. (It's free access. You can verify all this yourself.) It's always a good idea to read the original material and evaluate the evidence for yourself. What I saw in Brawand et al. is what prompted me to write my post.
My dispute with Torley (and Venema) is at bottom a dispute about the scientific interpretation of data, or should be. Therefore I am going to go through the data in some detail, to show why I reached the conclusions I did with regard to the human "VIT1" pseudogene, and where we differ in interpretations. This essentially covers Torley's points 1 and 2. I will address the points 3-7 in later posts, so as not to burden the reader with excess length.
There are three chicken egg yolk genes, VIT1, VIT2, and VIT3, all expressed and made into protein because chickens lay eggs. The Brawand paper set out to see if there was any evidence for a vitellogenin presence in the human genome, with the idea that we are descended from an egg-laying animal. They looked in the region of our chromosome that is analogous to the chicken genome, and aligned the two against each other. A dotplot from the Brawand paper (see below) shows where the human (Y axis) and chicken (X axis) DNA sequences align. A perfect alignment (for example if human sequence was aligned against human) should show a diagonal solid line.
All figures taken from Brawand, D., Wali, W., and Kaessmann, H. 2008. Loss of Egg Yolk Genes in Mammals and the Origin of Lactation and Placentation. PLoS Biology (6) 507-517. Creative Commons license.
The top panel illustrates the VIT1 alignment between the two sequences, chicken and human, and the bottom panel VIT2 and VIT3. Black dots show where sequence similarity exists. The colored stripes indicate coding sequences (exons) for each "gene." In between in the white regions are the non-coding introns and intergenic spaces (sequences between genes). ELDT1, FP, SSX2IP, and CTBS are functional genes in both human and chicken and show sequence similarity and synteny in all coding sequences (the yellow stripes). Even some intergenic spaces show evidence of synteny. Where the synteny disappears is where the VIT1, VIT2, and VIT3 coding sequences should be.
I found the VIT1, VIT2, and VIT3 alignments to be ambiguous at best. However, in the supplemental materials for the Brawand paper is another representation of the syntenic regions where the human VIT1, VIT2, and VIT3 remnants should be. That makes things clearer. It is reproduced below, but click on the image to see the figure properly:
The bars colored red and black represent the chicken VIT genes, showing only their exons (the parts of the gene that contribute to making protein), alternating as red and black segments along the VIT sequences. (There are 35 exons in VIT1 and 2, 36 exons in VIT3.) Above each bar and running parallel to it are thin red lines, indicating where similarity has been detected, with insertions, deletions and stop codons necessary to make the sequence line up also indicated. To find this alignment they used "highly sensitive similarity search algorithms," and ran repeated trials. From the paper:
The best scoring alignment chain was determined from the 2,000 best local alignments for each VIT region using dynamic programming. Importantly, the combined alignments of VIT coding sequences of the best chain for each of the opossum VIT1-VIT3 regions (aligned to chicken) showed significantly higher alignment scores than the genomic background (introns and intergenic regions) in the chain, as assessed by a Mann-Whitney U test (P < 0.05). This suggests that the obtained (pseudogenic) VIT remnants from opossum are nonrandom sequence matches and represent true VIT sequences. In the eutherian [human and dog] comparison, VIT1 coding sequences showed significantly higher scores than the genomic background [reported as P < 0.05 elsewhere] (the alignable regions for the other two VIT genes may be too short to provide statistical significance -- VIT3 -- or represent spurious matches -- VIT2). [Emphasis added.]
There was very little actual sequence alignment data given for the human syntenic regions, just the 150 base sequence from exon 3 that I mentioned in my post. Since I was asked to provide the source of my analysis, here is it, as obtained in the paper in a supplementary figure; again, click on the image to see it better:
Full disclosure: this is the best-reported evidence they have for human synteny. The rest is unconvincing to me, though it may be convincing to others. Surely if they had a better or more extensive alignment they would have reported it. This by the way, I would assume is the stretch of DNA used by Jeff Tomkins in his analysis of the region.
