Posted on 10/23/2003 6:16:48 PM PDT by Nebullis
Adaptive mutation is common in E. coli, say IU researchers
The quickening of genetic mutation rates in bacteria may not only happen when the microorganisms find themselves in strange and stressful circumstances. A new report in Molecular Microbiology by Indiana University Bloomington researchers shows that at least one bacterium, Escherichia coli, ratchets up its "adaptive mutation" machinery when it simply runs out of food.
Biologists Patricia Foster and Jill Layton found that as E. coli cells begin to starve, the bacteria quadruple their expression of DNA Polymerase IV (Pol IV), a mutation-causing enzyme that is notoriously bad at copying DNA accurately. The culprit, the scientists discovered, is sigma-38, a stress protein that appears to activate expression of the Pol IV gene.
"We've known that bacteria respond to different kinds of stress by activating 30 genes or so," said Foster, who led the study. "We now know Pol IV is part of the response to starvation, which E. coli experience regularly during their life cycles. This polymerase may provide the bacterium with new properties that help them get out of difficulty by, for example, giving them the ability to use other food sources for growth."
The identification of genes controlling increased mutation rates in other, more dangerous bacteria could arm hospitals with a new type of weapon that helps them keep up with nosocomial infections caused by quickly mutating bacteria.
But the discovery also feeds a fiery theoretical debate over when and why a bacterium might increase its mutation rate. Many scientists contend that dramatically increased rates of mutation are almost always bad for bacteria, while others believe the bacteria depend on adaptive mutation to outlast the trials of harsh environments. Previously, the increased expression of Pol IV was thought to be limited to weird, drastic circumstances, the kind which might force a bacterium to mutate or die. But Foster and Layton have shown that a very common situation in nature -- one in which bacteria use up available food -- is enough to cause bacteria to activate Pol IV's gene, which in turn leads to increased mutations.
"In many instances where a more accurate polymerase might work, this one could now be substituted, so more mutations will occur," Foster said. "This results in more genetic variation and more properties on which natural selection might act."
DNA mutations are usually bad for bacteria, since altered genes rarely work properly. But sometimes mutations give rise to genes with new functions, endowing offspring bacteria with new properties, such as resistance to antibiotics.
Whenever bacteria reproduce, they divide in two and must make a copy of everything inside them, including their chromosomes. E. coli's DNA polymerases are replication enzymes responsible for making copies of the bacterium's DNA. Among the bacterium's suite of different DNA polymerases, Pol I, Pol II, and Pol III are extremely accurate, making exact duplicates, or near-exact duplicates, of the DNA they copy. Pol IV and Pol V, however, are remarkably error-prone, mutating the copied chromosome so that it differs in sequence from the original chromosome. Pol IV and Pol V are also known to be the only DNA polymerases that can get past DNA lesions, such as DNA damage ccaused by a traumatic chemical event inside the cell.
Foster and Layton studied the Pol IV expression patterns of 24 experimental strains of E. coli. Some strains had a functional Pol IV, and some didn't. Some strains had a functional form of the stress protein sigma-38, and some didn't. Cellular levels of sigma-38 increase during stationary phase, a slow-growth behavior caused by starvation. Under starvation conditions, the researchers found that Pol IV expression is increased from basal levels, about 250 copies of Pol IV in a single cell, to as many as 1,000 copies of Pol IV in a cell. They also learned that levels of Pol IV were about as low in E. coli strains missing a functional sigma-38 as in normal strains growing in non-starving conditions. This led Foster and Layton to conclude that sigma-38 helps control to what extent Pol IV is expressed.
"Genetics shows us the impossibility of a mutation spreading throughout a species. DNA shows us the impossibility of a new useful gene ever occurring. Natural selection is only a destroyer, it cannot create anything.""...we have yet to see the first beneficial mutation in some 150 years of looking for them..."
"A mutation changing an existing gene to a new purpose would destroy the individual. In fact natural selection prevents the creation of new genes."
"DNA Polymerase III is just one of three genes required for cell replication, without the other two it is useless."
"...all our billions in research on DNA for decades have not shown a single favorable mutation has ever happened..."
"Mendellian genetics proved that the passing on of new mutations, new genes, new traits, is virtually impossible."
- some guy
Normally in the copy. There can be damage or incorrect repair to the original, but normally, even in eukaryotes, replication errors are found in the copy. Pol IV, discussed in the article, makes lots of mismatch errors and doesn't proofread and correct them.
- Vince Foster
"Play ball!"
- P.J. O'Rourke
:^)
Wait - when a bacterium divides, how do you tell which is the "original" and which is the "copy"? Aren't those concepts kind of moot here?So when a bacterium has errors in gene replication, who gets the mutation, the original organism or the copy?
Normally in the copy. There can be damage or incorrect repair to the original, but normally, even in eukaryotes, replication errors are found in the copy.
Well, there's the backup argument: Mutations can be beneficial, but only if they entail a loss of "information". But this study shows that the state of higher mutation levels occurs often - whenever a colony of bacteria run out of food, which is often. So you'd expect bacteria's genomes to be mutated down to nothing by now. (If mutations always decrease "information", that is.)
OTOH, ID advocates could point to this finding as proof that intelligent design was frontloaded into the bacteria, or perhaps that the cells are more intelligent than we think, so are consciously driving their own design.
Me? I think evolution works on many levels, and this is an example of the evolution of evolvability. It's very cool.
I also wonder if the error-prone Pol IV is ancestral to the more accurate Pol I, II, & III - and was kept around like an over-the-hill "situation pitcher" (who's kept on because he can still get lefty's out in specific situations, for example).
Cellular levels of sigma-38 increase during stationary phase, a slow-growth behavior caused by starvation. Under starvation conditions, the researchers found that Pol IV expression is increased from basal levels, about 250 copies of Pol IV in a single cell, to as many as 1,000 copies of Pol IV in a cell. They also learned that levels of Pol IV were about as low in E. coli strains missing a functional sigma-38 as in normal strains growing in non-starving conditions. This led Foster and Layton to conclude that sigma-38 helps control to what extent Pol IV is expressed.Do you know what the passage in bold means? There's always only one copy of Pol IV, isn't there? It's the gene. So when they refer to 250 or 1000 copies, what are they talking about?
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