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Friday, 15 July 2016

Spiders in the dock for design.

Spiders Have Eight (Well-Designed) Eyes
Evolution News & Views

Have you ever wanted eyes in the back of your head? Spiders have eight eyes, compared to our two. They can boast of better vision than ours on some counts; sharp, color vision that extends into the ultraviolet. Their ample set of peepers allows for division of labor: the main pair in front helps them see detail, while the smaller eyes wrapped around their heads warn them of looming threats. Stephanie Pappas wrote about spider eyes on Live Science recently.

"We see that division of labor within that visual system... That's pretty cool if you think about it, because we only have one pair of eyes."
That was actually a quote from Skye Long, a doctoral student at the University of Massachusetts at Amherst, who decided to test and find out what the extra eyes are for. She outfitted an enclosure for her 46 jumping spider subjects and used paint to "blindfold" the principal eyes on a third of them, and the adjacent, smaller eyes (anterior lateral pair) on another third, leaving one third blindfold-free. (Don't worry about the spiders; the paint could be easily removed.)
Then she used an iPod Touch to create images of a black dot growing or shrinking in size. When seeing the "looming threat," the spiders backed up quickly and raised their front legs in defense, as if they felt scared -- even when the principal eyes were covered. This means the anterior lateral pair are crucial for alerting the spider to potential dangers. What are the other four eyes used for? That's what Long wants to find out next.

This would have been a "pretty cool" Halloween animal story, featuring a nice, experimental science project, had not Skye Long wandered off into evolutionary tale-telling:

That means the secondary eyes are crucial for alerting the spider to dangerous motion, Long said. Spider eyes are a "really cool step in evolution," she added; insects have compound eyes with multiple lenses, and some areas of those eyes have certain functions. Spiders, on the other hand, separate out visual functions across their heads.
"This is a different pathway that evolution has taken to allow a very small animal to have a very extensive visual system," Long said.

Right. No matter how cool or well-designed the adaption, just say it evolved. It's a "really cool step in evolution." It's a "different pathway evolution has taken." The blind, aimless, purposeless process of natural selection gave spiders a "very extensive visual system." Turn in your paper and get an A.
Here's a better way. Look what researchers at the Optical Society of America are doing with spiders. Incredible as it sounds, they are taking spider silk and using it for fiber optics. Spider silk is already prized as an ideal material: it's strong, flexible, and biodegradable. Now, a team has found it can also transmit and guide light almost as well as glass fibers.

One team is using it as a light guide in photonic chips, while another is trying to imitate the proteins in silk from spiders and silkworms to be able to manufacture it. This second team has already made a silk-based "plastic" that can be used for everything from biodegradable cups to implantable devices that dissolve in the body. Fiorenzo Omenetto presented his work in a superb TED Talk that raised the audience to their feet without him once mentioning evolution. And he is getting grants from the NSF!


Evolution is a straw scarecrow whenever it appears in biological research. The whole story is intelligent design, in the animals and plants studied, in the experiments devised to gain knowledge about them, and in the applications they lead to. Animal tricks become science's treats.

The winged flocks v Darwin.

Starling Murmurations and Intelligent Design, Revisited
David Klinghoffer




A friend points out the bit of nice news that one of our favorite nature video clips, "‪Dylan Winter and the Starling Murmurations," from the Illustra film Flight: The Genius of Birds, has exceeded a million views on YouTube. Not bad. That's a million plus people exposed to one of the most remarkable demonstrations of the wonders of bird flight.

All those viewers may not know precisely how starling murmurations give evidence of intelligent design. We've discussed this in the past:

"Why Starling Murmurations Suggest Intelligent Design"

"'Not By Chance': Drone Engineers Try the Starling Trick"

"Fly Now; Swim Later"

As Dr. Timothy Standish explained, here in a nutshell is the challenge posed by starling murmurations to traditional evolutionary thinking:

In the cold hard world of survival of the fittest, starlings that stick with the group may enhance their odds of surviving predation. But such an effect is an emergent property of the murmuration. Attributing the origin of murmurations to enhanced survival requires first that murmurations exist, thus making for a circular argument. To circumvent this problem, a Darwinist might invoke cooption. Maybe the ancestors of modern starlings gathered together for some other practical purpose and then, in a lucky coincidence, gained the survival advantage provided by murmurations. But think about the resources consumed by daily migrations followed by considerable time flying about with other starlings. It's unclear why any other proposed reason for investing resources this way would not be equally vulnerable to the criticism of circularity.