Now for a general comment regarding the accusation of faulty statistics made against me by Torley and Swamidass. Here is the segment from Torley's post:
Professor Swamidass has two comments which are germane here. First, he points out that as a matter of standard practice, the data relating to similarity in the paper by Brawand et al. should be considered correct, unless proven otherwise. If Dr. Gauger thinks that the authors' claims of similarity are doubtful, then I would invite her to show the exact DNA sequence she used, so that interested readers can perform a BLAST by themselves (there is a website for this), to verify both the match to the vitellogenin chicken gene and to the human sequence. This doesn't resolve the issue of picking the right DNA sequence, but it is a start. Selecting the right parameters is important, too: if you use the wrong gapped parameter (a mistake Tomkins is notorious for making), then there will be discrepancies. [Emphasis added.]
I do not question the authors' data, but I do question their interpretation that it proves there is a VIT1 pseudogene in humans. Actually to be fair, they merely suggest it as evidence. They do not go much further than what I have quoted above: they point out a few deletions held in common by dogs, humans, and armadillo in the 150 base sequence I show above, arguing that they all share common ancestry. The bulk of the paper is about the remnants of opossum and platypus vitellogenin genes, perhaps because they recognize that the evidence is weak for dogs (for which they report no analysis I could find) and humans.
About the data being correct and my questioning it: All scientists are (or should be) taught in graduate school to critically evaluate conclusions. That is not the same as questioning original data, which I do not do. Questioning conclusions, evaluating them carefully to see if they are warranted, is something all scientists should do.
Again, I based my analysis on the data reported in the paper; I did not question the underlying data. The 150 base sequence I talked about was available as a supplementary figure in the paper itself, and I have already shown it to you. Careful reading of Brawand et al. would have revealed it -- it is the only sequence reported for human alignments. But since I am asked to provide the sequence I used, here it is. The 50 percent identity that is so disputed was simply calculated based on the percent identical positions for this 150 base alignment. I used the authors' own data. By the way, nowhere do they report a sequence identity for the region, probably because with poor alignment elsewhere, the percent identity would be considerably lower than 50 percent.
Lastly, I don't know where Torley's computer scientist friend Glenn Williamson got his figures, but they do not match the data reported in the paper. Says Williamson:
About 1,500 base pairs can be aligned with around 73% identity. That's much more than the 150 base pairs that Tomkins chose to focus on. Readers will recall that Tomkins claimed only a 62% identity, even for this short segment. [Emphasis in the original.]
If the alignment was as high as Williamson said over such a long stretch, surely it would have been reported by the authors. It certainly doesn't agree with the figures I have shown from the original paper itself. (See Figure S1 and S2.) The 150 base alignment shown in figure S2, with its 50 percent identity, is the little segment on the left side of VIT1, directly over exon 3 in Figure S1. There is no other alignment around it, let alone 1500 bases with 73 percent identity. I'll leave readers to judge whether Williamson's alignments are valid. But as Torley says, "if you use the wrong gapped parameter then there will be discrepancies."
Now for why I wrote the post. For this you will have to go to Dr. Dennis Venema's post that started it all, and which was mentioned earlier. (I do not think it is under the Creative Commons license so I won't reproduce his figure here.) I want you to compare his "redrawings" of the synteny between humans and chickens in the VIT1, VIT2, and VIT3 genes to the actual data reported in Brawand et al.'s paper. Does Venema's redrawing strike you as an exaggeration of the synteny for VIT1, as it did me? Compare it to the figures I have shown here from the original paper.
If all people did was to read Venema's post, the synteny would look pretty convincing. That's unfortunate. Those not trained in science will take his post at face value, and be convinced of VIT1 synteny and its status as a former vitellogenin gene. When the original data is examined, it's not nearly as convincing. Scientists have a duty to represent data accurately, even other people's data. Now I may not have access to information Dennis Venema has, so I will give him the benefit of the doubt. But I would be happier if he changed his figures, or revealed his source for any data that didn't come from the paper he cited.
