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Author Topic:   Problems with Chromosomal Evolution - From Circular to Linear
jt
Member (Idle past 5618 days)
Posts: 239
From: Upper Portion, Left Coast, United States
Joined: 04-26-2004


Message 31 of 58 (137131)
08-26-2004 4:21 PM
Reply to: Message 30 by jar
08-26-2004 4:01 PM


probability
IMHO, the issue of propabilities is simply another of the red herrings.
I don't think it is a red herring, it is integral to some things. Here is an (exagerated) example: There is a certain protein composed of 100,000,000 amino acids, and it is somehow known that it could not have evolved in more than 1 generation (I am not claiming the stuff with telomeres is near that, this example is hugely exagerated). What would that make you think about evolution, and why?
First when you start at one limit, as simple as things can get, the only direction that you can go is towards being more complex.
But in cells there is not a simple gradient from simple to complex - an enzyme either works or it doesn't. Natural selection sees no difference between "not working" and "almost working." Enzymes are hurdles - they cannot be taken by small amounts; the whole thing has to be cleared in one jump.
Second, you are dealing with very large numbers.
I'm aware of that.
Third, there is a filter. The things that work are kept, those random changes that don't work get discarded.
Exactly - and I think that the systems in question couldn't have gotten from non-existent to working, and would have been discarded.

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 Message 30 by jar, posted 08-26-2004 4:01 PM jar has not replied

Replies to this message:
 Message 32 by crashfrog, posted 08-26-2004 4:51 PM jt has replied
 Message 33 by Loudmouth, posted 08-26-2004 6:05 PM jt has replied

  
crashfrog
Member (Idle past 1489 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 32 of 58 (137151)
08-26-2004 4:51 PM
Reply to: Message 31 by jt
08-26-2004 4:21 PM


an enzyme either works or it doesn't.
Are you sure about that? It seems to me that since all enzymes do is reduce the activation energy of certain chemical reactions, there could easily be a complexity gradient - i.e. you might have two enzymes with active binding sites for the same molecules, but one of them is able to catalyze the reaction at a lower activation energy than the other.

This message is a reply to:
 Message 31 by jt, posted 08-26-2004 4:21 PM jt has replied

Replies to this message:
 Message 34 by jt, posted 08-26-2004 11:00 PM crashfrog has replied

  
Loudmouth
Inactive Member


Message 33 of 58 (137178)
08-26-2004 6:05 PM
Reply to: Message 31 by jt
08-26-2004 4:21 PM


Re: probability
quote:
But in cells there is not a simple gradient from simple to complex - an enzyme either works or it doesn't. Natural selection sees no difference between "not working" and "almost working." Enzymes are hurdles - they cannot be taken by small amounts; the whole thing has to be cleared in one jump.
And this sort of jump has been observed. Take the nylong bug, for example. A one base insertion caused a frame shift that resulted in a functional enzyme that cleaved one of the byproducts of nylon production (reference). So actually new enzymes with novel activity are able to arise in a one-time mutational event. You are correct in stating that natural selection can not select between "not working" and "almost working" (which are actually the same thing) but it can select against "suddenly working" and "not working".
Given this example, it is quite possible that the first telomerase could have arisen from one single mutation that was not planned and accidental just as we have observed in the nylon bug.

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 Message 31 by jt, posted 08-26-2004 4:21 PM jt has replied

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jt
Member (Idle past 5618 days)
Posts: 239
From: Upper Portion, Left Coast, United States
Joined: 04-26-2004


Message 34 of 58 (137242)
08-26-2004 11:00 PM
Reply to: Message 32 by crashfrog
08-26-2004 4:51 PM


It seems to me that since all enzymes do is reduce the activation energy of certain chemical reactions, there could easily be a complexity gradient - i.e. you might have two enzymes with active binding sites for the same molecules, but one of them is able to catalyze the reaction at a lower activation energy than the other.
True, once an enxyme is working it could be improved on (although for most enzymes I'm guessing it would take large changes to change anything and keep it functional). But the step from functional to non-functional protein or enzyme is what I was talking about when I said "hurdle."