Flying in formation has advantages that humans quickly recognized once we mastered powered flight. The most obvious of these involves multiple sets of eyes looking out for enemies or obstacles. If human intelligence can figure this out, perhaps clever starlings can as well. But if there is a genetic component to the behavior -- a reasonable assumption given that starlings form murmurations wherever they are in the world while other birds do not -- then a mechanism for creating the required genetic changes would need to anticipate the need fulfilled by murmurations. Darwinian evolution is blind and unguided, incapable by definition of anticipating anything. In the case of human flight, various types of formation flying were developed in anticipation of a need. Generally that was to survive during battles in the air. Formation flying is not something that pilots stumbled upon in the middle of a dogfight then stuck with; it is a solution to an anticipated need. Intelligence alone has been shown to have produced such solutions.


When it comes to design and murmurations, the elephant in the room is the other abilities birds must possess to achieve the phenomenon. They must have the inclination to fly long distances and to congregate. They must have the ability to navigate, the ability to fly, the ability to perceive and react to the other birds they are flying with, and any number of other wonders. Most people, scientists or not, can see this; but Darwinism demands that we turn a blind eye to such things.

The undeniable logic of the case for design.

Wednesday, 13 July 2016

File under 'well said' XXXI

Vague and mysterious forms of speech, and abuse of language, have so long passed for mysteries of science; and hard or misapplied words with little or no meaning have, by prescription, such a right to be mistaken for deep learning and height of speculation, that it will not be easy to persuade either those who speak or those who hear them, that they are but the covers of ignorance and hindrance of true knowledge.
John Locke

Demythifying peer review.

For Critics of Intelligent Design, There's No Hiding Behind Claims of "Peer Review" Anymore
David Klinghoffer


Darwinists have had to back off considerably from the once-confident assertion that peer review in science journals constitutes, as Jerry Coyne put it in 2005 inThe New Republic, the "gold standard for modern scientific achievement." The whole institution of peer review is so besmirched now as to arouse, not even amusement anymore, but something more like pity.

In the same article, Coyne maintained that it was precisely by "By that standard" that advocates of the theory of intelligent design "have failed miserably." You mean by the standard of what is now revealed as the intellectual and scientific equivalent of insider trading? Or more like racketeering and simple fraud.

The existence of a blog like  Retraction Watch  is, in this respect, a sign of the times, a measure of the extent to which science publishing has fallen into derision. Their post from a couple of days ago, on a "peer review and citation ring at the Journal of Vibration and Control," has been widely reported, including the retraction of 60 papers from that journal. Sixty!

"This one deserves a 'wow,'" observes author Ivan Oransky. Indeed. The cat is really out of the bag.

Slate:

It may not be entirely fair to liken a "peer review and citation ring" to the academic version of an extortion ring, but there's certainly fraud involved in both. Retraction Watch, a blog dedicated to chronicling which academic papers have been withdrawn, is reporting that SAGE Publishing, a group that puts out numerous peer-reviewed journals, is retracting 60 papers from its Journal of Vibration and Control after an internal investigation uncovered extensive evidence of severe peer-review fraud.

Apparently researcher Peter Chen, formerly of National Pingtung University of Education in Taiwan, made multiple submission and reviewer accounts -- possibly along with other researchers at his institution or elsewhere -- so that he could influence the peer review system. When Chen or someone else from the ring submitted a paper, the group could manipulate who reviewed the research, and on at least one occasion Chen served as his own reviewer.

The Washington Post:

Now comes word of a journal retracting 60 articles at once.

The reason for the mass retraction is mind-blowing: A "peer review and citation ring" was apparently rigging the review process to get articles published.

You've heard of prostitution rings, gambling rings and extortion rings. Now there's a "peer review ring."

The publication is the Journal of Vibration and Control (JVC). It publishes papers with names like "Hydraulic enginge mounts: a survey" and "Reduction of wheel force variations with magnetorheological devices."

The Guardian:

An academic journal has retracted dozens of articles and apologised to readers after falling victim to what it described as a "peer review ring" that appears to have involved more than 100 bogus scholars.

The Journal of Vibration and Control (JVC), a leading publication in the field of acoustics, said it was withdrawing 60 papers published in print and online over the past four years, after discovering that articles were being approved and cited by academics with "assumed and fabricated identities".

