I am having trouble following your logic. let me try

Comment on Gary Gilbert, Spectrum, and Pseudogenes by Sean Pitman.

I am having trouble following your logic. let me try to summarize

1] The fine structure within the globin genes across all species from monotreme to man is designed.

For functional sequences, like the eta-globin pseudogene, that is certainly the best hypothesis until the Darwinists can come up with something more scientific than non-testable non-observable just-so story telling.

2] Humans with higher levels of complexity and finer regulation of stage dependent forms was designed that way with pseudo genes.

Same answer…

3] The pseudogenes are critical for regulatory function because non-coding DNA is more important than coding DNA.

Yes. Non-coding DNA is responsible for using the same or similar genes (or basic “bricks and mortar” so to speak) to build very different functional systems and very different creatures.

4] Pseudogenes as common and critical builing blocks actually dont have to be used. Whether or not they are used doesnt have any effect on whether or not they are important.

In many cases that’s correct. You can live without an arm. That doesn’t mean your arm isn’t important or useful to you or that it wasn’t designed.

In other words the designer can arbitirarily use anything to do anything and yet it is clearly designed that way.

A designer can design any way he/she wants. The evidence for design isn’t based in the arbitrary ability of the designer to create, but in the inability for any known non-intelligent process to produce the artifact in question.

I really dont understand then how your design inference has any predictive value.

How do you think design inference works in forensics or anthropology? Hmmm? I’ve asked you this question many times before and you consistently avoid addressing it – for obvious reasons. The scientific basis for design inference has general application to any and all artifacts throughout the universe. The rational basis for detecting design is not limited to arrowheads, pottery shards, murder victims, or radio signals coming from space. It can also be applied to biological systems.

As Gilbert originally concluded it seems to me the sharing of genomic structure including a beta region pseudogene across primates and more particularly the sharing of an alpha gene between just man and chimps gives every appearance of common ancestory. Whether the pseudogenes are functional does not have anything to do with this conclusion particularly when you concede that the functional pseudogene in the beta region is not seen in other than primates when the designer hypothesis would predict that this essential building block for haemoglobin expression should be seen in all animals having hemoglobin.

This is a different argument from shared mistakes. This is the “nested hierarchical pattern” argument (NHP). The NHP argument is entirely based on sequence similarities without any consideration of the underlying functionality involved or the minimum sequences differences required to achieve the qualitatively novel differences in function. While the common descent hypothesis can explain sequence similarities quite well, to include the production of NHPs, the common descent hypothesis cannot explain functional differences beyond very very low levels of functional complexity – outside of invoking sequential design over time (i.e., “slow creation”).

You see, ID isn’t based on explaining sequence similarities, but on explaining functionally unique differences. The functional differences are key here – as I’ve pointed out many times for you before.

If you disagree I think you need to tell me the precise predictions of the design model. To me your model pales against a simple model of chance and contingency. Of gene duplication to give the alpha and beta cluster and then subsequent duplication within these 2 clusters gives the final primate form including almost identical structure between man and chimps. Variation and functional selection seems a compelling argument to me.

It would seem compelling to me too if I weren’t considering the minimum specific changes required to achieve the novel beneficial functions involved.

Sean Pitman
www.DetectingDesign.com

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Sean Pitman Also Commented

Gary Gilbert, Spectrum, and Pseudogenes

I was not clear enough in my comment. There are 14 ERV’s that are intact and able to produce virus that we share with the chimps.

This is not true. According to a study published in 2005, no human ERVs capable of replication have been identified; all appear to be defective as far as producing infective viruses is concerned due to major deletions or nonsense mutations.

Belshaw R, Dawson AL, Woolven-Allen J, Redding J, Burt A, Tristem M (Oct 2005). “Genomewide Screening Reveals High Levels of Insertional Polymorphism in the Human Endogenous Retrovirus Family HERV-K(HML2): Implications for Present-Day Activity”. J Virol. 79 (19): 12507–14.

These occur at the same location in the genome of both humans and chimps. There is no question as to the function of these 14 ERV’s. Some of these are associated with disease states in humans.

This is also not true. While many ERVs are being found to be functional, most of these functions are beneficial to one degree or another, and some are even vital to life. Also, there have been no proven cases of human ERVs causing disease.

“HERVs have frequently been proposed as etiological cofactors in chronic diseases such as cancer, autoimmunity and neurological disease. Unfortunately, despite intense effort from many groups, there remains little direct evidence to support these claims, and moreover some studies have served only to muddy the waters for others.” – http://genomebiology.com/2001/2/6/reviews/1017

“Many still manage to generate proteins, but scientists have never found one that functions properly in humans or that could make us sick.” – http://www.newyorker.com/reporting/2007/12/03/071203fa_fact_specter

It’s like arguing that regular genes cause disease. The real reason for disease is a loss of regulation of the normal function of regular genes, and perhaps ERV sequences on occasion, due to random mutations that destroy their original functionality.

