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Author Topic:   Convergent evolution in macaques
judge
Member (Idle past 6444 days)
Posts: 216
From: australia
Joined: 11-11-2002


Message 1 of 8 (62981)
10-27-2003 12:15 AM


Simlar sequences between humans and other apes are often cited as strong evidence of common descent.
The following paper (unfortunately I only have the abstract) details how six macaques developed similar mutations in independent lines.
The env gene of three simian immunodeficiency virus (SIV) variants developed convergent mutations during disease progression in six rhesus macaques. The monkeys had been inoculated with supercoiled plasmids encoding infectious proviruses of SIVmac239 (a pathogenic, wild-type strain), SIVdelta3 (the live attenuated vaccine strain derived from SIVmac239), or SIVdelta3+ (a pathogenic progeny virus that had evolved from SIVdelta3). All six monkeys developed immunodeficiency and progressed to fatal disease. Although many divergent mutations arose in env among the different hosts, three regions consistently mutated in all monkeys studied; these similar mutations developed independently even though the animals had received only a single infectious molecular clone rather than standard viral inocula that contain viral quasispecies. Together, these data indicate that the env genes of SIVmac239, SIVdelta3, and SIVdelta3+, in the context of different proviral backbones, evolve similarly in different hosts during disease progression.
http://www.ncbi.nlm.nih.gov...
{Shortened display form of URL, to restore page width to normal - Adminnemooseus}
If we observe similar mutations arising independently then how do we know when they arise independently and when the arise due to inheritance?
Thanks
[This message has been edited by judge, 10-27-2003]
[This message has been edited by Adminnemooseus, 10-27-2003]

Replies to this message:
 Message 2 by Rei, posted 10-27-2003 12:39 AM judge has not replied
 Message 3 by Mammuthus, posted 10-27-2003 3:19 AM judge has replied
 Message 4 by Dr_Tazimus_maximus, posted 10-27-2003 8:16 AM judge has not replied
 Message 5 by Coragyps, posted 10-27-2003 9:52 AM judge has not replied
 Message 6 by Ooook!, posted 10-27-2003 4:03 PM judge has not replied

  
Rei
Member (Idle past 7013 days)
Posts: 1546
From: Iowa City, IA
Joined: 09-03-2003


Message 2 of 8 (62986)
10-27-2003 12:39 AM
Reply to: Message 1 by judge
10-27-2003 12:15 AM


A whopping 3 genes converged, when placed in similar hosts, to a limited degree, while the rest of the virii diverged, and you come to the conclusion that this could explain the universal matchup of species with their phylogenic trees? How do you reach this conclusion?
------------------
"Illuminant light,
illuminate me."

This message is a reply to:
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Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 3 of 8 (63001)
10-27-2003 3:19 AM
Reply to: Message 1 by judge
10-27-2003 12:15 AM


The env gene is under intense selective pressure as it is what allows a virus to gain access to the host cell. env is structured into a transmembrane domain, an immunosuppresive domain (at least in HERVs), a surface moiety, and a domain that allows for interaction of the other domains. Thus, env is a highly constrained gene. It is hardly suprising then to see selection for similar or the same mutations (note the study found non-convergence as well). Env would hardly be the marker of choice for studying SIV evolution over long evolutionary time scales. On the other hand, from functional studies, we know which residues in env are highly conserved and can avoid them for such studies.

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 Message 1 by judge, posted 10-27-2003 12:15 AM judge has replied

Replies to this message:
 Message 7 by judge, posted 10-28-2003 7:21 PM Mammuthus has replied

  
Dr_Tazimus_maximus
Member (Idle past 3217 days)
Posts: 402
From: Gaithersburg, MD, USA
Joined: 03-19-2002


Message 4 of 8 (63015)
10-27-2003 8:16 AM
Reply to: Message 1 by judge
10-27-2003 12:15 AM


Judge, while I have not completely read the paper I did glance at it. It may be a case of the higher order of the DNA sequence (I hate that term but have not found one better) shifting the frequency and type of mutations that occur at that sequence in the viral genome. There was a thread on this board concerning Lynn Caporals book, Darwin in the Genome which deal quite well with this area. Here is some more info on a couple of areas related to this:
Molecular Strategies", Direction of mutations andSnail Toxins.
I particularly like the last one as the controlled hypervariability, i.e. hyprevariable in a discrete section of the gene, has a direct effect on the effectiveness of how the snail deals with it’s environment and therefore on one aspect of the natural selection of the organisms.
------------------
"Chance favors the prepared mind." L. Pasteur
and my family motto
Transfixus sed non mortis
Taz
{Added link to (closed) topic "Darwin in the Genome" - Adminnemooseus}
[This message has been edited by Adminnemooseus, 10-27-2003]

