evolution

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It takes a special kind of doggedness to make an “Infographic” that rehashes debunked stories as if the debunking had never happened, but that’s what the Discovery Institute did the other day. Perhaps some of this nonsense is down to the background of the author, who appears to have zero science credentials.

The other day, the wonderful xkcd published this satirical cartoon about Infographics (right).

I do tend to agree with this sentiment, though of course a well-structured infographic can be a useful and clear way of illustrating.

The dear old Discotute’s effort, though, is pretty pathetic (I haven’t embedded it here for copyright reasons). It’s apparently derived from what the Discotute rather grandly term “the Discovering Intelligent Design curriculum”.

Beginning with the rather grand (and incorrect) claim that

Intelligent Design uses the scientific method (e.g. observation, hypothesis, experiment, and conclusion) to make its claims.

Except that’s not really how ID creationism works. For starters, ID creationism was born as a cynical attempt to push creationism into US schools after successive court room defeats, and to do this by masquerading as science. The overall objectives can be seen in the Wedge document, after all. Accordingly, ID creation doesn’t really operate like science – it has a pre-determined conclusion that evolutionary biology must be wrong, and the only observations that the Discotute make are aimed at trying to make evolutionary explanations seem unreasonable (classic god of the gaps approach). They don’t really do experiments, and their labs appear to be greenscreens of stock photographs.

And then it’s on to the old canard that biological information is in some way directly comparable to language, computer programmes and the like, and that it can only be produced by intelligence.

The bonkers ID creationist concept of Irreducible Complexity (a.k.a. the Argument from Incredulity) is up next, illustrated by the bicycle (!) and the bacterial flagellum.

Bizarrely, the Discotute still think that bacterial flagella are in some way impossible to arrive at by natural processes, and must have been poofed into existence (by some as yet unknown mechanism) by some (unknown) sky fairy/alien genius/god, despite considerable evidence for how these structures did evolve. Anyway, get this tortured illogic:

In our uniform and repeated experience irreducibly complex systems (e.g., a bicycle) always originate from a mind capable of thinking with forethought and intentionality. Only intelligence can create the unlikely arrangement of parts that matches a specific pattern required for the machine to perform its function. ID predicts that natural structures will contain this same kind of information and complexity – patterns which we attribute to mind.

The problems with that are particularly obvious. On the one hand, we know from historical records who invented various aspects of a modern bicycle and when. Furthermore, we have an excellent understanding of how these inventions were made. On the other hand, the ID creationists are clearly being disingenuous when they claim not to identify the Judeo-Christian god as their designer of bacterial flagella, but in any case they are unable to point to specific evidence for their designer, when he/she/it did the design, and how he/she/it put the design into practice.

The concluding paragraph is lovely.

In the same way that we attribute the complex and specified information found on the Rosetta Stone and in machines to an intentional mind, the specified and even irreducible complexity found in living organisms points to an intelligent cause. By viewing biological systems as designed machines, ID opens up new avenues of scientific investigation to understand how life works.

The Discotute really needs to employ some scientists. We know that humans made the Rosetta stone. We know that humans made bicycles. The evidence there does point to intelligent cause. In the case of biological structures, there is zero evidence for a creator designer, zero evidence for how the supposed creator designer implemented his/her/its supposed design and nothing but wishful thinking and a deeply held desire for a resurgence of religious belief.

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I was idly perusing my rss feeds last week, when an article at The Dispersal of Darwin website (Hand-printed, hand-bound book about Wallace, Darwin, and natural selection) caught my eye. There are two attractive features: firstly, the physical attributes – this is a delightful hand-printed book – and secondly, the material in the book is of general interest to me. I should say that I have some of the contents in other books (notably a volume of Darwin and Wallace writing published in 1958 to coincide with the centenary of Origins), and that I have of course long been aware of Wallace in the context of natural selection. This is not a cheap book and it’s intended to contribute to a fund for the erection of a statue of Wallace. There’s a foreword by George Beccaloni which sets out the stall here.

