Whoops. Look at [deleted] on Wikipedia and the British use of the word (a person who is obnoxious or stupid). I completely understand your outrage - I would never use language like that.
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It’s not true for bacteria, but it’s very much true for vertebrates, and for most animals. Bacteria undergo lots of horizontal gene transfer, while vertebrates have very little. Vertebrates, not surprisingly, therefore yield very good, consistent phylogenetic trees when their DNA is analyzed.
I took another look at GULO, by the way, to see if some common mechanism really could explain the exons that were lost in both humans and guinea pigs. Your argument was that humans lost 7 out of 12 exons from the gene, and that it was unlikely that the exons guinea pigs happened to lose 2 and a half of the same exons by chance (exons 1, 5 and part of 6). Instead, they must have undergone similar deletions because they had similar genomes.
So what does the sequence actually look like when you compare the two? Conveniently, a pairwise alignment of the human and mouse genome is available online, as is an alignment of guinea pig vs mouse (yay, Jim Kent and UCSC). Since mouse has a functioning copy of the GULO gene, it provide a reference copy of the gene that has all of the exons intact. Here’s what the first half of the gene looks like:
In the plot, the x axis shows the position in the mouse chromosome and the y axis the equivalent position in the corresponding guinea pig chromosome. Blue segments show where the two still have similar DNA; where there is a gap, there has been an insertion or deletion in one of the two species. The green segments above that show the same thing for the human chromosome – the segments where it resembles the mouse gene. Along the bottom, the red blocks show where the GULO exons occur in the mouse. (They are numbered right to left because the gene lies on the reverse DNA strand.)
The first thing to note is that none of the genomes are very similar to one another, and that there are numerous insertions/deletions throughout the gene. Also, there is no sign that similar deletions are occurring at the same places. Exon 6 is completely missing from the human copy of the gene because a substantial deletion has taken out the entire region, while the guinea pig exon has been clipped by a different deletion.
Things are different in the case of the other two exons in question (exons 1 and 5): it turns out in both cases that one of the two species isn’t even missing the exon. Exon 1 is still present in guinea pigs, while exon 5 is still present in humans. I’m surprised that exon 5 was listed as missing in humans, since the sequence there isn’t that different from mouse. Here are the two lined up:
Exon 1 is much more heavily altered by mutation, probably because it’s almost all noncoding, and therefore mostly not constrained by purifying selection even for functioning copies of the gene. Here is that stretch of the gene in mouse and guinea pig:
You can sort of still see the resemblance, but it’s only because it’s part of a large block of similarity between gp and mouse that we can we sure they come from a common original state. For both of these exons, the matching sequence in the other species was completely removed by large deletions, a completely different mutation process.
Based on the actual sequence comparison, then, the argument is plainly wrong that humans and guinea pigs have lost overlapping exons because of common mutational processes in the two species.
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Is there a way I can recommend this comment as a candidate for its own blog post? There may be some need to boil down the prior comment thread with DCS (and, long ago, me) so people have some background, but when somebody puts so much effort into a clear exposition of something that really contributes to understanding why data doesn’t fit a YEC explanation, it’d be a shame to see it buried so deep in the comments section.
Just my $0.02.
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Despite my surprise, I see that doing the obvious, simplest comparison between mouse and human indeed fails to find exon 5 in humans. That comparison is a search using the program BLAST, with default parameters. (Anyone can try it for themselves. Go to Transcript: ENSMUST00000059970.9 (Gulo-201) - Exons - Mus_musculus - Ensembl genome browser 111
where you should see displayed the mouse exons for GULO. Highlighting some of the sequence should cause a box to pop up, offering to BLAST the sequence. Pain-free bioinformatics.)
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hey again glipsnot.
not according to those scientists:
“Charles Darwin’s “tree of life”, which shows how species are related through evolutionary history, is wrong and needs to be replaced, according to leading scientists.”