Finally, Torley makes a point about my having commented that the opossum alignment might show synteny better than the human or dog sequence. I didn't discuss it in my post beyond that comment because it wasn't the focus of my argument. I will turn to the discussion of the alignment between opossum and other genomes with the chicken, and the evidence for pseudogenes in another post. I will also answer Torley's question about logical inferences, and offer him my own logical puzzle.
I will deal with his other accusations along the way.
Thanks for sticking with the nitty-gritty analysis, dear readers. It's up to you to decide what you think about human synteny with VIT genes, whether it is strongly or weakly supported by the evidence, and whether we are justified in considering alternate explanations.
Too much of a good thing?
Objection to Intelligent Design -- Universe Is Too Big, with Too Much "Wasted Space"
David Klinghoffer
Thoughtful reader Eric points me to a fine article over that The Stream by Tom Gilson, addressing an objection to ID:
We don't know whether anyone is enjoying the view from some other planet. For all we know, we might be the only observers. Whether we are or not, the vastness of it all has led some skeptics to ask, why would God waste so much space on so few living creatures? Is this really a mark of intelligent design? It might surprise you to hear that I like that question, but I do: I enjoy answering it.
One of the better-articulated versions of that question goes like this:
Doesn't the way that 99.99999999% of the universe is absolutely inhospitable to any kind of life show you that it wasn't made for anybody? It is easy to imagine how a universe could have been more intelligently designed, with less wasted space and energy and more hospitality for life.
This objection is formulated by John R. Shook, of the Center for Inquiry, who also teaches philosophy at the University of Buffalo ("The Disappearing God"). Gilson goes on:
First, the "scientific" viewpoint of all this emptiness, when taken in full perspective, makes no strong statement against design. Quite the contrary, actually. I could mention the universe's fine-tuning for life, for one thing. For another, we know now that a large universe is necessary for life, at least according to physics as we understand it.
On that, Gilson cites "the principle of the galactic habitable zone."
[Its] implications include the principle that a certain amount of empty space, but not too much, is essential for life to thrive. (That's admittedly an oversimplification which I make for the sake of space here on the blog, but not, I take it, a distortion.) So it is premature at best to suppose that large amounts of space "inhospitable to any kind of life" really mean that "it wasn't made for anybody."
Second, that idea is not just premature; it's also incredibly short-sighted with respect to who Christians understand God to be. Is God concerned about the waste of energy and space?
Eric adds:
I think there is at least one other point that could be made. How does one recognize when something is rare? We see the extremely unusual state of this privileged planet precisely because it is in stark contrast to a vast inhospitable universe.
And we can see that contrast because we are also unusually suited for observation and scientific discoveries. Our state is both fine-tuned and knowable as fine-tuned.
Contrary to what Dr. Shook imagines, a vast universe is a key component in at least one line of argument for intelligent design. Articulated by Michael Denton and others, this argument points to the unique fitness of the universe and of our planet for upright bipeds like ourselves. The whole thing appears set up for us, and only for us. The vaster the cosmos, the more dramatically that point is underlined.
Denton's current focus is on the fitness of the universe for fire-using creatures like us. See the short documentary Fire-Maker.
What exactly is the size of the universe, as we observe it? Wikipedia says:
The proper distance -- the distance as would be measured at a specific time, including the present -- between Earth and the edge of the observable universe is 46 billion light-years (14 billion parsecs), making the diameter of the observable universe about 91 billion light-years (28×109 pc).
As Evolution News observed yesterday in a biological context, ID critics often end up playing the role of naïve theologian: What they "seem to want is a metric with The Human Body as God Would (or Should) Have Made It at one end of the measuring stick. As Dilley and Nelson have pointed out, contemporary Darwinian evolutionary thinking borrows heavily from theology for its justification." In this case it should be The Universe as God Would (or Should) Have Made It.