The book is hardback, hand printed andternate attractively bound in leather with printed design on paper. The contents are correspondence associated with the joint presentation to the Linnean Society, and the three documents that represent that presentation (and extract of unpublished work by Darwin; and abstract of correspondence from Darwin to Asa Gray; an essay by Wallace). The book concludes with correspondence between Darwin, Hooker and Wallace, and finishes with the text of Wallace’s acceptance speech on the award of the Darwin-Wallace medal in 1908.

This is all quite interesting material – I always feel that the private correspondence between Darwin, Wallace and the others reveals quite a bit about their nature. Of course, Wallace’s role on the discovery of evolution by natural selection isn’t new to me, but I do realise that many members of the public really aren’t aware of the circumstances around the discovery, nor of the theory’s antecedents or the social and scientific context in which evolutionary theories were discussed, presented and received during the 18th and 19th centuries. This is something that attempts are being made to rectify (see for example Bill Bailey’s recent BBC TV programme, and accompanying article in The Radio Times). That being said, I don’t quite buy in to the concept of the “Darwin Industry” excluding competing names from the history of natural selection: including Patrick Matthew as well as Wallace. It’s not helpful that ID creationists seem to have picked on Wallace as some kind of forerunner in Intelligent Design creationism.

Alfred Russel Wallace The Letter from Ternate (2013) is published by TimPress (Reigate, Surrey) in a limited edition of 100 copies. ISBN 1-905346-99-9

Further reading:
The Alfred Russel Wallace Website
Wallace Letters Online

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Courtesey of the BHA, I see that evolution is to be added to the primary curriculum! (BHA welcomes plans to add evolution to primary curriculum):

Evolution is to be included in the primary curriculum, it has today been announced. The Department for Education (DfE) has published its draft primary National Curriculum for science, which includes the teaching of evolution from year four (age 8-9). The British Humanist Association (BHA) spearheaded the‘Teach evolution, not creationism’ campaign calling for just this change, and is delighted at the news.

Hurrah!

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Via NCSE Evolution: Education and Outreach for free | NCSE) and Panda’s Thumb (Evolution: Education and Outreach free in December), I see that the Springer journal Evolution: Education and Outreach is offering open access until the end of the year.

RationalWiki has published an exhaustive list of scientific evidence that evolution is a hoax.

In summary:

h/t Panda’s Thumb

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On the gain of genes and gene function

Michael Behe recently published a review article in the Quarterly Review of Biology entitled Experimental evolution, loss-of-function mutations, and “the first rule of adaptive evolution” (subscription required), which consists largely of a review of laboratory experiments addressing the adaptive response of microorganisms to simple environmental changes. Behe generates a new definition – Functional Coded elemenTs (FCTs), essentially any segment of DNA that has a biological function, and a “rule”, the “first rule of adaptive evolution”, which essentially states that the majority of adaptive changes reflect mutational events are those which impair or eliminate FCT function.

Update: please note the first comment on this article, which outlines in more detail problems with Behe’s “first rule”.

My own view is firstly, that the data Behe relies on come largely from simple laboratory experiments on microbes (mostly bacteria) generally cultured as a monoculture away from other bacterial species and their bacteriophages (viruses), and secondly that the examples given for eukaryotic adaptation (of humans to endemic malaria) are peculiarly interpreted. Jerry Coyne has published several blog articles reflecting on this paper (Behe’s new paper; IDers already distorting Behe’s new paper; Casey Luskin distorts Behe’s paper; An experimental evolutionist replies to Behe), so there’s really no need to revisit it, other than to note the reservations I have.

What’s a bit more interesting is recently published evidence on the evolution of new genes in the fruit fly Drosophila (in fact these papers look as several species of Drosophila rather than just the common lab species Drosophila melanogaster).

In the first, Chen et al (2010) compared the genome sequences of different species of Drosophila. Again, Jerry Coyne’s beaten me to it with a detailed review of the paper (New genes arise quickly), but in essence, the authors investigated the gene differences between the species in the D. willistoni and D. melanogaster lineages, which diverged about 35 million years ago. Their aim was to evaluate how often genes appeared within the D. melanogaster lineage. In Behe’s new terminology, these would be gain-of-FCT. To summarise, Chen et al:

  • Identified 566 new genes in the D. melanogaster genome and dated their evolutionary ages through phylogenetic distributions.

