"You don't understand the history of transposons!"
Posted on 04/21/2006 9:17:58 PM PDT by Right Wing Professor
If we take the sample provided by you it is 100%.
Do you want to be silly or do you want to talk about evolution and the most recent aspects that are being elucidated in the genomic era?
It's not a false assertion and I actually demonstrated in your own example that the one article in that ToC on comparative genomics used transposable element distribution.
I'm beginning to think you don't quite grasp what a genome actually is.
"this type of DNA [repeat elements] is a major portion of the genome" is also false or nonsense?
I do not think you meant to say that this is nonsense and am giving you every opportunity to make clear what is nonsense so as to make no mistakes as to what you are saying.
How do you suggest this be resolved. You want to argue over the number of papers published that have done genomic comparisons using different methods.
OK. Rather a side issue, but it can be addressed by finding every article that has compared genomes and seeing what types of analyses were done. I would agree that number of genes, homology between gene sets, rRNA homologies were done. Transposable element analysis is much harder to do which is why it is a current focus.
I will initially refer you to the Chimp genome papers in Nature. Two were published One, the basic initial report:
Nature 437, 69-87 (1 September 2005) | Initial sequence of the chimpanzee genome and comparison with the human genome
including a section on genome evolution wherien nucleotide substitutions were examined, as well as insertions and deletions. Insertion of transposable elements were speficially looked at and catalogued.
The secomd sister article, Nature. 2005 Sep 1;437(7055):88-93. A genome-wide comparison of recent chimpanzee and human segmental duplications.
This touches exactly on the issue of transposable elements on genomic evolution. In the last pre-discussion paragraph the author's state the importance of transposons to genomic structure and evolution:
We propose that most of the asymmetrical increase of duplicated DNA in the chimpanzee lineage has emerged as a mechanistic consequence of changes in chromosome structure and not selection. The subterminal caps are an idiosyncratic structural aspect of African great ape chromosomes28, which are generally regarded as heterochromatic. Similar to human pericentromeric DNA, the regions have served as sinks for duplicative transposition and expansion of particular euchromatic segments. This process has led to an overall increase in chimpanzee genome size of at least 16 Mb since human and chimpanzee separated. It is interesting that the same region that represents the site of chromosome 2 fusion29 in the human lineage has undergone a segmental duplication hyperexpansion within the subterminal region of chimpanzee chromosomes. This may suggest an inherent instability of this segment of DNA, further extending the association of segmental duplication and chromosomal rearrangement without a direct cause and effect relationship
Science also did an article about the findings associated with the chimp genome and wrote:
But as suggested by earlier work on portions of the chimp genome, other kinds of genomic variation turn out to be at least as important as single nucleotide base changes. Insertions and deletions have dramatically changed the landscape of the human and chimp lineages since they diverged. Duplications of sequence "contribute more genetic difference between the two species--70 megabases of material--than do single base pair substitutions," notes Evan Eichler, also of UW, Seattle, who led a team analyzing the duplications. "It was a shocker, even to us."
From Chimp Genome Catalogs Differences With Humans, Elizabeth Culotta, 9-2-05 Science
The centrality of transposable elements to evolution is becoming more clear with every passing day.
The analysis consists pretty much only of breakpoints. Coincidntally to our discussion, this chromosome contains FRA3B.
Breakpoints were compared with other primates to look at evolutionary questions.
One excerpt here:
Further comparative FISH analysis revealed that a large-scale pericentric inversion occurred in the ancestor of the African apes and is present in modern human chromosome 3 as well as the chimpanzee and gorilla orthologues, but not in orang-utan or Old World monkeys14. Two scaffolds from the Baylor College of Medicine Human Genome Sequencing Center (BCM-HGSC) rhesus macaque Mmul_0.1 assembly were found to span both breakpoints of the human inversion (Fig. 2; see Supplementary Table 4 for breakpoint details). The macaque 5' breakpoint is characterized by a short homologous GTGG track (Fig. 2b) and by a mammalian interspersed repeat (MIR) that was split by a segmental duplication before the inversion resulting in one part, designated MIR A, present in boundary I and a second part, designated MIR B, present in boundary III (see Fig. 2a). The MIR at the 3' end of boundary III was present in the segmental duplication and may have been involved in the insertion event. A number of simple repeats and low complexity regions were found within 1 kb of the breakpoint (see Supplementary Table 5). Each of these elements, including retrotransposons15, short homologous sequence and alternating purine-pyrimidine tracks16 have been reported for many other breakpoints.
