Observing Evolution Over 40,000 Generations

[w1z4rd]

Last year we discussed the work of Richard Lenski, who has been breeding E. coli for 21 years in a laboratory in Michigan. Then, the news was that Lenski's lab had caught direct, reproducible evidence of a genetic mutation with functional consequences for an organism. Now Lenski's lab has published in Nature a major study comparing adaptive and random genetic changes in 40,000 generations of E. coli (abstract here).

"Early changes in the bacteria appeared to be largely adaptive, helping them be more successful in their environment. 'The genome was evolving along at a surprisingly constant rate, even as the adaptation of the bacteria slowed down,' [Lenski] noted. 'But then suddenly the mutation rate jumped way up, and a new dynamic relationship was established.' By generation 20,000, for example, the group found that some 45 genetic mutations had occurred, but 6,000 generations later a genetic mutation in the metabolism arose and sparked a rapid increase in the number of mutations so that by generation 40,000, some 653 mutations had occurred. Unlike the earlier changes, many of these later mutations appeared to be more random and neutral. The long-awaited findings show that calculating rates and types of evolutionary change may be even more difficult to do without a rich data set."

http://science.slashdot.org/story/09/10/18/1947238/Observing-Evolution-Over-40000-Generations

This is basically a major evolutionary change thats been observed in experimentation.

 

[davemc]

A mutation that affected metabolism increased the bacteria's metabolism, and therefore it's rate of mutation also increased.

The article really is an example of turning a one sentence story into a 1 page essay.

 

[w1z4rd]

This aint church, snappy one liners are not good enough in science. Also its kinda more than that:

But sometime around the 31,500th generation, something dramatic happened in just one of the populations - the bacteria suddenly acquired the ability to metabolise citrate, a second nutrient in their culture medium that E. coli normally cannot use.

 

[tco21]

And now we go to the creationists for their take on the study...

 

[davemc]

Oh, ty Wizard, next time I'll wait for the coffee to work.

 

[Phronesis]

Anybody looked at the actual data to make out how big this "leap/jump" is?

If not, here goes:
E. coli are facultative anaerobic organisms, meaning that in the presence of oxygen, pyruvate (from glycolysis) will enter the Krebs (citric acid) cycle to produce energy and in the absence of oxygen, pyruvate will ferment to form lactate and/or ethanol (depending on the organism). Thus, E. coli can metabolize intracellular citrate just fine. All the machinery necessary to metabolize citrate is present in E. coli and the biochemical processes/reactions are highly coordinated and complex. Therefore, the evolutionary "leap/jump" cited is not an example of a suddenly acquired ability to metabolize citrate as E. coli posses the necessary intracellular machinery to metabolize citrate. What did evolve then? The bacteria just lacked membrane proteins to import citrate, that is all.

First look at the experimental conditions.
The E. coli (subtype B) bacteria where grown in DM25, a minimal salts medium that has 139microM glucose and 1,700microM citrate for about 20 years. Meaning a lot of extracellular citrate and little extracellular glucose. This specific strain does not have a citrate symporter to import the extracellular citrate. Other strains of E. coli posses such membrane proteins (e.g. citT), however some of them are situated on plasmids and the researchers made sure that horizontal transfer of plasmids was not possible in this experiment. Basically, the bacteria were swimming in an ocean of food but could only use a fraction of it because they could not get their "hands" on the goods. At around the 31000-31500th generation the first citrate "importers" arose. It will be fascinating to see the actual mutations that gave rise to this function and it is probably more than one (article speculates on possibly three genetic events related to citrate imprt over many generations). E. coli has many other symporter membrane proteins for dicarboxylic acids and other molecules with similar properties to citrate (e.g. Tartrate or alpha-ketoglutarate). Citrate is a tricarboxylic acid and it is possible that a few key mutations from an existing symporter protein allowed citrate to be imported by an existing protein. If so, it would be interesting how the mutations affected the properties of the original symporter system. The researchers however have not tracked down the exact mutations. I wonder if w1zard could perhaps get access to an article showing these mutation, as that would really be fascinating.

30 000 generations is the equivalent of +-600 000 years of evolution in a species with an average generation of 20 years (like primates). Is this an example of a "leap/jump"? If you are lactose intolerant, it might very well take 600 000 years before a mutation makes your descendants lactose tolerant (lactase gene beneficial mutation if all your descendants are also lactose intolerant). So in the end it is more like an evolutionary stutter (without us knowing the full extent of the other mutations during the 30 000 generations), much like nylonase "evolution", which was a a pre-existing esterase with B-lactam folds that had minimal nylon hydrolysis activity from the start.

This is probably a very good example of a preadaptation being co-opted into a new function.


One thing that is interesting from the article is how these bacteria where able elevate their mutation rate in response to environmental pressure. This is context-dependent and under control.

A few examples of context-dependent mutagenesis:
1) The A-rule [a].
2) In Escherichia coli cells expressing the mutA allele, transitions are increased 13-fold (equally between G:C→A:T and A:T→G:C) and transversions are elevated 35-fold, with G:C→T:A, G:C→C:G and A:T→C:G elevated 28-, 13- and 27-fold, respectively, while A:T→T:A mutations are increased 348-fold .
3) Impaired Ump1 (Saccharomyces cerevisiae) function leads to an increase in spontaneous mutations whereby the majority where G:C→T:A transversions (50%) and G:C→A:T transitions (30%) [c].
4) SOS mutagenesis is well-known and likely due to the error-prone synthesis across a blocking lesion when a polymerase makes a misinsertion error. SOS-induced A:T→T:A errors are increased 10-fold and most-likely occurs in the lagging strand [d].
5) Transcription affects guanine to thymine mutations in the non-transcribed strand [e].

References.
[a] Strauss BS. The "A" rule revisited: polymerases as determinants of mutational specificity. DNA Repair (Amst). 2002 Feb 28;1(2):125-35.
Balashov S, Humayun MZ. Specificity of spontaneous mutations induced in mutA mutator cells. Mutat Res. 2004 Apr 14;548(1-2):9-18.
[c] McIntyre J, Baranowska H, Skoneczna A, Halas A, Sledziewska-Gojska E. The spectrum of spontaneous mutations caused by deficiency in proteasome maturase Ump1 in Saccharomyces cerevisiae. Curr Genet. 2007 Nov;52(5-6):221-8.
[d] Maliszewska-Tkaczyk M, Jonczyk P, Bialoskorska M, Schaaper RM, Fijalkowska IJ. SOS mutator activity: unequal mutagenesis on leading and lagging strands. Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12678-83.
[e] Klapacz J, Bhagwat AS. Transcription promotes guanine to thymine mutations in the non-transcribed strand of an Escherichia coli gene. DNA Repair (Amst). 2005 Jul 12;4(7):806-13.

Oh, ty Wizard, next time I'll wait for the coffee to work.

I suggest you ignore his anti-religious bigotry .