The journal's publisher, Sage, said in a statement that the ring appeared to centre around Peter Chen, a researcher formerly of National Pingtung University of Education, in Taiwan. Chen provided an "unsatisfactory response" when confronted, and has since resigned from his post.

Oh, it's just one unfortunate lapse, you say, not representative of anything much beyond itself? If you want to comfort yourself with that idea, first try following the reporting at Retraction Watch, which commonly posts two or three accounts of scholarly fraud and slipshod science per day.

With respect to what this means for the theory of ID, go back and read Casey Luskin's post, "Intelligent Design Is Peer-Reviewed, but Is Peer-Review a Requirement of Good Science" Casey concludes:

Despite the attempted lockout, ID proponents have published their ideas in peer-reviewed scientific journals. This shows that ID has academic legitimacy whether or not one applies the dubious "peer-review" test of good science.

That's right. Going forward, if you want to argue against ID, you are going to have to actually argue against it, critically analyze its arguments and its evidence, as opponents of ID so commonly refuse to do. There's no hiding behind claims of "peer review" anymore.

Monday, 4 July 2016

Darwin of the gaps just so stories re junk DNA becomoing harder to sell

Junk DNA: Is Preventing Breast Cancer a Function?
Evolution News & Views February 6, 2016 4:33 AM 

Each time a function is found for a piece of non-coding DNA, the "junk DNA" myth gets more mythological. Here's a function that has been revealed for a certain long, non-coding transcript of DNA into RNA (lncRNA). It helps prevent breast cancer and ovarian cancer.

Researchers at the University of Bath explain why it is difficult to find these functions for non-coding parts of the genome:

The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.

In recent years it has become apparent that a lot of this non-coding DNA is actually transcribed into non-coding RNA. However, there is still a debate as to whether non-coding RNA is just 'noise' or whether it serves any function in the cell.

Part of the reason for this uncertainty is that it is very difficult to knock-out non-coding RNA without damaging the DNA, which can lead to off-target effects and false results.

They are clearly aware of the "debate" about junk DNA and the results of ENCODE that found that the majority of the genome is actually transcribed (they referenced ENCODE in the paper). As we have reported often, some members of the evolution side of the debate expect most of the DNA is junk. The design side expects that much of it (but not necessarily all) is functional. Thanks to this research, we have a new case that may point the way to future discoveries.

The news release is titled, "'Junk' DNA plays role in preventing breast cancer." It's based on an open-access paper in Nature Communications. Most readers scanning the paper will see what researchers are up against. Discussion of the complex interactions of parts -- lncRNAs transcripts, small interfering RNAs (siRNAs), promoters, exons, introns, alleles, interference in cis and trans and all the rest -- gets into the technical weeds fast. Thankfully, the release simplifies the essence of the finding. Basically, a piece of non-coding DNA "keeps cells healthy" by preventing a genetic "switch" from getting stuck.

Dr Adele Murrell, from the University of Bath's Department of Biology & Biochemistry, led the study. She explained: "The number of cells in our body are balanced by the level at which cells replicate and replace the ones that die. Sometimes the switches that control this growth get stuck in the 'on' position, which can lead to cancer.

"As the tumour grows and the cancer cells get crowded, they start to break away from the tumour, change shape and are able to burrow through tissues to the bloodstream where they migrate to other parts of the body, which is how the cancer spreads. This process is called metastasis and requires a whole network of genes to regulate the transformation of cell shape and mobilisation.

Dr Lovorka Stojic, from Cancer Research UK Cambridge Institute, the first author of this work identified that GNG12-AS1, a strand of non-coding RNA, prevents the growth switch getting stuck and suppresses metastasis. The specific genomic region where this non-coding RNA is located often gets damaged in breast cancer patients -- this control is removed and the cancer cells spread.

The researchers found that the lncRNA GNG12-AS1 acts as a molecular "rheostat" (their term) that controls the expression of an adjacent gene, DIRAS3, a tumor suppressor. It does it by two mechanisms. One is by regulating the number of transcripts of the tumor suppressor. But if that gets out of control, it can even suppress the "network of genes that prepare cells to change their shape and prepare for metastasis."