  • Assayed the effects of loss of function by RNA interference – of 195 ‘young genes’ tested, 59 gave lethal phenotypes. In other words slightly more than 30%.

  • The frequency of young genes with essential function is not statistically different from the corresponding frequency of ‘old genes’, 35%.

Coyne notes in his blog article (New genes arise quickly) that

The presence of frequent gene duplications is supported by an independent study:  Emerson et al. (2008) found that in only fifteen lines of D. melanogaster from nature there were several hundred duplicate genes segregating as polymorphisms (that is, some individuals had one copy of a gene, some had two or more).  They estimated that 2% of the genome was tied up in this copy-number variation.  Clearly, there are a lot of duplicate genes variants floating around in nature.

Indeed, some years ago my laboratory identified a case of gene duplication in D. melanogaster that was presumably a recent event, being present in only some lab strains. It’s quite clear that these sorts of observations are widespread across genomes of species in which the genomes of many individuals have been looked at. Copy number variation is widespread among humans.  What is the usual fate of a duplicated gene?  In many cases, the duplicated gene may have lost vital elements required for correct expression (those sequences important for correct spatiotemporal expression patterns).  In such a circumstance it is likely to be non-functional (i.e. a pseudogene).  If the new copy has retained the capacity for expression, it may still acquire sequence changes which cause loss of function (i.e. it will become a pseudogene).  However, two other outcomes are possible: neofunctionalisation and subfunctionalisation.  In the former, one of the duplicate genes acquires a novel function, while in the latter, one of the genes performs a subset of the functions of the original gene.  Several mechanisms can lead to these outcomes.

In a second paper, Ding et al (2010) looked at the origins and function of young duplicated genes in Drosophila, and focusses on the members of the kep1 gene family, with particular reference to the appearance of new functions. In D. melanogaster, kep1 is a pre-mRNA splicing factor, influencing female fertility, eye development, and immune responses to bacterial infection.

The diagram shows the lineages of several Drosophila species (ana = anannasae; ere = erecta; yak = yakuba; sim = simulans; mel = melanogaster).  In these lineages, the points of origins of the members of the kep1 family are shown as horizontal bars.  Not all members of the gene have been named: those gene names in the form CGxxxx are working names allocated during the Drosophila genome project.

Loss of function mutants of each of the four functional additional members of the D. melanogaster kep1 family (CG4021, nsr, CG3927, CG33318) were analysed.  All of these mutant alleles involved deletion of some or all of the genes involved: two were obtained by targeted mutagenesis and two by imprecise excision of the transposable P element.  CR9337 is a pseudogene – a duplicated gene that has lost biological function.

Loss of nsr leads to almost complete male sterility (see Figure 3 for an illustration of the mutant alleles and the severely reduced fertility of nsr mutant males) – a phenotype distinct from that of kep1 mutants.  The authors analyse the biological function of nsr in considerable detail: it turns out to play its important role in male fertility by regulating several Y-linked genes that are known to be required for male fertility.  [In Drosophila, the Y chromosome does not itself specify male-ness as it does in humans: rather the primary sex determination signal is the ratio of X chromosomes to autosome sets.  Thus a fly with a single X chomosome will be male, though sterile because it lacks the Y chromosomal fertility factors.  The Y chromosome is also rather peculiar, both in terms of its gross structure but also in the structure of individual genes.]  Interestingly, loss of kep1 function leads to female, but not male fertility, while loss of CG4021 or CG3927 did not lead to male sterility.

So, do the analyses of nsr sequence and function suggest that it is derived from neofunctionalisation or subfunctionalisation forllowing the original duplication event?  Ding et al suggest their data point to the former, but do not exclude the latter.  In support of neofunctionalisation, they observe that:

  • kep1 is under strict purifying selection across the Drosophila lineage studied.
  • Comparative sequence analysis of nsr shows strong positive selection
  • kep1 expression in the testis could not be detected in D. yakuba, suggesting the ancestral function of kep1 did not involve testis development.