“We have no evidence at all that the tree of life is a reality,” Eric Bapteste, an evolutionary biologist at the Pierre and Marie Curie University in Paris, told New Scientist magazine."-
and its not just about bacteria:
“Last year, scientists at the University of Texas at Arlington found a strange chunk of DNA in the genetic make-up of eight animals, including the mouse, rat and the African clawed frog. The same chunk is missing from chickens, elephants and humans, suggesting it must have become wedged into the genomes of some animals by crossbreeding.”
not according to this paper:
http://www.jbc.org/content/267/30/21967.long
you can see that exon 1 is missing from the guina pig and rat comparison (fig 3). so you are claiming that you found what 2 scientific papers doesnt found? it will be interesting.
even if its true i can give you another examples. it doesnt change the fact that shared mystake can be found without a commondescent. so shared mystakes isnt evidence for a commondescent.
For completeness, here is the alignment of guinea pig and several primates for the entire mouse GULO gene.
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Nowhere does that article suggest that horizontal gene transfer is common in animals. As I said, it occurs but is not common. You can find a balanced (and later) assessment here. Relevant snippet: ‘The results suggest that “if we use the same yardstick to measure a variety of model organisms, it’s possible to say that mammalian genomes have also been subjected to low levels of HGT, although it happened only on very rare occasions at the early stages of evolution.’"
Read the paper. “On the other hand, regions corresponding to exons I and V were not identified in the guinea pig Lgulono-y-lactone oxidase gene homologue”, and “The regions corresponding to the rat GLO gene exons except for exons I and V were identified in the guinea pig gene, and their sequences were determined.” They didn’t show that exon 1 was missing: they failed to find exon 1. (They examined the sequence for exon 5 and showed that it wasn’t present, but did not do the same for exon 1.) Since they were searching for the gene by physically hybridizing the DNA, it would have been impossible for them to find exon 1, given how divergent the GP and mouse exons are.
As I said, I didn’t find anything. The finding was done by the comparative genomics folks at UC Santa Cruz. I just downloaded the files. They do their cross-species alignment using whole-genome sequence and the tool BLASTZ. That approach is dramatically more sensitive than the GP study (which was done 20+ years ago), and also more sensitive than the search that missed human exon 5, which used BLAST rather than BLASTZ.
Fine – let’s see the next example.
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true. i reffer to a different tree made by different (regular)genes, and not about lgt. we know that its very common that some genes tell different story. see this paper for example:
2)evolution cant explain how this lgt happan in animals. so even one event is a problem to the evolution senario.
fair enough. but still- why this result have not publish in a peer review article? why the new article from 2011 doesnt fix this? where is the peer review?
here is an example of 2 mutations without a commondescent:
and even in the gulo one rat share one base with chimp.
Sure, single-gene studies are noisy, but that is easily addressed by using more sequence. Incomplete lineage sorting means that closely spaced branches don’t actually have a unique tree, but that is expected and also easily dealt with. There are indeed real problems with ordering deep branches that are fairly close together: there simply isn’t enough information to determine the tree. But none of that changes the fact that DNA routinely produces reliable trees; it just means that there are well-known spots in the trees where the precise order is uncertain.
Sure it can (or rather, biology can – it’s not really the job of evolution). There are multiple plausible mechanisms for HGT in animals, several of which have been observed in intermediate states.
Because it’s trivial. Basically, no one cares. With whole-genome databases readily available, no one is going to go back and update all of the single-gene sequencing studies in the literature.
Which mutation do you mean? (It’s hardly surprising that the same mutation occurs independently in multiple lines, by the way. What we’re looking for is convergent mutations that happen more frequently than you would expect by chance.)