This message is a reply to:
 Message 32 by crashfrog, posted 08-26-2004 4:51 PM crashfrog has replied

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jt
Member (Idle past 5618 days)
Posts: 239
From: Upper Portion, Left Coast, United States
Joined: 04-26-2004


Message 35 of 58 (137245)
08-26-2004 11:06 PM
Reply to: Message 33 by Loudmouth
08-26-2004 6:05 PM


Re: probability
Given this example, it is quite possible that the first telomerase could have arisen from one single mutation that was not planned and accidental just as we have observed in the nylon bug.
This is another thing I'll have to research. I'm still working on your other post about t-loops, I'll post a reply to that soon-ish (I think).
You guys sure have a knack for making me spend inordinate amounts of time researching. Probably a standard evilutionist tactic...

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crashfrog
Member (Idle past 1489 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 36 of 58 (137262)
08-27-2004 12:18 AM
Reply to: Message 34 by jt
08-26-2004 11:00 PM


But the step from functional to non-functional protein or enzyme is what I was talking about when I said "hurdle."
Right, but that's a lot less of a hurdle than you made it out to be if there's varying levels of functionality.

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RAZD
Member (Idle past 1427 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 37 of 58 (137265)
08-27-2004 12:25 AM
Reply to: Message 29 by jt
08-26-2004 3:53 PM


more thoughts to ponder.
JT writes:
when a cell's chromosome became linear, the cell would die.
Immediately? Tomorrow? Next week? What is the time frame here? What kills it? There will always be some molecules available inside the cell that may be added to the end of the chromosome as it tries to close\repair itself ... what happens when one holds it together just enough ...
first, the protection system still would have had to evolve, which I think is implausible ... more implausible than it evolving in a line of cells already having DNA ... even if such a system was present in extremely early cells, the chances of it surviving very long after it stopped being needed is low ... didn't have to create/maintain the useless system would be less pressed for resources, and the system would soon degrade ...
Implausible is not impossible.
Why does it have to be DNA? We are talking the first replicating cell system and the environment then was totally alien to what we live in, the chemical energy system was different. Latest thought is that RNA could have just as easily been the best replicator before DNA evolved from it, perhaps there was a simpler but less effective molecule before that. The LUCA project is trying to determine just how little\simple the replicating molecule needs to be.
Why do you assume it stopped being needed? If circular chromosome breakage was common a stabilizing system could be maintained and even improved with time to hold things until circularity was re-established. Perhaps they are the molecules that first caused the circular chromosome to close, that becomes a repair molecule, that gets damaged while not needed but then employed in a new way ...
... and a molecule that was needed from time to time could then be fatal to the ones that lose it and then break open.
Certainly a linear molecule is simpler than a circular one, so evolution and probability would tend to favour the linear system first. A crude inaccurate system with a high degree of failure would still out compete pure chance combination of amino acids -- remember it does not have to be as good as the system today (in a different environment), it just needs to be good enough.
and the issue of improbability has been addressed on other threads -- think of a lottery: highly improbable that any one specific ticket will win, highly probable that one of all the tickets will win ...
see http://EvC Forum: the old improbable probability problem
and if it did "just happen" then the improbability is irrelevant.
enjoy.

we are limited in our ability to understand
by our ability to understand
RebelAAmerican.Zen[Deist
{{{Buddha walks off laughing with joy}}}

This message is a reply to:
 Message 29 by jt, posted 08-26-2004 3:53 PM jt has not replied

Replies to this message:
 Message 38 by Ooook!, posted 08-27-2004 9:26 AM RAZD has replied

  
Ooook!
Member (Idle past 5837 days)
Posts: 340
From: London, UK
Joined: 09-29-2003


Message 38 of 58 (137316)
08-27-2004 9:26 AM
Reply to: Message 37 by RAZD
08-27-2004 12:25 AM


Re: more thoughts to ponder.
Certainly a linear molecule is simpler than a circular one, so evolution and probability would tend to favour the linear system first.
Harking back to a previous thread concerning early life (about the origin of viruses):
What if the origin of the nucleus is a complex viral genome that got 'stuck' in a primitive archaea? That way, a linear genome (in the early pool of proto-cells) could be replaced by a circular one (in Archaea and Bacteria), which in turn got usurped by a more stable linear model (to produce an early eukaryote).
This is a paper suggesting just that (I think, I can't get access to the full text).
I don't know if the article is much cop, because I can't read the full text and its's only a 'comment' or 'letter'. I also have no idea whether it has been laughed at by all and sundry since then, but here's a snippet from the abstract:
quote:
It is proposed that several characteristic features of the eukaryotic nucleus derive from its viral ancestry. These include mRNA capping, linear chromosomes, and separation of transcription from translation.
Any thoughts?

