It is a nice effort but filled with numerous errors or misunderstandings and simple mistakes (e.g. "human DNA project", when it was the human Genome project.)
I am focusing on the repeating elements section where your mistakes include refering to repeating elements as "fossils" or "doing no harm" as if they are inert. And of course they do not integrate randomly. This non-randomness can be manifested at the DNA mechanistic level with repsect to the actual integration event or it can be conferered by selection after an integration event at the cellular level.
Further, you entirely misunderstand the nature of the evolution of repeating elements in the mammalian genome. There is an initial retroviral infection (which does not have to result in a "broken" virus as you described it) and the distribution of the repeat element is due to transposition events that occur subsequently over time. This initial insertion is called the "matser gene" or, to quote from Lebedev et al 2000 (cited by Theobald in 4.5):
These divergences can be used to calculate the age of the branch ancestor (master or source) gene, the retropositions of which gave birth to the branch members.
Sequence homologies of the repeat element family (in the example you used, Herv-2) distributed throughout the genome are used to compute the evolutionary time relative to initial retroviral insertion event. The loss of homology is due to the recombinant transposition events which increase the frequency of the element in the genome with each event and also cause a degenracy in the sequence integrity.
The retroviruses do not become fossilized, they are incredibly active as "jumping genes" and are believed to have been a strong driving force in mammalian evolution.
They currently are believed to be involved in regulating gene expression (with the first experimental observation of a transpositional event (induced) affecting a gene expression in neural progenitor cells and, given the specific nature (as opposed to random) of their activity, they are being used as a tool to identify oncogenes.
My comment is you are very enthusiastic (dare I say zealous), but don't really know or understand that much and it comes across.
Drop the dogma and the attitude and rejoyce in the wonder of nature and what we do not know about it as well as what is known.
The idea that retroviruses integrated randomly was common a long time ago. Still no one knows what the deterministic mechanisms are for the integration, so it was a fine working assumption to use that their integration was random. There was no way to assess if it was random or not, so it might as well be treated as if it were. But that idea has gone by the wayside in the same manner that the, at the time, perfectly reasonable idea that RNA was just scaffold for ribosomes or template for translation and all enzymatic activity resided in the proteins has been eradicated by Tom Cech and others.
Keep in mind Cech was not trying to provie anything about evolution or potential origins of life, he was simply trying to figure out why the tetrahymena RNA so painstakingly isoloated in his lab kept degrading in the fridge.
Open your mind and stop clinging to your dogma and biases. Use them as tool, not weapons.
I'm not angry at all. And I welcome comments. But I do feel disgust at disingenuous attempts to cloud the issue rather than bring light to it.
It is a nice effort but filled with numerous errors or misunderstandings and simple mistakes (e.g. "human DNA project", when it was the human Genome project.)
That's not a mistake, you idiot, I'm writing for a general audience, many of whom won't know what a "genome" is, so I used more generally recognizable terms and phrases. But then you knew that. Stop playing dumb, and especially stop doing it in order to have a cheap and dishonest excuse to insult me.
I am focusing on the repeating elements section where your mistakes include refering to repeating elements as "fossils" or "doing no harm" as if they are inert.
Muddying an already complex topic with additional side issues would serve no point. Despite the activity of some ERVs, the point remains that they are for the most part non-infectious.
And of course they do not integrate randomly.
Of course they do, just not uniformly. Stop beating this dead dishonest horse of yours.
This non-randomness can be manifested at the DNA mechanistic level with repsect to the actual integration event or it can be conferered by selection after an integration event at the cellular level.
...none of which invalidates the points being made in the essay, so stop pretending that they do.
If you want to be ridiculous and complain that I talked only about the aspects of ERVs which are directly relevant to the subject of determining common ancestry (which was my topic), without writing a whole freaking book on everything else about ERVs which has ever been written in a medical journal, I suggest that you stop being so jaw-droppingly anal.
Further, you entirely misunderstand the nature of the evolution of repeating elements in the mammalian genome.
No, I didn't, nor do you actually identify anything whch I have gotten wrong due to this alleged "entire misunderstanding". Yet again you use dishonest innuendo. How do you sleep at night?
There is an initial retroviral infection (which does not have to result in a "broken" virus as you described it)
It has to be "broken" in the sense that it fails to reproduce itself and spawn new viruses to be released, as is the normal life cycle of retroviruses. This should have been obvious to anyone with even the most basic reading comprehension.
and the distribution of the repeat element is due to transposition events that occur subsequently over time.
Yes it is, but it's not the repeat elements that provide the most direct evidence of common ancestry, so that advanced topic was left out of the basic presentation. Whoop-de-do -- do you have any other trivial gripes?