I'd want to ask John Shook, is it like going to the mall and looking for a pair of pants with the right waist and inseam measurements? 91 billion light-years is too big to be intelligently designed. Is there a size that would be too small? Just right?
Merely to ask such questions is to see how absurd the contention is that the universe has too much "wasted space."
Darwinism vs. the real world XXXIII
Liver Function and Its Effects
Howard Glicksman
Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News is delighted to offer this series, "The Designed Body." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.
Tim (not his real name) was a hard-working, hard-drinking man who had never stayed attached to anyone. He had contracted viral hepatitis which, combined with his alcohol abuse, had caused him to develop chronic liver disease. He had been hospitalized several times when I first met him at his sister's home after he was placed in hospice care. He was lying in a recliner looking pretty weak with a yellowish tinge to the whites of his eyes and skin. He had marked muscle wasting, scattered scratches and bruises on his arms, and a large belly with swollen red legs. I saw that he was confused and had problems expressing himself, so I turned to his sister and her son to get the history.
They told me that Tim had been declining for the last several weeks and that, although he had stopped drinking a few months ago, each time he came out of hospital he was worse than the last time. Now he needed a lot of help to dress, bathe, and use the bathroom. He could barely stand, even with significant assistance, to pivot and transfer to a wheelchair. He was more prone to confusion and slept most of the time, seemed to be itchy, ate very little and complained of abdominal and leg swelling and pain. When I examined him, not only was he confused and jaundiced, I also found that he had a fever, a quick pulse, and a relatively low blood pressure. I also noted that not only was his abdomen full of fluid but the redness in his swollen legs was due to infection.
His sister brought out the results of some of his recent blood work, which showed a very low serum albumin, elevated bilirubin and ammonia levels, and a moderate delay in his clotting test. I sat down with Tim's sister and nephew to explain the situation and what we might be able to do for him to keep him comfortable.
Next to the brain, the liver is the most versatile organ, performing over five hundred different tasks, and each is important for survival. Since the liver is capable of regeneration and has a large functional reserve, it usually requires a loss of over eighty percent of its cell function for the symptoms and signs of chronic liver disease to manifest. It is the liver that handles the metabolism of carbohydrates, proteins, and fats for the energy and nutrient needs of the body. It produces numerous different proteins for specific tasks and, using enzymes, chemically breaks down drugs, hormones and other substances so the body can maintain control of its chemical environment.
Evolutionary biologists are good at imagining how an ultra-complex organ like the liver could have come into being by talking about how it looks, but not how it actually works within the laws of nature to keep the body alive. But real numbers have real consequences and by using Tim's case to highlight just five of the over five hundred functions of the liver, we will see what would have happened to our earliest ancestors without any one of them. After all, evolutionary biology claims that life came about by chance and laws of nature alone, so it must explain how transitional organisms survived as the liver gradually acquired these vital functions while macroevolution was taking place.
First, the liver helps the body break down red blood cells and, using enzymes, chemically converts hemoglobin into bilirubin. It then takes bilirubin and joins it with cholesterol and other chemicals it produces to form bile. The liver sends the bile into the intestine so it can absorb fats and with it fat-soluble chemicals like vitamin A, for vision, vitamin D, for bones and calcium metabolism, and vitamin K, for clotting, all of which were necessary for our earliest ancestors. Just as we see for Tim, when the liver cells aren't working properly, the bilirubin they produce backs up and moves into the blood, making the bilirubin level rise and causing the whites of the eyes and the skin to turn yellow (jaundiced). People who are jaundiced often feel tired and weak, with a poor appetite and nausea, and may feel itchy.
Second, the liver produces albumin which represents over sixty percent of its entire protein output. One role for albumin is to help transport minerals like calcium and magnesium, fatty acids and other lipids, and steroid hormones like estrogen, progesterone, and testosterone in the blood so they can travel to where they are needed in the body. But one other very important function of albumin is to maintain the blood volume by keeping enough water in circulation. As blood enters the arterial side of the capillary under pressure and moves to the venous side, water is naturally pushed out of the circulation through the pores within the walls of the capillary and into the interstitial fluid, like soft boiled potatoes through a ricer.