On the other hand, the conclusion that nsr may have arisen by subfunctionalisation is still possible.  For example, kep1 my have lost its male fertility role in the D. yakuba lineage.  In any event, during the evolution of the melanogaster subgroup, nsr has not only arisen through gene duplication, but has been integrated into some pretty important biological processes.

How do these two papers relate to Behe’s proposal?  They do illustrate the extent to which novel gene functions arise during evolution, and that newly duplicated genes can be integrated into fundamental biological processes.  It’s interesting to note that the kind of experimental evolution experiments conducted using microorganisms and as reviewed by Behe are difficult (or at least time consuming)  to perform in eukaryotic laboratory organisms.  It’s clear from these two papers (and many other examples in the literature) that the increasing quantity of genome sequence data, not only of different species but of multiple individuals within species, has provided us with significant insight into the origins and diversification of genes.

References

Chen et al (2010) New Genes in Drosophila Quickly Become Essential. Science 330; 1682-1685. doi:10.1126/science.1196380. [Subscription required]

Ding et al. 2010. A Young Drosophila Duplicate Gene Plays Essential Roles in Spermatogenesis by Regulating Several Y-Linked Male Fertility Genes. PLoS Genetics 6; e1001255. doi:10.1371/journal.pgen.1001255. [Open Access]

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The Institute for Creation Research reveal their scientific illiteracy.

In a recent blog posting (No Fruit Fly Evolution Even after 600 Generations), Institute for Creation Research ‘science’ writer Brian Thomas misinterprets (deliberately or otherwise) two classic experiments in genetics, and one that has been recently published.  The ICR website doesn’t permit commenting, presumably to exclude people popping over to point out errors in their writing.

The first example concerns work conducted by Nobel prizewinners Christiane Nusslein-Volhard and Eric Wieschaus, and published in several peer-reviewed papers in the 1980s (see for example Nature 287, 795-801 (30 October 1980) | doi:10.1038/287795a0). The reason why Nusslein-Volhard and Wieschaus (along with Ed Lewis) won the Nobel Prize for Physiology or Medicine (there is no Nobel Prize for Biology) in 1995 was that they identified many of (if not most of) the genes that underpin the specification of body plan in the embryonic and adult development of the fruit fly Drosophila. The significance, of course, being the high level of conservation between these Drosophila genes and their counterparts in other animals, including humans. Of course the ICR don’t like this, since it correlates pretty well with evolutionary theory.

Now, what is it that Thomas thinks is the key take-home work from the ground-breaking experiments of Nusslein-Volhard and Weischaus?

If evolutionary biologists could document such evolution in action, they could vindicate their worldview and cite real research to support their surreal claims. In 1980, this search for proof led researchers to painstakingly and purposefully mutate each core gene involved in fruit fly development. The now classic work, for which the authors won the Nobel Prize in 1995, was published in Nature. The experiments proved that the mutation of any of these core developmental genes―mutations that would be essential for the fruit fly to evolve into any other creature―merely resulted in dead or deformed fruit flies. This therefore showed that fruit flies could not evolve.

This paragraph illustrates Thomas’ lack of understanding. Nusslein-Volhard and Weischaus clever stratagem was to realise that many of the genes that are required for correct embryonic development would be recessive lethal mutations, because loss of function would result in severely abnormal development. Nusslein-Volhard and Weischaus therefore generated collections of Drosophila strains bearing lethal mutations that cause death in the embryonic stages. They then examined embryos from each of these strains for embryos with evidence of abnormal development. Typical examples would include abnormal segmentation, embryos with incorrect specification of anterior and posterior and so forth.

So a real examination of Thomas‘ claims do not hold water: Nusslein-Volhard and Weischaus did not “painstakingly and purposefully mutate each core gene involved in fruit fly development”, they generated a large number of mutants and looked for those that specifically affected embryonic development. Also Thomas’ claim that the mutants “merely resulted in dead or deformed fruit flies” is also wrong: the whole point of the experiment was to identify mutations that yield abnormal embryos. Indeed the experiments were not aimed at demonstrating that fruit flies could evolve. On the other hand, the similarity between the Drosophila genes that Nusslein-Volhard and Weischaus identified and the counterparts found in all segmented animals provides very good support for the evolution of all these taxa.