But hey, if you want to write an essay yourself which details how the repeat elements provide *additional* evidence for common ancestry, as well as a kind of "clock" by which the age of the insertion event can be determined, and other phylogenetic "signal", go right ahead.
But don't be an a-hole and try to pretend that my providing the basics of the topic, instead of a full college course on it, is some kind of "mistake" or "misunderstanding" on my part, because it's not.
This initial insertion is called the "matser gene"
Try "master", Einstein. Gosh, by your nitpicking standards, I guess this means that you have a "total misunderstanding" of the topic after all.
or, to quote from Lebedev et al 2000 (cited by Theobald in 4.5): "These divergences can be used to calculate the age of the branch ancestor (master or source) gene, the retropositions of which gave birth to the branch members." Sequence homologies of the repeat element family (in the example you used, Herv-2) distributed throughout the genome are used to compute the evolutionary time relative to initial retroviral insertion event. The loss of homology is due to the recombinant transposition events which increase the frequency of the element in the genome with each event and also cause a degenracy in the sequence integrity.
Yes, thank you for *REINFORCING* my point. But what on Earth led you to falsely conclude that I didn't know this already or had "misunderstood" it?
The retroviruses do not become fossilized, they are incredibly active as "jumping genes" and are believed to have been a strong driving force in mammalian evolution.
Yup -- all of which is more advanced information than is necessary to impart in order to educate a lay audience in the basics of how ERVs are strong evidence of common ancestry, which is why I wrote an introductory essay instead of a PhD thesis.
As for your ludicrous nitpicking over the use of the term "fossil", the point is that they are something existing in modern times which is a leftover "mark" of an ancient event, just as a mineralized casting of a dinosaur footprint from 70 million years ago is.
They currently are believed to be involved in regulating gene expression (with the first experimental observation of a transpositional event (induced) affecting a gene expression in neural progenitor cells and, given the specific nature (as opposed to random) of their activity, they are being used as a tool to identify oncogenes.
Again, if you want to ramble on about ERVs other features, feel free, but none of this undermines the points made in my essay, and none of it was necessary background for the key explanations made in the essay about how ERVs get introduced into the genome, and about the most direct way in which they can be used as strong evidence of common ancestry.
You keep falsely accusing me of "misunderstandings" (without actually pointing out anything I have allegedly "misunderstood"), but your own bizarre list of nitpicks only reveals that you completely misunderstand the purpose and intended audience of the essay in the first place.
Or you actually do understand, and you're just getting your jollies by being a real jerk.
My comment is you are very enthusiastic (dare I say zealous), but don't really know or understand that much and it comes across.
Uh huh. Keep lying, jerk. I always appreciate it when folks who yap around my ankles keep torpedoing their own credibility, it saves me a lot of rebuttal time.
Drop the dogma and the attitude and rejoyce in the wonder of nature and what we do not know about it as well as what is known.
I always do.
The idea that retroviruses integrated randomly was common a long time ago. Still no one knows what the deterministic mechanisms are for the integration, so it was a fine working assumption to use that their integration was random. There was no way to assess if it was random or not, so it might as well be treated as if it were. But that idea has gone by the wayside in the same manner that the, at the time, perfectly reasonable idea that RNA was just scaffold for ribosomes or template for translation and all enzymatic activity resided in the proteins has been eradicated by Tom Cech and others.
Nice rambling innuendo. Feel free to actually *demonstrate* that independent same-locus events of natural retroviruses are actually as likely as you're trying to falsely imply. Oops, right, you can't, because they're NOT. Study after study which actually observes in vivo integrations demonstrates that they're not, they occur all over the damned place in the genome. So stop lying.
Also feel free to try to actually demonstrate that such independent "hits" on the same locus in independent integration *wouldn't* leave additional signs (such as differential sequence divergences) which would make it possible to distinguish them from actual ancestral events. Oh, right, you can't do that either.
You can *also* feel free to demonstrate your assertion that ERV integration is "deterministic" by predicting exactly where, and in what order, the first ten retroviral integration points will be when I bombard a cell culture with retroviruses of a given type. Oops, you can't do that, you say? The best you can do is describe a statistical distribution about the *probabilities* of those locations? That's because there's a RANDOM component to this process, no matter how much you try to hand-wave it away.
So you're just bluffing like a guy with his last few bucks in the poker pot, holding a busted flush.
Keep in mind Cech was not trying to provie anything about evolution or potential origins of life, he was simply trying to figure out why the tetrahymena RNA so painstakingly isoloated in his lab kept degrading in the fridge.
Keep in mind that your continued random "biology fact of the day" contributions still don't actually demonstrate any error in my essay, or invalidate its points about how ERVs are used to determine common ancestry.
No one's falling for your hand-waving.
Open your mind and stop clinging to your dogma and biases. Use them as tool, not weapons.
If ever there was a clearer case of what the psychologists call "projection"...