By experimentally reducing the amount of GNG12-AS1 produced, either by preventing its transcription or destroying the transcripts, they found that cells start becoming cancerous. This explains why in cancer patients, the switch is stuck:

DIRAS3 is downregulated in 70% of breast and ovarian cancer, and its loss of expression correlates with cancer progression and metastasis. The mechanism responsible for DIRAS3 downregulation to date involves different epigenetic mechanisms and loss of heterozygosity. We hypothesized that TI [transcriptional interference] by GNG12-AS1 could represent an additional layer of regulating DIRAS3 dosage.

The interactions are far more complex than can be described here. Suffice it to say that this long non-coding RNA, which would have been considered "junk" previously, plays a crucial role in regulating the amount of an important tumor suppressor gene. It's a "stable lncRNA localized in the nucleus" with a half-life of 20 to 25 hours, meaning it needs to be transcribed often. Other processes regulate the amount of the lncRNA in a very complex choreography of enhancers, suppressors, and feedback loops. Levels of expression also vary depending on the tissue involved.

It has become increasingly clear that non-coding parts of the genome play vital roles in regulating the coding parts. Regulation is an important function. A system that generates parts without regard to the amount needed is a system out of control. How cool is it to find a code that codes for products that regulate the amount of products in other parts of the code? Not only do we see function emerging for the non-coding regions, we see design on a more colossal scale than anyone could have imagined.

The University of Bath is an internationally recognized center of excellence in biological research. It's encouraging to see their biologists actively challenging the "junk DNA" myth:

Dr Kat Arney, science communication manager at Cancer Research UK, said: "Only a tiny fraction of our DNA contains actual genes, and we know that at least some of the bits in between -- often dismissed as 'junk' -- play important roles in controlling how genes get switched on and off at the right time and in the right place.

When the Human Genome project found that only 2 percent of the genome coded for proteins, the right question should have been, "What is all the rest doing?" Some evolutionists were too quick to dismiss it as a pile of useless leftovers from time and chance. Cancer patients around the world can be grateful that these researchers didn't buy that explanation, but looked beyond the unknown for greater understanding.

"Research like this is helping is to unpick the precise details about how these regions work, shedding light on their potential role in the development [or prevention] of cancer and pointing towards new approaches for tackling the disease."


If a system works, it's not happening by accident. That's the intelligent-design spirit that promises to shed more light into the genomic black box.

21st century divination.

 


Saturday, 2 July 2016

Darwinism Vs.The real world.XXXVII

Puberty, Maturation, and Fertility: The Role of Information in Human Sexuality
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.

The word sex comes from the Latin secare which means to separate or divide. Most one-celled organisms form offspring through asexual reproduction. It is asexual because there is no separation of genetic material. Therefore divided chromosomes do not need to be brought together and the new life produced is genetically identical to the original.

In contrast, most multi-cellular organisms form offspring in a much more complicated way called sexual reproduction. In humans, each of the chromosomes making up the 23 pairs containing the genetic material for life is separated from its partner and placed into gametes called male sperm and female eggs. Human reproduction involves sexual intercourse in which the male deposits sperm in the vagina of the female so they can move into the uterus and one of them can join its separated 23 chromosomes to the ones within the female egg in a process called fertilization. The fertilization of the female egg by the male sperm results in a one-celled zygote which then contains the full complement of genetic material and is distinct from its parents.

As difficult as it may be for evolutionary biologists to explain the blind and unguided development of the different organ systems and the body's ability to control them, because of the mechanism humans must use for reproduction they must also explain the simultaneous development of both males and females since neither is of any use to propagate the species without the other.

The three things needed for a human to reproduce are: (1) either be male or female and have all of the right sexual parts, (2) be able to produce enough sperm or release an egg into a fallopian tube, and (3) be able to participate in sexual intercourse so sperm is released into the vagina or have a clear path for sperm to swim toward the fallopian tubes.

In my last article, I showed that for the first few weeks of life the human embryo is asexual. That is because the primordial gonads have not declared themselves to be testes or ovaries yet. Notwithstanding where the embryonic structures that develop into mature sexual organs came from, the human embryo is destined to become female by default unless acted upon by specific chemicals. These include the Testis Determining Factor (TDF) (usually found on the Y chromosome), the enzymes needed to convert cholesterol into testosterone and testosterone into dihydrotestosterone, the androgen receptor on the Wolffian ducts and the tissue that will become male external genitalia, Anti-Mullerian Hormone (AMH) and the AMH receptor on the Mullerian ducts.

