Without Design Evolution Can Be Stopped?

Apparantly So, According to a The Scripps Research Institute and the University of Wisconsin by inhibiting LexA in E. Coli they were able to effectively stop all mutations in the bacteria.

In the June issue of the open-access journal PloS Biology, the team describes how a protein called LexA in the bacterium Escherichia coli promotes mutations and helps the pathogen evolve resistance to antibiotics. The scientists also show that E. coli evolution could be halted in its tracks by subjecting the bacteria to compounds that block LexA. Interfering with this protein renders the bacteria unable to evolve resistance to the common antibiotics ciprofloxacin and rifampicin.

LexA is a DNA-binding protein that regulates the synthesis of repair and recombination machinery. By taking out LexA, the bacteria cannot alter their own DNA, thus depriving them of the needed variation to find a solution to the challenge posed by antibiotics.

This research raises fundamental questions about evolution. Biologists have often thought about evolution in the same way many think about death and taxes—something inevitable. But Romesberg is a chemist, and he found himself asking not only how, but why evolution happens.

Now for the interesting part

Because of the potential harm of mutations, humans and other mammals have evolved to make as few as possible. The machinery inside our cells has the ability to replicate our genomes extremely well, and the “polymerase” enzymes that replicate our DNA rarely make mistakes. Even when they do, we have multiple, redundant repair and proofreading mechanisms that would make even the most six-sigma-compliant NASA engineer jealous.

Nevertheless, all organisms are prone to some level of damage because no replication machinery is perfect, and with large genomes of billions of bases of DNA to be copied many billions of times over the lifetime of an organism, a certain level of spontaneous mutations will occur—mistakes that escape repair and become part of the DNA of the cell in which they occur. Scientists have generally thought that slowly over time, these mutations accumulate and species diverge.

However, Romesberg and his colleagues believe that cells are not just the passive victims of random mutations, but have ways of initiating mutations in their own DNA. Evidence for this includes the fact that the rates of mutation in some cells does not seem consistent with the mutation rates associated with DNA replication.

This brought Romesberg to the conclusion that mutation is a programmed stress response—a survival mechanism. If the cell senses damage, and if the damage persists beyond its ability to repair it, the cell will turn on its mutation machinery and open the floodgates for evolution.

So the question is if this mechanism is needed to allow for evolution then how did this mechanism evolve in the first place? A real chicken and egg question that is central to proving evolution on a molecular level. It seems that without a designed mechanism to allow for mutation, evolution can be stopped.

Links

www.eurekalert.org...
biology.plosjournals.org.../journal.pbio.0030176

That's fascinating! Great find.

If the cell senses damage, and if the damage persists beyond its ability to repair it, the cell will turn on its mutation machinery and open the floodgates for evolution.

Being programmed to "start" evolving? That's insane. Sci-fi fanatics and scientists alike (is there a difference?) will have a field day with this find. If we could get this sort of trait to manifest itself in humans, then...

I bet it means a lot for the disease-curing/preventing people. Why use stem cells when the body does it itself? That's a giant leap, probably insurmountable, but the general idea is a good one.

[edit on 5/22/2005 by Amorymeltzer]

excellent find BlackJackal

Interesting to think that evolution might be an intelligently designed trait.

living things have by far the most compact information storage/retrieval system known. This stands to reason if a microscopic cell stores as much information as several sets of Encyclopaedia Britannica. To illustrate further, the amount of information that could be stored in a pinhead’s volume of DNA is staggering. It is the equivalent information content of a pile of paperback books 500 times as tall as the distance from earth to the moon, each with a different, yet specific content.

complicated nature of even the smallest cells adds further weight to ID(IMO)

Perhaps in no other area of modern biology is the challenge posed by the extreme complexity and ingenuity of biological adaptations more apparent than in the fascinating new molecular world of the cell… To grasp the reality of life as it has been revealed by molecular biology, we must magnify a cell a thousand million times until it is twenty kilometers in diameter and resembles a giant airship large enough to cover a great city like London or New York. What we would then see would be an object of unparalleled complexity and adaptive design. On the surface of the cell we would see millions of openings, like the port holes of a vast space ship, opening and closing to allow a continual stream of materials to flow in and out. If we were to enter one of these openings we would find ourselves in a world of supreme technology and bewildering complexity

Talk about beingirreducibly complex. The medical possibilities could be extraordinary indeed. They even have hopes for possible cancer treatments, perhaps leading to a cure.