My bold. Break point analysis, as Stultis brought up is extremely important to understanding evolutionary relationshsips and mechanisms and transposon and similar elements are associated with these breakage points.
It is a flat out lie to claim that only one paper in the issue was on comparative genomics. Almost all of them were.
I didn't say it was nonsense. Learn to read.
Indeed. And the evolutionary conclusions that could be drawn from the transposable elements were limited.A high-proportion of the HERV-K insertions occurred after hominoid chimp divergence, making them useless for interspecific comparisons. Some of the comparisons of subtypes of HERV-K were useful, but the transpositions themselves appear to occur largely on timescales that are fast compared with species divergence. There appears to be little diversity among humans in the HERV-K insertions, but that may be a result of our species' genetic homogeneity.
Comparison of SINEs between human and chimp genomes may be similarly disappointing. Humans have three times the number of lineage specific SINEs. And quoting the initial chimp genome paper "In any case, the presence of such anomalies suggests that caution is warranted in the use of single-repeat elements as homoplasy-free phylogenetic markers." The chimp genome paper discusses other classes of transposable elements, and some of them look more phylogenetically promising, but to claim they are likely to replace genes in comparative genomics is grossly optimistic and unwarranted.
Retract your false assertions and apologize. You breezed on this thread with a direct insult to me, and have continued throughout. I ignored your first few insults; then I asked you to stop; and when you refused, I decided that if you can't act like a civilzed human being, you don't deserve to be treated like one.
The first, Periodic Extinctions of Transposable Elements in Bacterial Lineages: Evidence from Intragenomic Variation in Multiple Genomes, was a comparative genomic study. -- and it was about transposons.
This, Explorative Genome Scan to Detect Candidate Loci for Adaptation Along a Gradient of Altitude in the Common Frog (Rana temporaria) is a genomic study, but not comparative.
One other, Genetic Structure and Evolutionary History of a Diploid Hybrid Pine Pinus densata Inferred from the Nucleotide Variation at Seven Gene Loci, seems related but looks only at 7 loci, not the genome.
Again, you seem not to know what genome or genomics means.
Research Articles:
Periodic Extinctions of Transposable Elements in Bacterial Lineages: Evidence from Intragenomic Variation in Multiple Genomes
Evolution of Circular Permutations in Multidomain Proteins
Diversity and Evolution of the Thyroglobulin Type-1 Domain Superfamily
Evolution of Programmed DNA Rearrangements in a Scrambled Gene
MBE Advance Access published on January 23, 2006
Diversification and Specialization of HIV Protease Function During In Vitro Evolution
Explorative Genome Scan to Detect Candidate Loci for Adaptation Along a Gradient of Altitude in the Common Frog (Rana temporaria)
The Evolutionary Rate of a Protein Is Influenced by Features of the Interacting Partners
An Analysis of Signatures of Selective Sweeps in Natural Populations of the House Mouse
A Tandem Gene Duplication Followed by Recruitment of a Retrotransposon Created the Paralogous Bucentaur Gene (bcntp97) in the Ancestral Ruminant
Genetic Structure and Evolutionary History of a Diploid Hybrid Pine Pinus densata Inferred from the Nucleotide Variation at Seven Gene Loci
Recombination Estimation Under Complex Evolutionary Models with the Coalescent Composite-Likelihood Method
Nuclear Gene Variation and Molecular Dating of the Cichlid Species Flock of Lake Malawi
The Evolutionary Origin of Peroxisomes: An ER-Peroxisome Connection
Genomic comparison that is possible today focus largely on repeat element distribution
You responded:
Your main point is nonsense in any case. Most molecular evolution analysis...