If all of these chemicals are present and working properly the human embryo will usually develop into a normal male. But if the TDF is absent it will usually develop into a normal female. However, if the TDF is present, directing the primordial gonads to become testosterone-producing testes, but the androgen receptor is absent or defective (Complete Androgen Insensitivity Syndrome (CAIS)), the result in an XY female. XY females occur in about one in twenty thousand "male" births and have testes instead of ovaries, no genital duct system and female external genitalia. So for the first decade of life they look like normal little girls. However, experience teaches that although humans are sexually differentiated as male or female at birth, they are not able to reproduce. Most children begin to show signs of their sexual development to come by the end of the first decade. Over the following years they will undergo sexual and bodily development in a process called puberty. Puberty is a constellation of physiological changes that, except in, for example, XY females, not only enables human beings to reproduce but also prepares them for their natural role in the family. Let's consider how this happens.

The hypothalamus and pituitary work to control many different vital hormones in the body. For example, the hypothalamus secretes Growth Hormone-Releasing Hormone, which stimulates the pituitary to release Growth Hormone (GH). As its name implies, GH is very important in the overall growth and development of the body. The hypothalamus also sends out Thyrotropin-Releasing Hormone (TRH), which tells the pituitary to send out Thyroid Stimulating Hormone (TSH). It is TSH that controls the production of thyroid hormone from the thyroid gland, which mainly affects the body's metabolic rate. Furthermore, the hypothalamus sends out Corticotropin-Releasing Hormone, which tells the pituitary to send out Adrenocorticotropin Hormone (ACTH). ACTH stimulates the adrenal glands to produce cortisol, another hormone that is important in the body's metabolism, in addition to androgenic hormones.

The hypothalamus and pituitary together control the production of a hormone such as thyroid hormone, or others, through a process called feedback inhibition. For example, the hypothalamus and the pituitary have specific receptors that allow them to sense the blood level of thyroid hormone. If it rises above what is needed the hypothalamus reduces its output of TRH and the pituitary lowers its output of TSH. The feedback of the thyroid hormone level in the blood serves to inhibit the release of TRH and TSH to maintain control of the blood level of thyroid hormone.

The production of the sex hormones is regulated in the same way by the hypothalamus and the pituitary. The hypothalamus secretes Gonadotropin-Releasing Hormone (GnRH) which attaches to specific receptors on certain cells in the pituitary and tells them to send out the gonadotropins, Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH). It is FSH and LH that attach to specific receptors on the testes or the ovaries to produce the sex hormones, testosterone and estrogen, respectively.

In the first decade of life it appears that the hypothalamus and the pituitary are very sensitive to the feedback inhibition of the sex hormones. This means that prior to puberty, very low levels of testosterone and estrogen are able to prevent the hypothalamus from releasing its GnRH and the pituitary its FSH and LH. This results in the blood levels of testosterone and estrogen being very low prior to puberty.

A few years before puberty the adrenals increase their output of androgenic hormones which causes a small growth spurt and the development of pubic and axillary hair. What actually triggers the beginning of puberty is, as yet, poorly understood. However, what is known to happen is that the hypothalamus and pituitary start to become progressively less sensitive to the sex hormones. The gradually diminishing feedback inhibition of the sex hormones on the hypothalamus and pituitary results in their slowly increasing their output of GnRH and the gonadotropins, FSH and LH, respectively. By the time puberty is in full swing, the levels of gonadotropins and the sex hormones have risen significantly.

During male puberty, more FSH and LH attach to specific receptors in the testes and cause an increase in testosterone production, while at the same time giving them the ability to produce sperm. Puberty in the male also results in the progressive increase and coarsening of facial, chest, axillary, abdominal, extremity, and pubic hair, with enlargement of the vocal cords and deepening of the voice. Moreover, with the associated increase in the pituitary output of Growth Hormone (GH), the male experiences a significant linear growth spurt and the development of his musculoskeletal system as well. Furthermore, along with the capacity for sperm production, puberty brings on enlargement of the penis, scrotum, and testes. Finally, testosterone not only plays a major role in sexual differentiation, development, and maturation, but also in the desire for sexual relations. In addition, testosterone is important in giving the male the ability to maintain an erection for adequate penetration into the vagina and ejaculation during sexual intercourse. All these developments prepare the boy to become a man and later a father.

