Evolving New Information

But for some reason actual evolutionary biologists know less about evolution than you do? Indeed you are prepared to believe Stephen Meyer, a historian and philosopher of science on the details rather than people doing actual primary research? Well sure, you already agree with them and apparently you think the word of an ID proponent is always better than that of someone arguing for evolution. It certainly is casual. These sort of ad hoc explanations have no value, like many of the speculative strong adaptationist 'just so' stories that plague evolutionary biology. You haven't really given me much to go on here. Are we talking insect wings? Bird wings? I'm going to assume you mean insect wings, although I wouldn't be at all surprised to find homologous genes in bird wings as well. Indeed I just found one on google in about 10 seconds.I suspect that a number of these genes we are discussing are in fact common also to the crustacean and insect leg. The genes engrailed and Distal-less are expressed in both the developing wings and legs of insects and in the compound arthropod leg which includes the 'leggy' bit, the endopod, and the 'gilly' bit, the epipod. Both of these genes also have homologues involved in the patterning of vertebrate limbs, including birds wings. The engrailed homologues are called Engrailed-like 1 and 2 and the principal Distal-less homologues are called Dlx genes which stands for 'distal-less homeobox' genes.The more wing/gill specific genes discussed by Averof and Cohen (1997) which I think you were refering to are called apterous and nubbin or pdm, Interestingly while these genes are, with the exception of a small region in the leg for apterous, not expressed in the leg they do have homologues in vertebrate limb development. The homologues of apterous are called Lmx-1 and Lhx2 while nubbin has a homologue called Pou2F1. This isn't how darwinian theory would explain it. Evolutionary biologists would look at the fossil and currently extant species of insects and crustacea and realise that in fact you don't need to lose your gills and regain them as wings. You just hang on to your gills and over many many generations they become modified and allow for a new function to be acquired such as modifying descent (pun unintentional) and eventually allowing powered flight. I admit that the last elements are true conjecture and just the sort of 'just so story' I was complaining about myself, but it hardly seems unreasonable. The larval mayfly has gills highly remiscent of the crustacean gill and also structurally similar to the insect wing. It isn't in one place, it is throughout the whole of developmental biology. Your own gill/wing example is just one where we see a pattern of one or 2 genes in what are considered more 'primitive' organisms, i.e. the invertebrates, which in the vertebrates have diversified snd giving rise to homologous gene families which have both retained and modified the function of the ancestral proteins from which both they and their invertebrate homlogues derive.Virtually any developmental pathway tells the same story. I'd be happy to discuss some of them with you since developmental biology is both my job and my passion.As I say, I don't really know what a good place to start is for a novice. Apart from some SJ Gould articles I hadn't really encountered development until I got to university. There are plenty of evo-devo blogs out there, including the infamous Pharyngula. Maybe Sean Carroll's book would be good, but I haven't read it myself.So I can't point you to a place which will tie this all together with a bow, science doesn't usually work like that, but I can certainly elaborate on evo-devo if you like, and direct you to the primary literature which discusses these things.TTFN,WK

Meh, this is developmental biology, not rocket science. It isn't like reading a maths heavy physics paper or an abstruse information theory argument. There are pretty pictures and once you understand really only a few key techniques, in fact you might get by with just understanding what an in-situ hybridisation was for the majority of papers, the only tricky things to interpret are some of the comparative anatomies.Anyway I prefer to explain things in my own words and use the primary literature simply as a reference as your title suggests.I may not have a very objective view on this I realise. One commentary on the wing/gill relationship was on the old Pharyngula site here.The only real problem I see with references to the primary literature is that so much of it is still not open access.As to homologues, Drew seemed to have understood the way I have been using the term previously in the thread and my reply was specifically directed to him, but I agree that for some lay lurker it might be quite unclear and it would be good to make posts as accessible to all as possible.TTFN,WK

