Posted on 08/07/2007 9:30:37 AM PDT by GodGunsGuts
RIVERSIDE, Calif. – A research team, including UC Riverside biologists, has found experimental evidence that supports a controversial theory of genetic conflict in the reproduction of those animals that support their developing offspring through a placenta.
The conflict has been likened to a “battle of the sexes” or an “arms race” at the molecular level between mothers and fathers. At stake: the fetus’s growth rate and how much that costs the nutrient-supplying mother.
The new research supports the idea of a genetic “arms race” going on between a live-bearing mother and her offspring, assisted by the growth-promoting genes of the father...
(Excerpt) Read more at eurekalert.org ...
==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?
Well, this was your challenge in post 104
Why is the Vitamin C synthase gene broken in the exact same place in humans and apes? Why would an animal be designed with a broken Vitamin C synthase gene in the first place, and what theory could explain the fact that they are broken in the same place.
The vitamin C questions are the ones that I addressed. I believe the paper GGG cites indirectly in post 274 by Inai et al. supports my position. So I conclude that your specific challenge as I have cited above has been answered.
ERV’s and pseudogenes are not functional, this explains the observation that the measured neutral mutation rate of that species can be used to predict its time of divergence from related species
Again, this is an assumption.
Gene-breaking: A new paradigm for human retrotransposon-mediated gene evolution
Transposable elements are neither "junk DNA" nor mere curiosities to be categorized taxonomically and relegated to dusty catalogs; rather, they can affect gene expression in important ways and are a dynamic and significant part of our evolutionary history (Boissinot et al. 2000; Meischl et al. 2000; Myers et al. 2002; Brouha et al. 2003; Salem et al. 2003; Kazazian Jr. 2004). Transposons comprise nearly 45% of the human genome (International Human Genome Sequencing Consortium 2001) and include DNA transposons, LTR retrotransposons, and non-LTR retrotransposons such as LINEs and SINEs. Each class can be divided into several subgroups, each with a unique evolutionary history. Most elements are currently inactive, but the active elements shape the genome through continued expansion, transduction, chromosomal rearrangements (Gilbert et al. 2002; Symer et al. 2002), and even direct effects on gene expression (van de Lagemaat et al. 2003; Druker et al. 2004; Han and Boeke 2004). The related endogenous retroviruses have also been implicated in affecting gene expression, inserting new promoters and/or 3' end forming sequences into many human genes (Landry 2003).
Dr. James Shapiro is being confirmed day after day.
If common circumstance can lead to similar mutations in similar species and different mutations in different species; wouldn’t one expect that Old World vultures and New World vultures would be more similar in genetic sequence to each other than either would be to eagles?
Why then do Old World vultures more closely resemble eagles than New World vultures in their DNA sequences?
You have to laugh at a Creationist who buys into a literal meaning of 66 books, gospels and letters that recognize a flat eath ....
==Many elements in DNA are highly divergent and shown to be selectively neutral.
I understand divergence, such as a limb changing over time, but I’m not sure I know what you mean by DNA that are highly divergent. Divergent from what?
An example of a conserved sequence would be the gene that codes for hemoglobin. It is necessary for blood cells to carry oxygen so would be under stringent selection. When comparing the hemoglobin molecule between species one notices that there are no differences between the human hemoglobin and the chimp hemoglobin, but several differences between the human and chicken hemoglobin. Among the differences some positions seem to be “free” positions where any of several amino acids can appear in different lineages without changing the ability of the molecule to bind oxygen. Several others at the ‘active domain’ of the protein are highly conserved, they are seldom any amino acid but the one necessary for the active site of the protein to be active. This reiterates the linkage between function and conservation.
A divergent sequence would be a pseudogene or ERV that doesn’t have a function and changes at the neutral mutation rate. When comparing the gene for hemoglobin to a pseudogene just as long and shared between species, one would expect a couple changes between humans and chimps (compared to none in hemoglobin) and many more changes between human and chicken in a pseudogene than would be observed when comparing the hemoglobin sequence.
One can also tell if a DNA segment is being transcribed to a protein and is under selection if the pattern of mutations across species tends to accumulate at the third position of the codon within an open reading frame (third position wobble, it doesn’t change the amino acid coded for, or it codes for a related amino acid). DNA sequences that do not make proteins accumulate mutations at any of the three positions of the codon with equal likelihood.
Great presentation (IMHO) of the issues we have been discussing. I think some of the material was added as a direct result of our discussion/debate. All the best—GGG
http://www.detectingdesign.com/pseudogenes.html
I enjoyed their presentation, although it doesn’t take them long to diverge into misrepresentation.