Since albumin cannot escape from circulation through the walls of the capillary, it naturally applies an osmotic pull back on the water trying to leave, acting as a counterbalance to the pressure pushing the water out. The degree of osmotic power applied by albumin to pull back on the water trying to escape from circulation is directly related to how much albumin is in the blood. When the liver doesn't produce enough albumin, more water tends to move out of the circulation and into the interstitial fluid, which reduces the blood volume and can cause blood pressure to drop. One of the main causes of Tim's low blood pressure and increased fluid in his abdomen (ascites) and legs (edema) was due to a very low level of albumin in his blood.
Third, besides albumin and other transport proteins, the liver produces most of the clotting factors. Hemostasis is the process by which the body prevents itself from bleeding, something that would have been vital for the survival of our earliest ancestors. Damage to the blood vessel wall triggers the muscles surrounding it to contract and close off the opening as much as possible. It also causes the platelets in the blood passing by to stick together, forming a soft plug to cover the opening and limit blood loss.
But, for many blood vessel injuries, this is not adequate to achieve hemostasis. The clotting factors must swing into action to produce a fibrin clot strong enough to permanently seal the defect, stop the bleeding, and allow healing to take place. When the clotting factors are released from the liver into the blood they are inactive and do not interact with each other unless they encounter a damaged blood vessel. This is very important because if fibrin clots formed within normal blood vessels they could block blood flow and lead to organ damage and death. When the clotting factors encounter a damaged blood vessel, and the platelet plug trying to seal it, this triggers them to interact like dominos to form a fibrin clot in a process called the coagulation cascade. When the liver isn't making enough clotting factors, this makes the body prone to bleed easier as we see with Tim, whose clotting test was prolonged. That was why his arms were bruised due to minimal trauma from scratching.
Fourth, another set of proteins the liver makes is complement which consists of over thirty proteins that, when activated, work together to help the immune cells fight infection. Just like the clotting factors, the complement proteins are inactive when the liver releases them into the blood. Encountering microbial infection triggers them to interact like dominos to aid in the immune defense of the body. They increase inflammation in the area of infection, kill microbes, and attract immune cells to the battlefield and help them attach to microbes so they can literally swallow and destroy them. When the liver isn't working as well as it should, it produces less complement, which along with other factors, makes the body more susceptible to infection. Clinical experience shows that this would have made the survival of our earliest ancestors impossible.
Fifth, another important job for the liver is to convert ammonia, a highly toxic byproduct of protein metabolism, into urea, so it can be released from the body through the kidneys.
This requires five specific enzymes working together in what is called the urea cycle. Elevated blood levels of ammonia are toxic to the nervous system and the absence of any one of these five enzymes would have made life impossible for our earliest ancestors. When the liver isn't working properly, it may allow ammonia, and other toxic substances that it usually metabolizes, escape into the blood, causing a condition called hepatic encephalopathy. In its milder form, this manifests as irritability, poor attention, anxiety, and insomnia. But if the ammonia level rises further, this can progress to imbalance, lethargy, confusion, slurred speech, difficulty swallowing, and be fatal. Returning to Tim, we see that with his confusion, difficulty speaking, and need for lots of assistance, that he is probably showing signs of hepatic encephalopathy.
Having detailed to his sister and nephew what was going on with Tim, I also explained that his leg infection could be responsible for his functional decline and confusion. In other words, if we could treat some of his problems with medications and provide him with good nutrition and support, he may improve and be able to live a little longer. We started him on antibiotics to treat his infection, diuretics to push excess salt and water out of his body and reduce the swelling in his legs and abdomen, and medication to reduce the ammonia level in his blood. Over the next several weeks Tim's condition improved so that he was lucid, had a better appetite, and could be up on his own with a walker. The transformation was remarkable and he became very animated about how he had a "new lease on life."
