==Why is it that ERV’s that are common in some human populations but not in all humans have reverse transcriptase genes that are nearly perfect?
Could you please explain the relavence of your question so I have something better to go on. I’m just an amateur ya know!
==Why is it that ERV’s that are shared between all humans but not shared by chimpanzee’s are MORE preserved than ones that are common among all apes?
Again, please explain what you are driving at, and please provide links/sources.
==Why is the Vitamin C synthase gene broken in the exact same place in humans and apes?
Already answered...Common mechanism/mutational hotspots.
==Why would an animal be designed with a broken Vitamin C synthase gene in the first place
Already answered...we were created with a functional GULO gene that has since mutated. It is broken in the same place because of common mechanism/mutational hotspots
==what theory could explain the fact that they are broken in the same place
Already answered...creatures that share similar body plans, occupy similar environments, and have similar functional needs will have a similar hot spots for certain functional elements such as “pseudo”-genes and ERVs.
When sequencing the human genomes, it was noticed that the most recognizable sequence (usually mutated beyond repair) is Reverse Transcriptase, the protein that retrovirus uses to make RNA into DNA, and situated in the context of other viral protein coding DNA.
It seems obvious that these are nonfunctional DNA elements (other than that one rare case you brought up), and just as predicted by their non-functionality - when comparing ERV’s shared between species (human-chimp) and a gene shared between species (human-chimp), one notices that the ERV’s are more divergent than the genes.
Johnson WE, Coffin JM.
Department of Molecular Microbiology, Tufts University School of Medicine, Boston, MA 02111, USA.
The genomes of modern humans are riddled with thousands of endogenous retroviruses (HERVs), the proviral remnants of ancient viral infections of the primate lineage. Most HERVs are nonfunctional, selectively neutral loci. This fact, coupled with their sheer abundance in primate genomes, makes HERVs ideal for exploitation as phylogenetic markers. Endogenous retroviruses (ERVs) provide phylogenetic information in two ways: (i) by comparison of integration site polymorphism and (ii) by orthologous comparison of evolving, proviral, nucleotide sequence. In this study, trees are constructed with the noncoding long terminal repeats (LTRs) of several ERV loci. Because the two LTRs of an ERV are identical at the time of integration but evolve independently, each ERV locus can provide two estimates of species phylogeny based on molecular evolution of the same ancestral sequence. Moreover, tree topology is highly sensitive to conversion events, allowing for easy detection of sequences involved in recombination as well as correction for such events. Although other animal species are rich in ERV sequences, the specific use of HERVs in this study allows comparison of trees to a well established phylogenetic standard, that of the Old World primates. HERVs, and by extension the ERVs of other species, constitute a unique and plentiful resource for studying the evolutionary history of the Retroviridae and their animal hosts.
PMID: 10468595 [PubMed - indexed for MEDLINE]
If we were separately created de novo with a functional GULO gene that has since mutated, does that mean you are conceding the functionality of the GULO sequence in humans? How does that fit in with...
“similar hot spots for certain functional elements such as “pseudo”-genes and ERVs.”
I can see how common circumstance, similar morphology, etc could lead to identical seemingly meaningless changes in sequence when comparing similar species when compared to divergent species in functional sequences. Maybe an amino acid that seems to be a “free” position when comparing several different species (i.e. it is the same protein doing the same job with ‘mostly’ the same sequence; and that spot seems fairly “free” of evolutionary constraints because it is several different amino acids in several different species) really does has a deeper significance than has thus far been determined and it does make a difference that those “free” positions are the same amino acid in humans and chimps, and a different one in bovine and pigs, and yet a third in mice and rats. The overall pattern is pretty impressive evidence for the similarity/difference of living things down to a molecular level.
But if the GULO gene did mutate from a working copy, what mechanism introduced an identical deletion in ape lineages, but more similar mutagenic pressure between chimps and humans than was experienced by orang’s? Why would a gorilla’s mutations be more similar to a human or a chimps than to an orang? What mechanism would make mutations selectivly of that type and at those locations that has not been detected when looking at the mutations of cell lines of that lineage?