“So, the persistence of a non-functional DNA sequence in an entire lineage for such a supposed long period of time seems remarkable in the context of the gene duplication hypothesis. The very fact that pseudogenes are still present and recognizable after tens of millions of years without any beneficial function just doesn’t seem to make sense.”
With the neutral rate measurable what kind of Scientist says “it just doesn’t SEEM” (emphasis mine) “to make sense”. The divergence of this pseudogene is about one fifth as divergent as what one would expect from the neutral mutation rate (based upon measurements of the divergence of other pseudogenes) and a comparison of two lineages that share the pseudogene.
So they take an exceptional example of a psuedogene that shows conservation and try to use it to establish that all pseudogenes have function, even the ones that do not show conservation. I am less than impressed.
Also they go on to suggest (with emphasis) that “The failure to recognize the full implications of this particularly the possibility that the intervening noncoding sequences may be transmitting parallel information in the form of RNA molecules—may well go down as one of the biggest mistakes in the history of molecular biology.” Despite the fact that they introduce the eta pseudogene with the relavant fact that it “has no start codon (AUG) and it has several stop codons. So obviously, no mRNA is made”.
So which tact are they taking? That all pseudogenes have function, or only the ones that show conservation? That all psuedogenes transmit information in the form of mRNA molecules, or only the ones that allow RNA polymerase to make a mRNA of their sequence? That all psuedogenes have a regulatory function like the ‘gene switching’ putative function of the eta psuedogene, or only the ones that change between lineages at one fifth the expected neutral mutation rate?
I think they are throwing mud and trying to see what sticks. It is good mud though, the only misrepresentation is in the relative numbers. MOST ERV sequences and pseudogenes do change at the neutral mutation rate, so latching onto the putative functions assigned to sequences that are conserved to try to ascribe function to sequences that are not conserved is complete obfuscation.
J Mol Biol. 1984 Dec 25;180(4):803-23.Links
The eta-globin gene. Its long evolutionary history in the beta-globin gene family of mammals.Goodman M, Koop BF, Czelusniak J, Weiss ML.
In phylogenetic reconstructions by the parsimony method, utilizing 62 sequenced globin genes and pseudogenes (including 34 of the beta-globin gene family from eutherian orders Primates, Lagomorpha, Artiodactyla and Rodentia), the branch of primate psi beta pseudogenes and the goat embryonically expressed epsilon II gene group monophyletically together as orthologues of a common ancestral gene (labelled eta) distinct from orthologues of epsilon, gamma, delta and beta. This primate psi eta-goat eta branch is cladistically closer to epsilon and gamma than to delta and beta branches. In each eutherian order gene conversions replaced portions of delta by beta sequences, whereas in descent of Primates epsilon, gamma and eta mostly retained their separate ancient identities predating the radiation of Eutheria in all their exons and non-coding regions. The loci of the ancestral beta-globin gene cluster in basal eutherians and proto-primates, as deduced from beta-clusters representing the four eutherian orders, were linked 5’-epsilon-gamma-eta-delta-beta-3’ with epsilon, gamma and eta being embryonically expressed genes, and delta and beta ontogenetically later expressed genes. Through deletions gamma was lost in artiodactyl evolution, eta in lagomorph and rodent evolution, and all DNA between exon 2 3’ boundaries of eta and delta in prosimian lemuriform evolution (lemur having the hybrid pseudogene psi eta delta). Simian primates retained intact the five loci of the ancestral cluster. Not only did eta, after it became a pseudogene in the basal primates, persist intact in descent to present-day simians but in the line to hominoids it evolved during the last 40 million years at the decelerated rate of 1 X 10(-9) substitutions/site per year which is one-fifth the expected neutral rate. The possibility is suggested that the psi eta locus situated between fetal and adult chromosomal domains of the simian beta-globin gene cluster might play some role in a mechanism for ontogenetic switches of globin gene expression. However, not enough sequence data on genes and intergenic regions in DNA of species of primates and other mammals as yet exist to know if the slow rate of 1 X 10(-9) reflects the rate of a conserved functional gene or primarily reflects a decelerated neutral rate of hominoid DNA evolution, conceivably from enhanced DNA repair and longer generation times in hominoids. The further possibility is raised that gene correction (repair of damaged DNA that prevents emergence of new alleles) and gene conversion both more often involve strand copying of conserved than of rapidly evolving DNA.
PMID: 6527390 [PubMed - indexed for MEDLINE]
Thanks for your reply. If you don’t mind, I would like to pose your questions to the auther and see if he replies. If he does, I’ll post it here. Thanks for your response—GGG
PS I think he is clearly implying that most or all of pseudogenes will be shown to have function. But I could be wrong. Let’s see if he replies.