Tim's nephew was due to go back to college for his pre-med courses in biology and he was perplexed. He believed in neo-Darwinism, and was exposed to the rhetoric that those who don't believe Darwin really don't understand science. But what he had learned about the liver and just five of its vital functions, and what he had seen happen over the last several weeks, gave him pause. He had seen someone who believes in intelligent design prove his knowledge of how science, and life, really works by bringing his uncle back from the brink. I told him that being a physician means having the responsibility to seek out and speak the truth so that those who are vulnerable will not be misled and being humble enough to admit that we don't always have all of the answers, and probably never will.
Howard Glicksman
Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News is delighted to offer this series, "The Designed Body." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.
Tim (not his real name) was a hard-working, hard-drinking man who had never stayed attached to anyone. He had contracted viral hepatitis which, combined with his alcohol abuse, had caused him to develop chronic liver disease. He had been hospitalized several times when I first met him at his sister's home after he was placed in hospice care. He was lying in a recliner looking pretty weak with a yellowish tinge to the whites of his eyes and skin. He had marked muscle wasting, scattered scratches and bruises on his arms, and a large belly with swollen red legs. I saw that he was confused and had problems expressing himself, so I turned to his sister and her son to get the history.
They told me that Tim had been declining for the last several weeks and that, although he had stopped drinking a few months ago, each time he came out of hospital he was worse than the last time. Now he needed a lot of help to dress, bathe, and use the bathroom. He could barely stand, even with significant assistance, to pivot and transfer to a wheelchair. He was more prone to confusion and slept most of the time, seemed to be itchy, ate very little and complained of abdominal and leg swelling and pain. When I examined him, not only was he confused and jaundiced, I also found that he had a fever, a quick pulse, and a relatively low blood pressure. I also noted that not only was his abdomen full of fluid but the redness in his swollen legs was due to infection.
His sister brought out the results of some of his recent blood work, which showed a very low serum albumin, elevated bilirubin and ammonia levels, and a moderate delay in his clotting test. I sat down with Tim's sister and nephew to explain the situation and what we might be able to do for him to keep him comfortable.
Next to the brain, the liver is the most versatile organ, performing over five hundred different tasks, and each is important for survival. Since the liver is capable of regeneration and has a large functional reserve, it usually requires a loss of over eighty percent of its cell function for the symptoms and signs of chronic liver disease to manifest. It is the liver that handles the metabolism of carbohydrates, proteins, and fats for the energy and nutrient needs of the body. It produces numerous different proteins for specific tasks and, using enzymes, chemically breaks down drugs, hormones and other substances so the body can maintain control of its chemical environment.
Evolutionary biologists are good at imagining how an ultra-complex organ like the liver could have come into being by talking about how it looks, but not how it actually works within the laws of nature to keep the body alive. But real numbers have real consequences and by using Tim's case to highlight just five of the over five hundred functions of the liver, we will see what would have happened to our earliest ancestors without any one of them. After all, evolutionary biology claims that life came about by chance and laws of nature alone, so it must explain how transitional organisms survived as the liver gradually acquired these vital functions while macroevolution was taking place.
First, the liver helps the body break down red blood cells and, using enzymes, chemically converts hemoglobin into bilirubin. It then takes bilirubin and joins it with cholesterol and other chemicals it produces to form bile. The liver sends the bile into the intestine so it can absorb fats and with it fat-soluble chemicals like vitamin A, for vision, vitamin D, for bones and calcium metabolism, and vitamin K, for clotting, all of which were necessary for our earliest ancestors. Just as we see for Tim, when the liver cells aren't working properly, the bilirubin they produce backs up and moves into the blood, making the bilirubin level rise and causing the whites of the eyes and the skin to turn yellow (jaundiced). People who are jaundiced often feel tired and weak, with a poor appetite and nausea, and may feel itchy.