Again, you don't seem to know what a genome is and don't know the difference between a molecular evolutionary analysis and a genome comparison.
Again, genomic comparison today focuses largely on repeat element distribution.
I disagree and this has all ready taken place to a large extent. Fundamental to this is that it turns out that the repeat elements are such a major component of genomes and this wasn't known until the full genomes were sequenced.
The Science article I linked to article addresses this to some degree in relating how looking only at genes there is very little difference between chimp and human and the reasosn for our differences are in no way apparent. Gene relationships have been extensively examined over decades (hence my comment to you the other day that you have reached the 1980's) and the very high degree of homology doesn't seem to be able to explain the differences in species.
A clue that transposable element activity of some sort did appear in the 1980's and 90's with the sequencing of a number of G-Protein coupled receptor genes. It was found that many of these genes surprisingly were intronless. This was indicative of class I transposition having been involved in the evolution of this large and important class of genes. Other intronless genes have been found as well.
Breakage and recombination that can be mediated by transposons and repeats elements provide a mechanisms for chromosomal rearrangements (as McClintock was the first to discover) which fits well with an mechanisms for mutations over the course of evolution. This is combined with the epigentic understanding of gene regulation and eu/heterochromatin strucure/function associated with high repeat regions provides a basis for not only the structural chromosomal changes which define species and reflect evolution but a genetic regulatory mechanisms whereby regulation of genes which are essentially interchangable between species can provide for the vast differences in phenotype not reflected in the genotypes (ie the genes are pretty much the same so how do they specify human vs chimp).
As I pointed out, the most recent authoritaive genome study from the sequencing consortium just published in nature and analyzed these sort of questions.
"In any case, the presence of such anomalies suggests that caution is warranted in the use of single-repeat elements as homoplasy-free phylogenetic markers."
is that what I am talking about is not their uitilty as homoplsy-free markers, but their distribution (and discovery via analysis) throughout geneomes at regions of divergence.
Treating them as if they are genes with sequences that can be used to compare phylogeny based on homology would require probably more than caution, it just wouldn't be the thing to do.
Much of the focus in this area is to actually identify repeats. Using the first known characterized repeats or elements as if they are genes is not what is being addressed. So, yes, I agree with you about the approach you outline. But that is not what I am talking about.
Oh yeah, I don't know what a genome is. That is almost so imbecilic it isn't even an insult.
Look at the chimp genome comparson paper you yourself cited. It is a direct comparison between the genomes of Homo sapiens and Pan troglodytes. How much of the comparison is a comparison of transposable elements? In the section on genome evolution, there are subsections on nucleotide substitutions, insertions and deletions, transposable element insertions, and large scale rearrangements. One subsection out of four, in other words, concerns transposons of various kinds. The next section, on gene evolution, does not touch on transposition at all. And in fact, the only really detailed quantitative consideration of evolutionary rates is in the section on gene evolution. Then there's a section which you claim is handwaving, on human population genetics. A 18 1/2 page paper, in other words, on comparative genomics, between two very closely related species where the transposons have been well studied and where they should provide more information than usual, actually deals with transposons for less than two pages, and largely reaches negative conclusions.
And this is the area that you claim has eclipsed gene analysis, which is '1980's genetics'!
and don't know the difference between a molecular evolutionary analysis and a genome comparison.
Nor, evidently, do the authors of 'Initial sequence of the chimpanzee genome and comparison of the human genome', since they spend a far larger fraction of the paper on moleuclar evolutionary gene analysis than on transposed element analysis.
You make sweeping, broad statements that are utterly unwarranted, and then defend them, if at all, by claiming the rest of the world doesn't know what it's talking about.
"You don't understand the history of transposons!"
Size isn't everything.
The Science article I linked to article addresses this to some degree in relating how looking only at genes there is very little difference between chimp and human and the reasosn for our differences are in no way apparent. Gene relationships have been extensively examined over decades (hence my comment to you the other day that you have reached the 1980's) and the very high degree of homology doesn't seem to be able to explain the differences in species.
