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Sci Scavenger Hunt Answers

Yesterday’s Science Scavenger award goes to jadarm for his answer: “Humans, the little rat/piggie thingies that scientists experiment things with, and some monkeys…the kind of monkey that swings on trees.”

Close enough. A correct answer would include simian primates and guinea pigs. Put another way humans, other apes, monkeys, and guinea pigs. So jadarm misses a point for missing the non-human apes. It would present a difficulty if neither monkeys nor humans had a working copy of the L-Gulono-gamma-lactone oxidase (GULO) gene that all other mammals (besides Guinea pigs) share and that is responsible of the final step of ascorbic acid synthesis, but that apes did have a working copy. That would imply that either monkeys were more closely related to humans than apes (which would undermine most of what we know about the primate phylogenetic tree), or that basal apes had a very fortuitous back-mutation restoring this gene’s functionality and humans subsequently lost it again (this is very unlikely for reasons I can’t go into here). The final possibility would be that evolution was wrong – also unlikely due to heaps & heaps of other evidence for evolution.

Humans and other primates (apart from prosimians) share mutations to the GULO gene that render it unable to produce the enzyme necessary for ascorbic acid synthesis but preserve what is called GULOP – or GULO pseudogene that does carry some of the same codons as the functional gene that other mammals share. Humans, apes and monkeys all share a common ancestor with one another more recently than they do with prosimian primates or other mammals. This means that the mutation took place in the simian line after it diverged from the prosimian line, and was preserved in all of the descendants of that line, including ourselves.

Guinea pigs also carry mutations to the GULO gene that render it unable to produce the enzyme, but preserve a pseudogene. The Guinea pig pseduogene is significantly different from the human one, indicating that the mutation that inactivated the gene in Guineas was a separate event.

Subsequent to the deactivation of GULO, in both Guineas and in primates, there was no selective pressure to maintain the structure of the GULO gene, so a number of other mutations have accumulated, separately in each line. It is a difficult matter to isolate which mutation(s) were originally responsible for each line’s loss of Vitamin C for this reason. And, for that reason, I’ll leave it to the professionals to sort that out. But, for interesting further reading, see why a favored hypothesis is that simians lost Vitamin C synthesis to a retroviral insertion, and why they speculate that this event might have contributed to the diversity of primates, including human evolution.

4 comments to Sci Scavenger Hunt Answers

  • Stan Parker

    True scientists have proven this wrong. Our gene is closer to the guineau pig gene than to the so called working gene. If you need a “reference” for this then I have http://www.answersingenesis.org/tj/v18/i3/mistakes.asp

  • Hi, Stan!

    I’ve actually come across that article before, and I’m afraid that your “true scientist” is a creationist, and he made some major errors in that article.

    His biggest problem is with his assertion that “shared mistakes” between Guineas and humans, but (presumably!) not shared by other mammal species that do synthesize ascorbic acid. He claims that this shows that “shared mistakes” can arise from something other than common ancestry – therefore are not evidence of it. But, he didn’t check to see if what he counts as “lesions” – changes in base pairs between humans (and Guineas) and rats actually show a history of having arisen independently in Guineas and humans. It turns out that they arose only once – in the rat line. Actually, of the 47 base pair changes he identifies as “shared lesions”, all but about one in ten of them are shared between most mammal groups. In other words, these aren’t “lesions” on the pseudogene in either Guineas or humans. They are mutations on the rat gene (which nevertheless do not render the rat gene inoperable).

    The remainder of his article is pleading that the GULOP pseudogene may have an undiscovered purpose and that therefore the mutations shared between the members of the primate line (which are not known to do anything other than to prevent our synthesis of Vitamin C) are examples of “common design” rather than inherited mistakes. This is a weak argument. It’s true that even “junk DNA” is often put to structural or non-coding use (sometimes in ways that are not currently very well understood). However, the sequences of these genes are not random and it isn’t very probable at all that GULOP is anything but a true pseudogene – a gene that lost its function and was subsequently inherited by all of the species descended from the population that lost it. If it were anything else, we could expect to find something like what he thought he saw with the comparison to rats – or we would find that some group within that array of organisms actually had a functioning GULO gene or no GULOP pseudogene at all. Instead the base pair comparisons match very closely with the phylogeny of simians that we know from every other line of evidence.

    So, I’m afraid this isn’t proven wrong at all. But I’m glad you’re here & I’m glad you’re paying attention!

  • I have the same problem Stan has. Differentiating between true scientists and false scientists. It gets so confusing.

    But not nearly as confusing as trying to understand the real answer. When you start talking about GULO’s and GULOP’s and shared mistakes and lesions I find myself wondering how was that retroviral inserted and if Tennessee will be able to take care of Oklahoma State in the tournament today.

    Teacher, is this a 101 class or am I in the wrong room?

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