I didn't mean that you necessarily agreed with any and all claims a creationist/IDist might make on this site. Rather that you seem to have already decided that ID is correct and seem to lend much more weight to arguments that agree with this conclusion than those against it. I understand that you may well think the same about me from the other side, but in my defence, I know a lot more about the actual science than you do, and certainly more about evo-devo and molecular biology than Stephen Meyer.As for Mike Behe, the gaps for him to fit ID into in his conception of life's history are getting almost infinitesimally small. He is uncharacteristic of the ID crowd in his acceptance of an awful lot of mainstream evolutionary biology. If it wasn't for his belief that he can detect ID no one would think he was anything other than an invisible hand sort of theistic evolutionist, the sort of person who thinks that god interferes at an unobservable quantum level to influence mutation in such a way as to direct evolution at a level not detectable scientifically. One of our participants here, Randman, used to put this sort of thing forward as a mechanism, but he also insisted that the resulting pattern of intervention should be detectable. Cellular pH is regulated by a number of things including proteins in the cell membrane which can move sodium and hydrogen ions into and out of the cell. I wasn't drawing any specific connection between pH and phosphorylation state, there are lots of other post-translational modifications which can change the functional state of a protein. I was just pointing out that analysing protein function isn't as simple as just looking at the primary/secondary sequence. Its certainly complex, I have no idea why you assume it is irreducibly so. If I showed that you could entirely remove one proton transport protein and an organism still survived would that mean you were wrong? What evidence would you consider sufficient to discount IC, short of a step by step evolutionary history of every ancestral genome for the past 2 billion years?That is even before we get into the which of Behe's various definitions of IC you are actually using and whether IC systems cannot come about by natural evolutionary pathways. Thanks. I really think that if you took some time to actually understand evolutionary theory and look at the wealth of published research you would appreciate that we aren't just making stuff up for ideological reason there simply isn't any compelling argument against evolution and there is a wealth of data from multiple disciplines which are consilient with it.TTFN,WK

It may surprise you Drew, but I agree to an extent. I think this is something of a caricature since most evolutionary biologists are happy to accept a broader range of mechanism than simply "Darwinian processes". But I would agree that science tends to assume the things are the result of material processes, but then that has turned out to be the case in almost everything that science has investigated.To some extent this turns on a semantic issue of design, after all intelligent design theory obviously draws a distinction between different types of design, so perhaps rather than discounting something as the mere appearance of design we should think of it as being simply naturally designed, over a very long term of development by natural processes. We know of many natural processes that can produce the necessary sorts of genetic variation after all, and of a mechanism for maintaining/promoting traits favoured by a particular environment. Your words not mine . The problem here is that you are assuming that all 200 parts of a cilium and "10,000 protein binding sites in cells" whatever that is supposed to mean, are evidence for irreducible complexity, but you haven't provided any evidence to support this, I doubt you have even been presented much in the way of evidence in the sites you got this information from.You assume it is true because they tell you so, why should anyone else assume it is true in turn in the absence of evidence? Especially anyone who is actually at all familiar with real cellular biology? Indeed, I'm sure there is quite enough space in the realms of quantum weirdness to accommodate many forms of god. I have no scientific issue with this because Ken miller doesn't claim to have scientific evidence that this is the case. He believes it as a matter of faith and that is between him and his own conception of god. I'm not sure what you are saying here. Is your argument 'no but its really, really, reeeeeally complex. Because if so it is no more convincing than when you were just saying how complex it was.Otherwise I can't make this out Again you make an assumption. The fact that an organisms gross morphology has remained essentially consistent, the sort of thing we see in the fossil record, is not evidence that it is remaining unchanged genetically. It is also a somewhat disingenuous argument since the IC flagellum is a bacterial structure. How much data relevant to the evolution of the bacterial flagellum do you really think we can get out of fossilised fish? Maybe I missing the point of your bacteria comment. Arguably this has been done its just that the clues are still tentative and a lot of the details are still unclear. We touched on this in another thread at Message 361. But surely you accept that the fact that this hasn't been done yet doesn't constitute evidence that it can't be done? The problem here is that Behe is using a term devolution, which is barely a scientific term at all, there are probably about 20 papers on pubmed which use the term in the context of evolutionary biology. To describe an organism becoming better adapted, which is what these bacteria are doing when they lose the genetic material for synthesising amino acids which are being freely supplied to them in their amenable culture broth environment, is simply evolution. It takes energy to synthesise DNA, why synthesise DNA for a function you no longer need?Having said that, the fact that it is easier for evolution to break things is of course facilely obvious. It is a consequence of the way it is so much easier for mutations to break things. It doesn't stand as any sort of evidence that evolution can't also make things though. Not 'intelligent', there is plenty of science that allows the involvement of intelligence. What science cannot deal with is immaterial, untestable or supernatural entities which can interact with a system undetectably and leave no trace. If you have a testable mechanism by which you think ID has acted then by all means tell me about it and I will consider it.After that your post degenerated into woo, so I'll leave well enough alone.TTFN,WK