Interesting that he buys into the conservation-function paradigm in ascribing putative function to conserved sequences, yet also thinks to ascribe function to non conserved sequences.
If he is holding out for the idea that every jot and tittle of DNA sequence has function then how can he explain why some sequences are not at all conserved, can be deleted entirely without any phenotype, and change between lineages at the neutral mutation rate?
I think he likes to only believe the data which supports his ‘every DNA sequence has function’ hypothesis and completely ignore all the sequences that have clearly been shown to not have a function and to not show conservation between lineages.
I guess one has to do something to try to hold the line against a reality which frightens and disturbs them.
I guess I was a bit mistaken. I sent him your reply and he sent back the following:
“I don’t get the argument . . . I’m not saying that there are no neutral genetic sequences. I’m saying that those that are concerved between species are likely functional and that many of these have been proven to be functional.”
I sent him your last reply as well. At this point, I’m just as curious as you about his position re: pseudogenes that do not show conservation.
Seems that he and I are saying the same thing on this point. The next subject would be the relative abundance of sequences that show conservation versus sequences that change between lineages at the neutral mutation rate. I think only about 10% of the human genome shows conservation between lineages, but am going from memory....a bit of trouble tracking down the actual number so don't take my word for it. ;)
RESEARCHING....... If your interested I’ll post the answer to you with citation when I find it.
In this paper they point out that 97% of the human genome is non-coding.
“In this issue, Frazer et al. (2001) describe the large-scale identification of conserved noncoding elements
from human chromosome 21 using oligonucleotide array technology. In a twoway comparison between mouse and human,
they found that the amount of conserved noncoding sequence was roughly equal to the coding sequence in this region.”
So about 6% of the human genome shows conservation between lineages based upon this finding. That leaves 94% that changes between lineages at the neutral mutation rate. Interesting though that there is as much conserved non-coding DNA (i.e. probably fully functional and under selective pressure) as there is conserved coding DNA. Obviously a lot is going on in this 3% of the genome that is conserved but non-coding, and the function of these conserved sequences are probably just as important as the 3% of the genome that codes for proteins.
Exciting times, and lots of work to do. FUN FUN STUFF!!!
Thanks for making me look all that stuff up, its good to know and makes me excited about the future of Biology. And every step we make further exemplifies what a miraculous and wonderful creation we are, and shows the POWER and the GLORY of our creator who brought us forth from specks of dust and set us as stewards over the earth that he created from matter forged in the heart of stars.
==In other words, as a Biologist I have to say that we have a LOT of work to do.
I’ll say! Check out this fascinating article from Science News. I would not be surprised if they someday soon announce that almost everything we thought about genes/genomes was wrong. I suspect that one of the items in the announcement will almost certainly contain a blurb explaining why “junk DNA” isn’t junk at all:
“Researchers slowly realized, however, that genes occupy only about 1.5 percent of the genome. The other 98.5 percent, dubbed “junk DNA,“ was regarded as useless scraps left over from billions of years of random genetic mutations. As geneticists’ knowledge progressed, this basic picture remained largely unquestioned....”
“Closer examination of the full human genome is now causing scientists to return to some questions they thought they had settled. For one, they’re revisiting the very notion of what a gene is.”
http://www.sciencenews.org/articles/20070908/bob9.asp
Creationists look at the same evidence:
Many previous entries have dealt with these subjects (e.g., 06/15/2007, 12/29/2006 bullet 2, 11/09/2006, 07/06/2006). This is a classic case of a paradigm change in science occurring before our eyes. Even what we mean by an intuitively-obvious word like gene is being questioned: is there such a thing? Does it have physical reality, or is it a mental picture humans have imposed on a much more subtle reality? The new buzzword is network, but is that an accurate characterization? Networking is concerned more with the interactions of entities than with the entities themselves; this means that the rules of the game are more important than the nodes of the network. How could that fit within a materialistic world view?
Whatever comes in the days ahead, it appears that there is far more information processing occurring in the cell than even Watson and Crick imagined – and that was startling and elegant enough. Barry states that the raw genetic information transcribed in DNA now appears to be 62 times what genes alone would produce. The fundamental operational unit of life may, therefore, be nonphysical: information, not molecules. These are exciting times for science – troubling times for Darwinists. Don’t expect them to have any remorse over leading mankind into a “modern orthodoxy” that was mistaken.
For full article:
http://creationsafaris.com/crev200709.htm#20070912a
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