If these are a product of design by God then why is reverse transcriptase part of the code in these viruses? They could have been placed directly in the genome as DNA. Did God design us to have disease? Would it not be more likely that these represent the past viral attacks on a common ancestor which were then incorporated into the germ cell and passed on the future generations of descendants? It would only require one ERV to prove common descent and we have 14. Ask yourself what is more reasonable?

Your knowledge about ERVs is very inaccurate. There are many rational reason for ERV-type sequences to be included, by design, in our genome. As already mentioned, many ERV sequences are being discovered to produced beneficial effects – some are even vital to life. Some ERVs have even been shown to fight against infection by exogenous retriviruses:

“The HERV-W env gene product has also been shown to block infection by an exogenous retrovirus, suggesting that the expressed HERV-W env gene could have a beneficial function to the host (Ponferrada et al., 2003).” – http://vir.sgmjournals.org/cgi/content/full/85/5/1203

“However, in the case of both Fv4 and Rmcf, the mode of defense is by the domesticated env gene blocking the receptor required for retrovirus entry.” – http://genetics.plosjournals.org/perlserv/?request=get-document&doi=
10.1371%2Fjournal.pgen.0010044

Beyond this, the theory that the ERV sequences within the human gene pool were derived from external viral infections is untenable given the population bottlenecks that would have been required to achieve this effect within the germline of humans or any other animal. Even modern retroviral infections never insert themselves within the germline cells of their host. Such a theory is based on something that is so extraordinarily unlikely that it hasn’t even been observed.

“No current transposition activity of HERVs or endogenization of human exogenous retroviruses has been documented so far.” – http://www.pnas.org/cgi/content/full/101/suppl_2/14572

“Most of these elements represent ancient retroviral infections, as evidenced by their wide distribution in primate species, and no infectious counterparts of human endogenous retroviruses (HERVs) are known to exist today.” – http://www.pnas.org/cgi/content/abstract/101/6/1668

In any case, for further details along these lines, please refer to these detailed discussions of ERVs:

http://www.detectingdesign.com/pseudogenes.html#Endogenous
http://www.whoisyourcreator.com/endogenous_retroviruses.html

Sean Pitman

Gary Gilbert, Spectrum, and Pseudogenes
We share far more than 14 ERVs with chimps.

Not too long ago it was thought that around 30,000 ERVs existed within the human/ape genomes, comprising between 1-8% of each. As of the 2005 Chimpanzee Sequencing and Analysis Consortium, where the entire chimpanzee genome was compared to the human genome, it is now thought that approximately 200,000 ERVs, or portions of ERVs, exist within the genomes of both humans and apes – totaling around 127 million base pairs (around 4% of the total genomic real estate). Some authors suggests a 45% ERV origin for the human genome at large (Mindell and Meyer 2001) and 50% for mammalian species in general, if all small fragments of ERV sequences are included in the estimate. In any case, of these hundreds of thousands of recognizable portions of ERVs, the vast majority of them seem to match up, at the very same loci, between humans and chimps. Less than 1% of the ERVs are lineage specific for either humans or apes. In other words, the vast majority of ERVs are shared or “orthologous” between humans and chimps (a significant increase from the seven or so that were once thought to infect both humans and chimps at identical locations).

So, doesn’t this make the case all that much stronger than humans and apes share a common ancestor? After all, what kind of intelligent designer would have put so much shared “junk” in both of our genomes?

Well, recent research is turning out some surprising discoveries on what was once thought to be junk-DNA. Much of what was thought to be junk is turning out to be functional to one degree or another – to include ERVs.

For more information on this most interesting topic, please visit:

http://www.detectingdesign.com/pseudogenes.html

Sean Pitman

Gary Gilbert, Spectrum, and Pseudogenes
Now you’re just projecting. How about putting your own ideas to the test and see where they stand? Isn’t it a bit strange that I’m willing to respond to questions and challenges regarding my position, but you are not? Are you willing to even consider that you might be wrong? What kind of evidence or demonstration would that take? – short of a conversion of most scientists?

I’ve spelled out quite clearly that my position is easily falsifiable and that I’d be more than willing to leave Adventism and even Christianity behind as convincingly falsified if reasonable evidence supporting the creative power of the Darwinian mechanism, or any other mindless naturalistic mechanism, could be produced… or that life has actually existed and evolved on this planet over hundreds of millions of years. I have no desire to believe in any falsehood – not matter how attractive it may seem to me. I really do desire to know the truth and follow where it leads as I am able to discover it.

What about you? What would make you leave agnosticism behind and consider that a personal God who thinks about you and cares for you and died for you actually exists?

Sean Pitman
www.DetectingDesign.com

P.S. By the way, science is also required to make leaps of faith. Science isn’t about absolute proof or demonstration. Science is about taking what little is known and using it to make educated leaps of faith into that which is not and cannot be known with absolute confidence.