During puberty in the female, more FSH and LH attach to specific receptors in the ovaries and cause an increase in estrogen production while at the same time giving them the ability to develop an egg. Puberty in the female results in an increase in mainly pubic and axillary hair that is not as coarse as in the male. Moreover, breast development takes place so that the potential mother will be able to provide breast milk for her infant. In addition, an increase in Growth Hormone (GH) results in a significant linear growth spurt and development of her musculoskeletal system as well. Puberty also brings on enlargement of the external genitalia and increased mucous production within the vagina and uterus. Finally, along with the capacity for egg development, the increase in FSH, LH, and estrogen allows for ovulation, where the egg is released and can enter the fallopian tube.

Inside the fallopian tube the egg can meet and join with the sperm, which has been deposited into the vagina by the male during sexual intercourse, to form new human life. After ovulation, the ovaries mainly secrete the pregnancy hormone called progesterone. The estrogen before ovulation, and the progesterone after ovulation, attach to specific receptors in the lining of the uterus to make it thicken up and produce more mucous helping it to prepare for pregnancy. If a pregnancy does not take place, the gonadotropins (FSH, LH) and the female sex hormone levels (estrogen, progesterone) drop precipitously to cause the lining of the uterus to shed in the process called menstruation. The first menstrual period generally marks the beginning of female fertility and usually takes place on a monthly basis for the next thirty or forty years.

All these developments prepare the girl to become a woman and later a mother. However, during puberty an XY female will develop normal breasts and in every way look like a normally maturing woman, except when she fails to menstruate. Investigation will then uncover her as yet unknown (even to her) secret.

Remember that an XY female has Complete Androgen Insensitivity Syndrome (CAIS). In this case, the testes form testosterone, but since the androgen receptors are absent or not working, the Wolffian ducts degenerate and the external genitalia become female. However, in addition to testosterone the testes also produce Anti-Mullerian Hormone (AMH), which attaches to specific AMH receptors on the Mullerian ducts and makes them degenerate as well. So the XY female has neither a male nor female genital duct system and her vagina ends in a blind pouch. If an XY female has testes instead of ovaries how can she develop breasts during puberty?

The answer lies in the fact that breast development does not, per se, depend only on estrogen but rather the ratio between estrogen and testosterone. Since during puberty the normal XY male produces lots of testosterone and relatively small amounts of estrogen, his breast tissue does not develop. During puberty the normal XX female produces lots of estrogen and only relatively small amounts of testosterone, so her breast tissue does develop. Although an XY female has testes that produce lots of testosterone, because there are no androgen receptors for it to take effect, this allows the small amount of estrogen she produces to dominate and cause breast development. In fact, without any androgenic effects in their bodies, XY females are some of the most femininely attractive women in the world.

As noted above, the human embryo is destined to become female by default unless several other chemicals swing into action to make it become a normal male. But that's only part of the story because for the first several years of life, humans, whether male or female, cannot reproduce. Puberty first involves an as yet unexplained reduction in feedback inhibition so there can be a significant increase in the release of GnRH from the hypothalamus and FSH and LH from the pituitary. This also requires the presence of specific receptors on their target tissues. It leads to the testes being able to produce sperm and more testosterone and the ovaries being able to release an egg and more estrogen (and progesterone) so males and females can reproduce.

It is information, wrapped in chemical signals, that makes the embryo become male or female and initiates puberty, thus making human reproduction possible. As Stephen Meyer observes in the Discovery Institute film The Information Enigma, the major discovery of the last half of the 20th century was that it is information that drives biology. In generating information, all human experience points to a mind rather than a random and unguided material process.


But clinical experience teaches that just having all of the parts present for reproduction doesn't automatically guarantee fertility and the natural ability to bring about new human life. That's what we'll begin to explore next time.

On the collapse Darwinism's prima facie case.

Alleged Instances of Observed Speciation -- Evolution's Smoking Gun Is Still Missing
Editor's note: William Dembski and Jonathan Wells, leading figures in the intelligent design movement, are co-authors of The Design of Life: Discovering Signs of Intelligence in Biological Systems. Originally published by the Foundation for Thought and Ethics, this path-breaking work explores some of the most important arguments for intelligent design in biology. To celebrate the launch of Foundation for Thought & Ethics Books as an imprint of Discovery Institute Press, we will be publishing excerpts from the book here at Evolution News. Through July 8, we will also be making the book available for only $10 -- that's more than a 70 percent discount, and it includes both the full-color hardcover and an accompanying CD with additional materials. If you haven't read this classic book, now is your chance! Order now, because this special discount won't last long.