On the subject of Richard Lenski’s E. coli experiments, I refer Brian Thomas to P. Z. Myers’ Pharyngula blog, which discussed the paper (Historical contingency in the evolution of E. coli), and dealt with the creationist misunderstanding (wilful or otherwise): creationists across the internet have spent a good deal of time trying to discredit Lenski’s work and failing.

Thomas also reveals his poor grasp of biology in his discussion of a recent paper in Nature (Burke et al (2010) Genome-wide analysis of a long-term evolution experiment with Drosophila. Nature 467, 587–590 doi:10.1038/nature09352), which describes a lengthy experiment in which a population of Drosophila was selected for rapid development over about 600 generations. Normal Drosophila can develop from egg to adult in about 10 days at 25oC: this experiment yielded flies that developed about 20% faster. As an experimental biologist (rather than an armchair creationist) might expect, a number of correlated phenotypes also evolved, including shorter lifespan, smaller body size and reduced starvation resistance.

To simplify the findings of the paper, detailed and extensive DNA sequencing revealed that in comparison between selected and unselected populations:

  • One sequence variant every 175 bases

  • Over 37000 of these variants potentially impact on gene function

  • 662 variants in 506 genes are predicted to have a significant effect on function

  • The majority of the genes are known or predicted to play a roles in development

I wonder whether the ICR don’t have a subscription to Nature or that they are unwilling to pay for the pdf – it certainly seems as though Thomas’ reading is limited to the abstract. Thomas’ conclusion from his ‘reading’ of the paper is:

The study’s authors wrote, “In our sexual populations, adaptation is not associated with ‘classic’ sweeps whereby newly arising, unconditionally advantageous mutations become fixed.”

They suggested that perhaps there has not been enough time for the relevant mutations to have become fixed. They also suggested an alternative—that natural selection could be acting on already existing variations. But this is not evolution, and it is actually what creation studies have been demonstrating for many years.

The abstract, which is freely available on the Nature website, reads (in part):

[…] in our sexual populations, adaptation is not associated with ‘classic’ sweeps whereby newly arising, unconditionally advantageous mutations become fixed. More parsimonious explanations include ‘incomplete’ sweep models, in which mutations have not had enough time to fix, and ‘soft’ sweep models, in which selection acts on pre-existing, common genetic variants. We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time.

Actually, may take on this paper (and bear in mind that this population genetics is not my field in Drosophila genetics) is that it has demonstrated the genetic consequences of long term artificial selection for a characteristic which probably leads to pretty disadvantageous outcomes for the animal (reduced lifespan, reduced body weight, reduced starvation resistance), and the point the authors make is that the dynamics of genetic diversity under selection is rather more complex than seen is simpler, asexually reproducing organisms. None of this is particularly contentious, and it in no way represents evidence against evolution.

Except in the eyes of the ICR and its staff writers.

H/T: Psiloiordinary (BCSE)

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The Daily Telegraph reported yesterday that a new hominid had been discovered in South Africa (Missing link between man and apes found – Telegraph).  Apparently the discovery is of a skeleton (or, as it turns out from a quotation from Phillip Tobias skeletal remains from several individuals) and this is quite exciting since hominid fossils are usually pretty fragmentary. Apparently the fossils represent an intermediary between Australopithecus and Homo habilis and are about 2 million years old. There’s to be an announcement on Thursday, followed by a TV series.

The find is deemed to be so significant that Jacob Zuma, the South African president, has visited the university to view the fossils and a major media campaign with television documentaries is planned.

This all sounds a little familiar – remember the Darwinius masillae frenzy (see Darwinius masillae and Darwinius masillae – the BBC World Service gets it…)?  Hopefully this fossils will live up to the promise. The eminent human anatomist and anthropologist Phillip Tobias, who is one of the few scientists to see the fossils, is certainly excited, and is quoted as saying:

He said: “To find a skeleton as opposed to a couple of teeth or an arm
bone is a rarity.