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Coragyps
Member (Idle past 735 days)
Posts: 5553
From: Snyder, Texas, USA
Joined: 11-12-2002


Message 5 of 8 (63021)
10-27-2003 9:52 AM
Reply to: Message 1 by judge
10-27-2003 12:15 AM


details how six macaques developed similar mutations in independent lines.
Errrmm....I don't see anything about mutations in macaques. Just in virii.

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 Message 1 by judge, posted 10-27-2003 12:15 AM judge has not replied

  
Ooook!
Member (Idle past 5815 days)
Posts: 340
From: London, UK
Joined: 09-29-2003


Message 6 of 8 (63043)
10-27-2003 4:03 PM
Reply to: Message 1 by judge
10-27-2003 12:15 AM


Oh come on, this is just like the old "we all are closely related to cats and whales according to genomic analysis" argument, and just as flawed.
Understand the science and then comment on it. As has already been pointed out it's not the macaques that are converging it's the viruses, and if you think that is nitpicking ask your self how many generations of macaques were used and how many virus replication events occur?
On top of this, the convergent mutations (most of which are I think are single point mutations), are in the epitopes of antibodies. Is it any surprise that these type of random mutations are selected for extremely strongly, and therefore appear independently in many instances.
[This message has been edited by Ooook!, 10-27-2003]

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judge
Member (Idle past 6444 days)
Posts: 216
From: australia
Joined: 11-11-2002


Message 7 of 8 (63168)
10-28-2003 7:21 PM
Reply to: Message 3 by Mammuthus
10-27-2003 3:19 AM


Thanks for all the replies (particularly to Taz for the links).
I am just an amatuer so I may have to ask a couple of dumb questions here..(And it is so difficult to find creationist discussions of this stuff, which is why I am trying to lok at papers themselves).
The similar mutations happen in independent lines of the gene in the virus and yet these mutations are selected for during the life of the macaque?
If I understand this correctly ..how long does it take for these muations to be selected for?
Have i understood? (I'm not sure I have)
[This message has been edited by judge, 10-28-2003]

This message is a reply to:
 Message 3 by Mammuthus, posted 10-27-2003 3:19 AM Mammuthus has replied

Replies to this message:
 Message 8 by Mammuthus, posted 10-29-2003 2:51 AM judge has not replied

  
Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 8 of 8 (63250)
10-29-2003 2:51 AM
Reply to: Message 7 by judge
10-28-2003 7:21 PM


Hi judge,
quote:
The similar mutations happen in independent lines of the gene in the virus and yet these mutations are selected for during the life of the macaque?
If I understand this correctly ..how long does it take for these muations to be selected for?
What you have to keep in mind is that the viral lifecycle is not the same as its hosts. The virus infects the macaque and if an active infection is established, you will have thousands of generations of virus occuring in the infected individual..meanwhile each host represents a single generation. So a lot more evolution is occuring in the virus relative to the monkey. And in the case of retroviruses like SIV, they have a really error prone reverse transcriptase so they produce massive numbers of mutated viral copies on which the hosts defenses select against. But with such a massive population size potential and so much variation, you will almost always stumble accross variants that have an advantage (that is why so many single drug treatments against HIV fail..a variant arises that is resistant and becomes frequent). The constraints on the env gene mean that mutations outside these specific residues for the most part have been selected against, not that they do not occur. If a mutation deletes the transmembrane domain, the virus is dead. Thus they converge, even independently, on a few specific mutations even if the infection was in different individual monkeys. The dead copies (well not all inactive or so dead) of viruses often show up in our genome such as human endogenous retroviruses (HERVs) which often show key deletions for example, most lack the env gene entirely so they have lost the ability to escape the cell and cause active infection.
Assigning a specific time until selection occurs would be near impossible given all the variables. It would vary from individual to individual since our own host defenses are themselves variable.
Hope this helped.
Cheers,
M

This message is a reply to:
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