My answer would be that the information or complex specified information, if we wish to use an ID term, in the genome is the result of the interaction between the environment and the genome over long periods of time. Genomes are unstable things and will naturally vary in a population. Environments are a many splendoured thing and can be variable, stable and catastrophically unstable in different areas at different times. The degree to which any genome proliferates is in large part a function of how well adapted it is to its environment.Raw non-specific novel informational variation is consistently generated by mutation. Most of this is functionally neutral, much is deleterious but a small proportion has beneficial functional effects that allow an organism to survive or proliferate in an environment better than its fellows. The environmental pressures favour the preservation of such changes and over time this gives rise to large complex assemblies of favoured traits in the genome, which form the CSI.Mutation acts as a monte-carlo process for generating random informational change and the environment acts as a filter to preserve those changes in patterns determined by that environment.If you want to know the originator of a meaningful message in the Gitt sense of information, I don't think there is one.TTFN,WK

It's worth bearing in mind that a bacterium and oocytes are pretty radically different. The fact that a genome transplant works in one does not neccessarily mean it will work in the other.That caveat aside however there is plenty of evidence that genome transplants into oocytes do work, even across species boundaries in some cases. There are a number of ongoing projects to find ways to increase population numbers of endagered species by using related species as a form of surrogate mother. These have had varied degrees of success, for a review off mammalian attempts see Loi et al. (2007).Part of the issue here is that LTA is at least half right. The oocyte isn't a clean neutral template that will accept any nuclear content and produce a viable organism of the genome donor's species. Cross species hosts need to be carefully matched and the further apart species are the less succesful such attempts appear to be. Even in the bacterial example the two bacteria are forms of mycoplasma, allowing the tried and tested creationist response of 'but they are still mycoplasma!'As I say LTA is only partly right because when these transplants are successful the offspring are genetically and as far as can be determined phenotypically of the donor's species. The one area where the hosts genetic complement can be seen to persist is in the mitochondrial genome inherited from the oocyte. Except for the mitochondria and proteins derived therefrom everything is based on the donor's genome, all donor species proteins and what have you. One might make an attempt to argue that some structural information is passed on from the oocytes centrosomal structures and associated proteins to the daughter cells, but these structures don't tend to differ radically between closely related species and the accessory protein complement from the oocyte would very rapidly be superceded by new proteins generated from the donor genome.TTFN,WKEdited by Wounded King, : No reason given.

I'm not sure why it should particularly, can you explain? Because influenza isn't a retrovirus with the capacity to insert itself into a genome.TTFN,WK

I assume you mean do we know where retroviruses came from originally. In terms of how new retroviral vectors are formed during viral replication we have a pretty extensive understanding.The short answer is not exactly, but most current genetic research points to retroviruses being derived from transposable elements native to organismal genomes called Long Terminal Repeat (LTR) retrotransposons.TTFN,WK

This may still be the case in many cases as there is clearly a complex dynamic between LTR transposable elements and retroviruses. It is also possible that there is a viral, but not retroviral, origin for such elements.Phylogenies of ribonuclease H (RNH) suggest that LTRs and retroviruses arose quite late in eukaryotes possibly derived from a fusion of DNA mediated transposon and non-LTR retrotransposon (Malik and Eickbush, 2001; Malik, 2005).There is also evidence suggesting that in some cases env genes conferring infectivity have been co-opted from non-retroviral viruses (Malik et al., 2000; Havecker et al., 2004; Eickbush and Jamburuthugoda, 2008).TTFN,WK