“It is one thing to find a lower jaw with a couple of teeth, but it is
another thing to find the jaw joined onto the skull, and those in turn
uniting further down with the spinal column, pelvis and the limb bones.

“It is not a single find, but several specimens representing several
individuals. The remains now being brought to light by Dr Berger and his
team are wonderful.”

All very exciting, and I’m looking forward to Thursday already!

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The Theos think tank invites entries in a competition to summarise The Origin of Species in a tweet:  Darwin’s Origin of Species evolves to a Tweet.  Whether this turns out to be a good thing is probably rather moot!  Theos say:

Fans of Britain’s most famous scientist are being asked to encapsulate the over 600-page seminal work into 140-character tweets on the popular Twitter website.  The competition comes ahead of tomorrow’s (Tuesday) 150th anniversary of the publication of the book, which sets out Darwin’s theory of evolution.

The Origins twittercomp was actually announced on 20th November, but it didn’t cross my radar till just now.  The Theos article also punts their recent report, being the fourth and final report in the Theos Rescuing Darwin series: Doubting Darwin.  It’s succeeded, I just downloaded it and will take a look.
One final comment: how does one enter the competition?

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One of the great stories about American cinema is that in credits for the 1929 Pickford-Fairbanks film version of “The Taming of the Shrew” was the line “With Additional Dialog by Sam Taylor”. Most unfortunately, it would seem that this just isn’t so, and it’s an urban legend. So, why is this turning up in my atheism blog?

The (unfortunately) well-known creationist Ray Comfort, who runs a number of websites aimed at discrediting evolution and/or atheism has re-published Darwin’s “On the Origin of Species”. Rather cheekily, this seems to be credited at amazon.co.uk as being written by Charles Darwin and Ray Comfort (it has to be said, in the interests of truth, that the cover image provided by Amazon.co.uk – pictured right – makes no mention of Ray banana man Comfort). Furthermore, judging from the reviews of this edition at amazon.co.uk, the initial listing conflated reviews of this version (bowdlerised not only by inclusion of Comfort’s crass creationist introduction but also by excision of key material) mixed with reviews of more acceptable editions. It would seem that the resounding raspberry of the seven reviews to date are now specifically associated with this version.

There has been an ongoing debate over this edition of Origins over at the US News website, beginning with NCSE Director Eugenie Scott’s piece (How Creationist ‘Origin’ Distorts Darwin) and Comfort’s attempts at justification. Scott pointed out Comfort’s evisceration of Origins:

Unfortunately, it will be hard to thoroughly read the version that Comfort will be distributing on college campuses in November. The copy his publisher sent me is missing no fewer than four crucial chapters, as well as Darwin’s introduction. Two of the omitted chapters, Chapters 11 and 12, showcase biogeography, some of Darwin’s strongest evidence for evolution. Which is a better explanation for the distribution of plants and animals around the planet: common ancestry or special creation? Which better explains why island species are more similar to species on the mainland closest to them, rather than to more distant species that share a similar environment? The answer clearly is common ancestry. Today, scientists continue to develop the science of biogeography, confirming, refining, and extending Darwin’s conclusions.

Likewise missing from Comfort’s bowdlerized version of the Origin is Chapter 13, where Darwin explained how evolution makes sense of classification, morphology, and embryology. To take a simple example, why do all land vertebrates (amphibians, mammals, and reptiles and birds) have four limbs? Not because four limbs are necessarily a superior design for land locomotion: insects have six, arachnids have eight, and millipedes have, well, lots. It’s because all land vertebrates descended with modification from a four-legged (“tetrapod”) ancestor. Since Darwin’s era, scientists have repeatedly confirmed that the more recently two species have shared a common ancestor, the more similar are their anatomy, their biochemistry, their embryology, and their genetics.

The blogosphere has been full of protests about this edition of Origins – I can’t list all articles, but here are two links to PZ Myers’ Pharyngula: Ray Comfort is a parasite (in relation to which, I note that Comfort’s bowdlerised version no longer tops the list in the search results at amazon.com) and Ray Comfort Replies to Eugenie Scott.

(This post was composed offline and submitted via Bilbo Blogger, now sadly renamed Blogilo. Let’s see how well it works!)

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