Despite the absence of evidence for the ability of reproductive isolation to harness the mechanisms of genetic change and thereby to produce new species, some Darwinists still claim that there are many instances of observed speciation.1 But most of these alleged instances are in fact analyses of existing species that are used to defend one or another theory of how they might have originated -- such as the theories of allopatric and sympatric speciation, or the bottleneck and founder effects. Analyzing existing species to support one or another theory of speciation, however, is not the same as observing speciation in action.

There actually are some confirmed cases of observed speciation, but these are due to an increase in the number of chromosomes, or "polyploidy." Such cases, however, are limited to flowering plants and result from hybridizing two species to form a new one.2 Furthermore, according to evolutionary biologist Douglas Futuyma, speciation that results from polyploidy (also called "secondary speciation") "does not confer major new morphological characteristics . . . [and] does not cause the evolution of new genera" or higher taxonomic levels.3 Darwinian evolution, by contrast, depends on taking a single existing species and splitting off new species from it (called "primary speciation"), which then in turn diverge and split, diverge and split, over and over again. Only primary speciation, and not secondary speciation, could produce the branching-tree pattern required by Darwinian evolution.

Of the many instances of observed speciation alleged by Darwinists, only five come close to claiming observed primary speciation. First, in 1962, from a single lab population of Drosophila (fruit flies), J.M. Thoday and J.B. Gibson bred only those flies with the highest and lowest number of bristles (the insect equivalent of hair). After 12 generations, the experiment produced two populations that not only differed in bristle number but also showed "strong though partial isolation." Yet Thoday and Gibson not did claim to have produced a new species. Furthermore, other laboratories were unable to reproduce their results.4

Second, in 1958 Theodosius Dobzhansky and Olga Pavlovsky started a laboratory population of fruit flies using a single female of a strain from Colombia. Crosses between that fly and several other strains produced fertile hybrids in the laboratory. In 1963, however, similar crosses yielded sterile hybrids. In 1966, Dobzhansky and Pavlovsky concluded that the strain they had introduced in 1958 had become "a new race or incipient species . . . in the laboratory at some time between 1958 and 1963."5 But Coyne and Orr, writing in 2004, suspect their results were "due to contamination of cultures by other subspecies."6 In any case, Dobzhansky and Pavlovsky reported only a "new race or incipient species," not a new species.

Third, in 1964 biologists collected some marine worms in Los Angeles Harbor and used them to start a lab colony. When they went back to the same location 12 years later, the original population had disappeared, so they collected worms from two other locations several miles away, and these were used to start two new lab colonies. In 1989, researchers found that the two new colonies could interbreed with each other but not with the Los Angeles Harbor colony that had been started 25 years earlier. In 1992, James Weinberg and his colleagues called this an observed instance of "rapid speciation," based on the assumption that the original colony had "speciated in the laboratory, rather than before 1964."7 A few years later, however, tests performed by Weinberg and two others showed that the original population was "already a species different from" the two new colonies "at the time when it was originally sampled in 1964."8 No speciation had occurred.

Fourth, in 1969 E. Paterniani reported an experiment on maize in which breeding was permitted only between individuals possessing two extremes of a particular trait. Paterniani noted the development of "an almost complete reproductive isolation between two maize populations" but did not claim that a new species had been produced.9

Fifth and last, in the 1980s William R. Rice and George W. Salt subjected a population of fruit flies to eight different environments. They then took the flies that preferred the two most extreme environments and allowed only them to breed. Within thirty generations the flies had sorted themselves into two populations that did not interbreed. Even so, Rice and Salt did not claim to have produced two new species. More modestly, they believed only that "incipient speciation" had occurred.10

So, of the five alleged instances of observed primary speciation, only one (Weinberg's) claimed to have observed actual speciation -- and it was later retracted. The other four (one of which could not be reproduced by other scientists and one of which was not controlled for contamination) claimed only some degree of reproductive isolation or "incipient speciation."

What is "incipient speciation"? Darwin wrote: "According to my view, varieties are species in the process of formation, or are, as I have called them, incipient species."11 But how can we possibly know whether two varieties (or races) are in the process of becoming separate species? St. Bernards and Chihuahuas are two varieties of dog that cannot interbreed naturally, but they are members of the same species. Maybe they are on their way to becoming separate species, or maybe not. The two varieties of Rhagoletis pomonella described in the previous section do not interbreed in the wild, but they look exactly alike and are still capable of mating in the laboratory. Like different breeds of dogs, they are still members of the same species. Calling them "incipient species" amounts to no more than a prediction that they will eventually become separate species. But maybe they won't. Short of waiting to see whether the prediction comes true, we can't really know. And given our limited lifespans, we don't have time to wait (at least not by conventional evolutionary timescales).