This message is a reply to:
 Message 37 by RAZD, posted 08-27-2004 12:25 AM RAZD has replied

Replies to this message:
 Message 39 by RAZD, posted 08-27-2004 10:40 AM Ooook! has replied

  
RAZD
Member (Idle past 1427 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 39 of 58 (137336)
08-27-2004 10:40 AM
Reply to: Message 38 by Ooook!
08-27-2004 9:26 AM


Re: more thoughts to ponder.
Hmmm a DNA viral mechanism could also hark back to a more primitive organism overshadowed by later evolved more complex cells. Certainly by the time we are talking about developing eukaryotes, life has been around for a while.
This talks about the first predator engulfing others for raw materials, while the viral model is to enter the 'prey' and attack\co-opt from inside? This also leaves the original outershell as camoflage in case of colonies.
Other papers have suggested a lot of DNA\RNA interchange between early cellular organisms. A form of group sex?
These viral remnants would still have already developed the capping\telemere solution by this time as well. Thus this does not solve our OT problem.
One thought this brings to the OT problem though is that dead and dying cells would be consumed by others, cells that had broken circular chromosomes could be incorporated, and in the process get combined with other remnants, one becoming a cap for another.
interesting thoughts.
Going off on a tangent I posit that a virus entering a cell is similar to a sperm entering an egg ... perhaps this mechanism is behind the evolution of sex (once a symbiotic relationship has become established)? The idea of males as viruses would, I'm sure, amuse many. Could be an interesting new topic?

we are limited in our ability to understand
by our ability to understand
RebelAAmerican.Zen[Deist
{{{Buddha walks off laughing with joy}}}

This message is a reply to:
 Message 38 by Ooook!, posted 08-27-2004 9:26 AM Ooook! has replied

Replies to this message:
 Message 40 by Loudmouth, posted 08-27-2004 1:23 PM RAZD has replied
 Message 46 by Ooook!, posted 08-28-2004 5:42 AM RAZD has replied

  
Loudmouth
Inactive Member


Message 40 of 58 (137385)
08-27-2004 1:23 PM
Reply to: Message 39 by RAZD
08-27-2004 10:40 AM


Re: more thoughts to ponder.
quote:
These viral remnants would still have already developed the capping\telemere solution by this time as well. Thus this does not solve our OT problem.
The host cell could use the viral long tandem repeats (LTR's) through retrotrasposition to solve the problem of end deletion in linear DNA replication. A similar mechanism is used in Drosophila, although the whole viral genes are used instead of LTR's.

This message is a reply to:
 Message 39 by RAZD, posted 08-27-2004 10:40 AM RAZD has replied

Replies to this message:
 Message 41 by RAZD, posted 08-27-2004 3:57 PM Loudmouth has replied

  
RAZD
Member (Idle past 1427 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 41 of 58 (137427)
08-27-2004 3:57 PM
Reply to: Message 40 by Loudmouth
08-27-2004 1:23 PM


Re: more thoughts to ponder.
has anyone tried to remove the end caps from straight chromosomes and see if a protection system evolves?
are there molecules that cause circular chromosomes to open, and are they catalytic or do they combine in the process?

we are limited in our ability to understand
by our ability to understand
RebelAAmerican.Zen[Deist
{{{Buddha walks off laughing with joy}}}

This message is a reply to:
 Message 40 by Loudmouth, posted 08-27-2004 1:23 PM Loudmouth has replied

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Loudmouth
Inactive Member


Message 42 of 58 (137453)
08-27-2004 5:11 PM
Reply to: Message 41 by RAZD
08-27-2004 3:57 PM