Second, the liver produces albumin which represents over sixty percent of its entire protein output. One role for albumin is to help transport minerals like calcium and magnesium, fatty acids and other lipids, and steroid hormones like estrogen, progesterone, and testosterone in the blood so they can travel to where they are needed in the body. But one other very important function of albumin is to maintain the blood volume by keeping enough water in circulation. As blood enters the arterial side of the capillary under pressure and moves to the venous side, water is naturally pushed out of the circulation through the pores within the walls of the capillary and into the interstitial fluid, like soft boiled potatoes through a ricer.
Since albumin cannot escape from circulation through the walls of the capillary, it naturally applies an osmotic pull back on the water trying to leave, acting as a counterbalance to the pressure pushing the water out. The degree of osmotic power applied by albumin to pull back on the water trying to escape from circulation is directly related to how much albumin is in the blood. When the liver doesn't produce enough albumin, more water tends to move out of the circulation and into the interstitial fluid, which reduces the blood volume and can cause blood pressure to drop. One of the main causes of Tim's low blood pressure and increased fluid in his abdomen (ascites) and legs (edema) was due to a very low level of albumin in his blood.
Third, besides albumin and other transport proteins, the liver produces most of the clotting factors. Hemostasis is the process by which the body prevents itself from bleeding, something that would have been vital for the survival of our earliest ancestors. Damage to the blood vessel wall triggers the muscles surrounding it to contract and close off the opening as much as possible. It also causes the platelets in the blood passing by to stick together, forming a soft plug to cover the opening and limit blood loss.
But, for many blood vessel injuries, this is not adequate to achieve hemostasis. The clotting factors must swing into action to produce a fibrin clot strong enough to permanently seal the defect, stop the bleeding, and allow healing to take place. When the clotting factors are released from the liver into the blood they are inactive and do not interact with each other unless they encounter a damaged blood vessel. This is very important because if fibrin clots formed within normal blood vessels they could block blood flow and lead to organ damage and death. When the clotting factors encounter a damaged blood vessel, and the platelet plug trying to seal it, this triggers them to interact like dominos to form a fibrin clot in a process called the coagulation cascade. When the liver isn't making enough clotting factors, this makes the body prone to bleed easier as we see with Tim, whose clotting test was prolonged. That was why his arms were bruised due to minimal trauma from scratching.
Fourth, another set of proteins the liver makes is complement which consists of over thirty proteins that, when activated, work together to help the immune cells fight infection. Just like the clotting factors, the complement proteins are inactive when the liver releases them into the blood. Encountering microbial infection triggers them to interact like dominos to aid in the immune defense of the body. They increase inflammation in the area of infection, kill microbes, and attract immune cells to the battlefield and help them attach to microbes so they can literally swallow and destroy them. When the liver isn't working as well as it should, it produces less complement, which along with other factors, makes the body more susceptible to infection. Clinical experience shows that this would have made the survival of our earliest ancestors impossible.
Fifth, another important job for the liver is to convert ammonia, a highly toxic byproduct of protein metabolism, into urea, so it can be released from the body through the kidneys.
This requires five specific enzymes working together in what is called the urea cycle. Elevated blood levels of ammonia are toxic to the nervous system and the absence of any one of these five enzymes would have made life impossible for our earliest ancestors. When the liver isn't working properly, it may allow ammonia, and other toxic substances that it usually metabolizes, escape into the blood, causing a condition called hepatic encephalopathy. In its milder form, this manifests as irritability, poor attention, anxiety, and insomnia. But if the ammonia level rises further, this can progress to imbalance, lethargy, confusion, slurred speech, difficulty swallowing, and be fatal. Returning to Tim, we see that with his confusion, difficulty speaking, and need for lots of assistance, that he is probably showing signs of hepatic encephalopathy.
Having detailed to his sister and nephew what was going on with Tim, I also explained that his leg infection could be responsible for his functional decline and confusion. In other words, if we could treat some of his problems with medications and provide him with good nutrition and support, he may improve and be able to live a little longer. We started him on antibiotics to treat his infection, diuretics to push excess salt and water out of his body and reduce the swelling in his legs and abdomen, and medication to reduce the ammonia level in his blood. Over the next several weeks Tim's condition improved so that he was lucid, had a better appetite, and could be up on his own with a walker. The transformation was remarkable and he became very animated about how he had a "new lease on life."