Darwinists therefore discount the lack of observed instances of primary speciation by saying that it takes too long to observe them. But if it takes too long for scientific investigators to observe primary speciation, then there will never be anything more than indirect evidence for the first and most important step in Darwinian evolution. Darwinists claim that all species have descended from a common ancestor through variation and selection. But until they can point to a single observed instance of primary speciation, their claim must remain an unverified assumption, not an observed scientific fact. University of Bristol bacteriologist Alan H. Linton made precisely this point when in 2001 he assessed the direct evidence of speciation: 

None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of twenty to thirty minutes, and populations achieved after eighteen hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another. . . . Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic [e.g., bacterial] to eukaryotic [e.g., plant and animal] cells, let alone throughout the whole array of higher multicellular organisms.12

So except for secondary speciation, which is not what Darwin's theory needs, there are no observed instances of the origin of species. As evolutionary biologists Lynn Margulis and Dorion Sagan wrote in 2002: "Speciation, whether in the remote Galápagos, in the laboratory cages of the drosophilosophers, or in the crowded sediments of the paleontologists, still has never been directly traced."13 Evolution's smoking gun is still missing.

References:

(1) See Catherine A. Callaghan, "Instances of Observed Speciation," The American Biology Teacher 49 (1987): 34–36; Joseph Boxhorn, "Observed Instances of Speciation," The Talk.Origins Archive, September 1, 1995, available online (last accessed January 9, 2007); Chris Stassen, James Meritt, Annelise Lilje, and L. Drew Davis, "Some More Observed Speciation Events," The Talk.Origins Archive, 1997, available online (last accessed January 9, 2007).

(2) See Justin Ramsey and Douglas W. Schemske, "Neopolyploidy in Flowering Plants," Annual Review of Ecology and Systematics 33 (2002): 589–639; D. M. Rosenthal, L. H. Rieseberg, and L. A. Donovan, "Re-creating Ancient Hybrid Species' Complex Phenotypes from Early-Generation Synthetic Hybrids: Three Examples Using Wild Sunflowers," The American Naturalist 166(1) (2005): 26–41.

(3) Douglas J. Futuyma, Evolution (Sunderland, Mass.: Sinauer Associates, 2005), 398.

(4) J.M. Thoday and J. B. Gibson, "Isolation by Disruptive Selection," Nature 193 (1962): 1164–1166. J. M. Thoday and J. B. Gibson, "The Probability of Isolation by Disruptive Selection," The American Naturalist 104 (1970): 219–230. Coyne and Orr, Speciation, 138.

(5) Theodosius Dobzhansky and Olga Pavlovsky, "Spontaneous Origin of an Incipient Species in the Drosophila Paulistorum Complex," Proceedings of the National Academy of Sciences 55 (1966): 727–733.

(6) Coyne and Orr, Speciation, 138.

(7) James R. Weinberg, Victoria R. Starczak, and Daniele Jörg, "Evidence for Rapid Speciation Following a Founder Event in the Laboratory," Evolution 46 (1992): 1214–1220.

(8) Francisco Rodriquez-Trelles, James R. Weinberg, and Francisco J. Ayala, "Presumptive Rapid Speciation After a Founder Event in a Laboratory Population of Nereis: Allozyme Electrophoretic Evidence Does Not Support the Hypothesis," Evolution 50 (1996): 457–461.

(9) E. Paterniani, "Selection for Reproductive Isolation Between Two Populations of Maize, Zea mays L.," Evolution 23 (1969): 534–547.

(10) William R. Rice and George W. Salt, "Speciation via Disruptive Selection on Habitat Preference: Experimental Evidence," The American Naturalist 131 (1988): 911–917. See also Coyne and Orr, Speciation, 138–141.

(11) Darwin, Origin of Species, 111.

(12) Alan Linton, "Scant Search for the Maker," The Times Higher Education Supplement (April 20, 2001), Book Section, 29, available online with registration (last accessed January 9, 2007).


(13) Lynn Margulis and Dorion Sagan, Acquiring Genomes: A Theory of the Origins of Species (New York: Basic Books, 2002), 32.