I don't see that either article leads to a conclusion of "intelligent design," though it does support evolution. And yes, it can certainly develop on its own.

Remember that we don't live in a stable, static, climate-controlled world and we sure didn't emerge in one. Climate has fluctuated over billions of years, changes in numbers of plants and animals has changed the ratio of carbon dioxide in the air, changes in landscape affects wind and rain patterns...

If creatures couldn't evolve as a group, the group of creatures would become extinct the first time that wind patterns shifted on a semipermanent basis.

If I'm not mistaken, even if the evolution, adaptation or mutation mechanisms in the human genome are disabled in every person, the mechanism of female/male genome blending at the point of conception is still a form of mutation or evolution, that isn't disabled by this.

What you could have by this though is that the people with this part of their genome disabled will be unable to procreate, have offspring with messed up DNA or still have perfectly normal children with a brand new set of DNA with its own features.

I sure hope that its the last, because if this mechanisme to repair and evolve our own DNA is needed to make a working DNA set from the blending of male/female DNA at conception, the true reason for the existence of this mechanisme will be procreation and not mutation or self repair.

Procreation is a form of evolution by itself.

Originally posted by Byrd
I don't see that either article leads to a conclusion of "intelligent design," though it does support evolution. And yes, it can certainly develop on its own.

Remember that we don't live in a stable, static, climate-controlled world and we sure didn't emerge in one. Climate has fluctuated over billions of years, changes in numbers of plants and animals has changed the ratio of carbon dioxide in the air, changes in landscape affects wind and rain patterns...

If creatures couldn't evolve as a group, the group of creatures would become extinct the first time that wind patterns shifted on a semipermanent basis.

Well, Byrd you can interupt the study anyway you would like but the actual study findings listed here

biology.plosjournals.org.../journal.pbio.0030176

indicate that a mechanism that can either be turned on or off controls evolution. Also, Romesberg indicated that he did not know how the mechanism itself evolved and would be researching that next so if you already know that it can develop on its own I guess thats all the proof we need?

Consider me stupid because I don't understand that study well. In layman's terms what exactly does it mean? I'm surprised this thread hasn't gotten more hits.

I'm currently studing cells in my science class. And (keep in mind that I am not fully educated and may not know some of the more complicated things about cells)I was under the impression that cells can only be produced by other cells. If thats true then why are we studying evolution in the first place?

For starters, Behe is not correct in his findings.

Originally posted by Voidmaster
I'm currently studing cells in my science class. And (keep in mind that I am not fully educated and may not know some of the more complicated things about cells)I was under the impression that cells can only be produced by other cells. If thats true then why are we studying evolution in the first place?

You'll see when you get to that point in your biology class, apparently. No offense.

Zip

Originally posted by BlackJackal
preventing induction of the SOS response by interfering with the activity of the protease LexA renders pathogenic Escherichia coli unable to evolve resistance in vivo to ciprofloxacin or rifampicin, important quinolone and rifamycin antibiotics

This, importantly, is stating that they've evolved a mechanism by which there is an increase in the mutations relevant to anti-biotic resistance, not all mutations throughout the genome.

Further evidence that the resistance-conferring mutations are induced is provided by the fact that deletion or mutation of several genes, including lexA, renders cells unable to evolve significant levels of resistance.

This is definitly intruiging information nonetheless. The bacteria seemed to have evovled a system bywhich, when challenged by the environment, specifically anti-biotics, they 'run the risk' of producing deleterious mutations by upping the mutation rate on specific parts of their genome, parts that are strongly associated with resistance to that anti-biotic that is so deadly for the bacteria.

This is an interesting example of the complexity and novelty that natural selection can result in.