Re: more thoughts to ponder.
quote:
has anyone tried to remove the end caps from straight chromosomes and see if a protection system evolves?
are there molecules that cause circular chromosomes to open, and are they catalytic or do they combine in the process?
There are some tantalizing hints that this work has been done, but I haven't been able to find free access to any of the primary literature as of yet.
From The Rockefeller University » testpost for LDAP authorlogin :
E. coli has a mechanism to deal with this. Enzymes take the extruded DNA and reinsert it back into the genome. This reaction is similar to the formation of a t-loop. Through regular DNA synthesis, you have the chance to extend the end of the inserted DNA in the t-loop, just as the telomerase enzyme does, de Lange says. All you need to get this primitive telomere system to work are a few repeats at the end of the linear DNA.
As proof of this notion, de Lange points to several proteins that currently act at telomeres that have evolved from the enzymes in E. coli that are involved in replication restart events. There are also prokaryotic relics of this system de Lange calls them living fossils in which linear chromosomes have repeats of varying sequences and sizes at their ends. These living fossils survive with linear chromosomes because they have miniature t-loops, de Lange says.
And from de Lange's Rockefeller university page The Rockefeller University : (this is just a snippet, the whole description is worth a read)
Our long-term goal is to understand how the human telomeric complex executes its two main functions: to protect chromosome ends and mediate their replication. Telomeres shield chromosome ends from extensive degradation and fusion and allow cells to discriminate between broken DNA and natural chromosome ends, thus ensuring that DNA damage checkpoints are not activated in undamaged cells. Our research is aimed at determining how cells distinguish natural chromosome ends from DNA breaks and what happens when telomere protection is lost. . .
The protection of chromosome ends is mainly executed by TRF2, a TRF1-related telomeric DNA-binding factor. TRF2 recruits additional proteins to the telomere, including the TRF2 interacting protein hRap1 and the Mre11 recombination repair complex. Loss of TRF2 leads to immediate deprotection of chromosome ends as evidenced by the loss of the telomeric 3'-tail and fusion of chromosome ends. . .
We found that removal of TRF2 from human telomeres and the ensuing deprotection of chromosome ends induced immediate premature senescence, even though the telomeric tracts remained intact. This premature senescence was indistinguishable from replicative senescence and could be mediated by either the p53 or the p16/RB pathways. Telomere deprotection also induced a growth arrest and senescent morphology in mouse cells.
de Lange seems to be the most active researcher on the evolution of early telomere systems and human telomere control, at least during my brief searches. I have found some of her papers but they are not free-access. I could order through my job, but it really wouldn't be that ethical.
I will keep looking, but I thought it might go faster if two people were looking down the same path. If anyone else has access to more of de Lange's work feel free to post it here.

This message is a reply to:
 Message 41 by RAZD, posted 08-27-2004 3:57 PM RAZD has not replied

  
jt
Member (Idle past 5618 days)
Posts: 239
From: Upper Portion, Left Coast, United States
Joined: 04-26-2004


Message 43 of 58 (137478)
08-27-2004 5:59 PM


Everybody,
I'm leaving on a two week or so vacation in a couple days, so this'll be my last post for a while. When I get back I'll keep researching all the arguments, and hopefully soon after my return I'll start rebutting them.
Later,
JT

Replies to this message:
 Message 44 by RAZD, posted 08-27-2004 6:30 PM jt has replied

  
RAZD
Member (Idle past 1427 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 44 of 58 (137494)
08-27-2004 6:30 PM
Reply to: Message 43 by jt
08-27-2004 5:59 PM


Have Fun
OK. We'll try to keep it down to a dull roar so theren won't be too much to cover.
You may want to bookmark your last post on this topic so you can get back to it even if it has dissappeared from the radar?

we are limited in our ability to understand
by our ability to understand
RebelAAmerican.Zen[Deist
{{{Buddha walks off laughing with joy}}}

This message is a reply to:
 Message 43 by jt, posted 08-27-2004 5:59 PM jt has replied

Replies to this message:
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jt
Member (Idle past 5618 days)
Posts: 239
From: Upper Portion, Left Coast, United States
Joined: 04-26-2004


Message 45 of 58 (137530)
08-27-2004 10:21 PM
Reply to: Message 44 by RAZD
08-27-2004 6:30 PM


Re: Have Fun
Thanks, I will. Although having your guys' arguments floating around in my head for two weeks without my having a rebuttal is going to drive me nuts...
Also, you guys can post as much as you want in this thread, the more the better. I'll just start where I left off and work through it. (I appreciate your consideration, though.)
Later,
JT

This message is a reply to:
 Message 44 by RAZD, posted 08-27-2004 6:30 PM RAZD has not replied

  
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