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there is a lot of problems with this method that we can discuss about. but the main point is that this tree isnt evidence for a commondescent more then a commondesginer.
can you give an explanation for lets say this one:
http://www.biolbull.org/content/227/3/300.abstract
about the uox pseudogene- i reffer to those mutations:
" One exceptional change is a duplicated segment of GGGATGCC in intron 4 which is shared by the gorilla and the orangutan. However, because this change is phylogenetically incompatible with any of the three possible sister-relationships among the closely related trio of the human, the chimpanzee, and the gorilla, it might result from two independent duplications"-
and the mutation at codon 107:
“The nonsense mutation (TGA) at codon 107 is, however, more complicated than others. It occurs in the gorilla, the orangutan, and the gibbon, and therefore requires multiple origins of this nonsense mutation”
Sure it is. Common designers routinely violate hierarchical trees. In fact, that’s an important component of intelligent design – any software engineer can tell you that good design involves reusing components across diverse applications.
That’s an interesting one. It will take me a while to dig out the sequence to look at it.
That’s not an interesting one. That a recurring mutation at a “CG” dinucleotide, better known as a CpG. That particular combination of nucleotides mutates to T at a very high rate (because the C in that pair is usually methylated, and methylated C spontaneously deaminates to thymine). They’re routinely discarded from many comparative analyses because recurrent mutations are so common at such sites. So multiple independent mutations at this site are not surprising. (Something I believe is mentioned in the paper somewhere.)
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true. but the same can be find in nature. unless you refer to a non-hierarchical tree. so what tree are you refer to?
i will wait.
its very interesting because now we have 2 share mutations without a commondescent. therefore a shared mutations cant be evidence for a commondescent.
Where there is little horizontal gene transfer, living things do not routinely violate hierarchical trees.
False. You can’t just lump all mutations together; you have to try to understand what you’re looking at. Highly mutable sites will frequently appear as multiple mutations in different parts of the tree. Other kinds of mutation will rarely appear independently in different parts of the tree. That’s the actual expectation of common descent – not that all mutations should follow the tree perfectly. And that’s what we see.
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ok. lets check this. take for example the tetrapod evolution. the phylogenetic tree base on molecular evidence show one tree and the fossil one show another. i also gave this one:
http://www.nature.com/news/phylogeny-rewriting-evolution-1.10885
“This family tree is backed up by reams of genomic and morphological data, and is well accepted by the palaeontological community. Yet, says Peterson, the tree is all wrong.”
and i can show you a lot more examples.
true according to evolution. but then the main argument that shared mutations is evidence for a commondescent is false. because there is a lot of examples for a shared mutations without a commondescent.
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I said I’d look into this one, and I did. Here is the sequence from humans, gorillas and orangutans:
Chimpanzees are the same as humans there, and gibbons look similar. The anomaly is that gorillas and orangutans share a chunk of sequence not found in humans/chimps or the more distantly related gibbons, even though gorillas are more closely related to humans than they are to orangutans.
You may recall that I previously said that deletions tend to occur where there are stretches of nearly identical, duplicated sequence. (The same is also true of duplications, by the way.) And that’s what we’ve got here. Gorillas and orangutans have three (nearly identical) copies of an 8-base-pair repeat, while humans and gibbons have two. (Specifically, it’s a direct tandem repeat, meaning that the copies go in the same direction and are placed next to one another.) This should indeed be a hotspot for both insertions and deletions of copies of the repeat, and finding violations of the tree here is not surprising. I wouldn’t want to venture a guess as to whether it was two independent duplications in orangs and gorillas, or two independent deletions in gibbons and the human/chimp ancestor, that led to the incongruity. More distantly related primates (monkeys and prosimians) have only one copy of that segment, so it was probably first duplicated in an early ape.
We expect to find some disagreements at the cutting edge of science. At the time of the Nature article, Peterson had not yet accumulated enough data or performed enough analysis to even publish an article on the implications of miRNA for mammalian phylogeny. So how does the article somehow disprove our understanding of the standard phylogeny?
Second, Peterson does not for a second think that his analysis, such as it was/is, disproves evolution. He is looking to refine the phylogeny; he does not contend that miRNA deals a blow to the theory of descent with modification from common ancestors.
Third, subsequent analysis of the miRNA theory shows that it is–so far–highly unreliable as a method of inferring phylogeny.
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true. because evolution cant be falsified. so its not a science.
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