Tim's nephew was due to go back to college for his pre-med courses in biology and he was perplexed. He believed in neo-Darwinism, and was exposed to the rhetoric that those who don't believe Darwin really don't understand science. But what he had learned about the liver and just five of its vital functions, and what he had seen happen over the last several weeks, gave him pause. He had seen someone who believes in intelligent design prove his knowledge of how science, and life, really works by bringing his uncle back from the brink. I told him that being a physician means having the responsibility to seek out and speak the truth so that those who are vulnerable will not be misled and being humble enough to admit that we don't always have all of the answers, and probably never will.
It was just a matter of time.
Oregon court allows resident to change sex from female to nonbinary
Faith Karimi and Dani Stewart, CNN
regon resident Jamie Shupe, who identifies as neither male nor female, can legally be considered nonbinary, a judge ruled.
In what legal experts believe is the state's first such ruling, Judge Amy Holmes Hehn ruled Friday that Shupe's sex has been changed from female to nonbinary.
READ: One transgender woman's long road to finding herself
"It feels amazing to be free from a binary sex classification system that inadequately addressed who I really am, a system in which I felt confined," the Portland resident said.
The Army veteran was assigned the gender of male at birth, but Shupe started transitioning to a female in 2013, more than a decade after leaving the military, according to The Oregonian newspaper.
Shupe said male or female titles didn't seem fitting, and preferred to use the first name, Jamie, instead of a pronoun. In April, Shupe filed a petition for a gender change.
"Oregon law has allowed for people to petition a court for a gender change for years, but the law doesn't specify that it has to be either male or female," said civil rights attorney Lake J. Perriguey, who filed the petition.
"The law just says, 'change.' Historically, people have asked for a gender change from male to female and the other way around, but Jamie is the first to ask for the gender of "nonbinary," Perriguey, said.
The lawyer said the standard form provided by the court clerk listed only male or female as options, so he inserted "nonbinary."
Their wish was granted Friday.
The judge said she has determined Shupe underwent surgical, hormonal or other treatment for the purpose of gender transition.
"The sexual reassignment has been completed," the judge wrote in the ruling. "No person has shown cause why the requested general judgment should not be granted."
Faith Karimi and Dani Stewart, CNN
regon resident Jamie Shupe, who identifies as neither male nor female, can legally be considered nonbinary, a judge ruled.
In what legal experts believe is the state's first such ruling, Judge Amy Holmes Hehn ruled Friday that Shupe's sex has been changed from female to nonbinary.
READ: One transgender woman's long road to finding herself
"It feels amazing to be free from a binary sex classification system that inadequately addressed who I really am, a system in which I felt confined," the Portland resident said.
The Army veteran was assigned the gender of male at birth, but Shupe started transitioning to a female in 2013, more than a decade after leaving the military, according to The Oregonian newspaper.
Shupe said male or female titles didn't seem fitting, and preferred to use the first name, Jamie, instead of a pronoun. In April, Shupe filed a petition for a gender change.
"Oregon law has allowed for people to petition a court for a gender change for years, but the law doesn't specify that it has to be either male or female," said civil rights attorney Lake J. Perriguey, who filed the petition.
"The law just says, 'change.' Historically, people have asked for a gender change from male to female and the other way around, but Jamie is the first to ask for the gender of "nonbinary," Perriguey, said.
The lawyer said the standard form provided by the court clerk listed only male or female as options, so he inserted "nonbinary."
Their wish was granted Friday.
The judge said she has determined Shupe underwent surgical, hormonal or other treatment for the purpose of gender transition.
"The sexual reassignment has been completed," the judge wrote in the ruling. "No person has shown cause why the requested general judgment should not be granted."
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