You don't know that. Nobody knows that. Nobody really has a clue if the differences in non-coding regions have much effect at all; and until the relevant knockout experiments have been done, nobody will know. There are literally hundreds of thousands of differences in our coding DNA between humans and chimps.
Breakage and recombination that can be mediated by transposons and repeats elements provide a mechanisms for chromosomal rearrangements (as McClintock was the first to discover) which fits well with an mechanisms for mutations over the course of evolution. This is combined with the epigentic understanding of gene regulation and eu/heterochromatin strucure/function associated with high repeat regions provides a basis for not only the structural chromosomal changes which define species and reflect evolution but a genetic regulatory mechanisms whereby regulation of genes which are essentially interchangable between species can provide for the vast differences in phenotype not reflected in the genotypes (ie the genes are pretty much the same so how do they specify human vs chimp).
Whether transposition is an important source of genome variability is an entirely different issue from whether transposon analysis predominates in current comparative genomics. As I've said a hundred times, the source of genome variability is unimportant to the possibility of evolution; what matters is that variability exist and be heritable. However, Darwin knew no more about point mutations than he did about transposons. What he appreciated was that heritable variability was important.
Yes because it was the section on gene evolution at the protein coding level: We next sought to use the chimpanzee sequence to study the role of natural selection in the evolution of human protein-coding genes..
Again, you don't seem to know what gene means compared to genome.
As far as your other point, yes, the initial report didn;t focus on this, but the second sister report, A genome-wide comparison of recent chimpanzee and human segmental duplications, was specific to these questions of chromosome structure.
Actually, no. I have always said this is coming from stidies that are ongoing made possible by the various genome projects.
Here is an example from a recent Genome Research Identification of transposable elements using multiple alignments of related genomes:
Repeat elements make up a large fraction of many eukaryotic genomes. Within these regions, the occurrence of Transposable Elements is rampant. The term Transposable Elements (TEs) groups several subclasses of elements that replicate in the genome, either through the reverse transcription of an RNA intermediate (class I elements), or autonomously from DNA to DNA by excision and repair (class II elements). Class I elements are further grouped by the presence (LTR elements) or absence (LINE and SINE elements) of long terminal repeats. Class II elements are largely comprised of elements with terminally inverted repeats (TIR elements). TEs make up large portions of the middle- and high-repetitive segments of genomes and are mostly found in the heterochromatin and centromeric regions (Pardue et al. 1996Go; Junakovic et al. 1998Go). Studies show TEs can be deleterious to hosts (Green 1988Go; Deininger and Batzer 1999Go) and approximately one-half of Drosophila melanogaster mutations are attributed to TEs (Finnegan 1992Go). Increasingly, evidence points to other contributions of TEs in the evolution of the host genome and even in shaping chromosome structure (Pardue et al. 1996Go; Kidwell and Lisch 1997Go; Labrador and Corces 1997Go; Pardue and DeBrayshe 1999Go). They are also the chief cause of gapped regions and poor annotations in up to 10% of currently sequenced genomes. Despite some knowledge about sequence structure in transposons, for example, they typically contain open reading frames in the interior or some characterizing repeat sequences at the ends, their mechanisms for replication are poorly understood, and their classification into families is far from complete. An accurate catalog and phyletic mapping of the instances of TE insertions will help elucidate TE contribution to genetic variability in eukaryote genomes, and refine assemblies of sequenced genomes (Holmes 2002Go; Bennett et al. 2004Go).
My bold, but all the paragraph is pertinent to this discussion.
In no way is this some sort of claim that the rest of the world doesn't know what it is talking about.
Please, try to be stay on subject (as you have at times) and refrain from speciousness.
You don't know that. Nobody knows that.
I agree, which is why I wrote "doesn't seem".
Nobody really has a clue if the differences in non-coding regions have much effect at all;
No, people have clues. I linked to the Science comment article that talked about this.
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