In Yeast Survive as They ‘Fail to Optimize’ (10 April 2013) Brian Thomas stumbles upon an important biological truth: what looks better on paper, when considering only a single part of a biological system, can still be bad for the survival of the organism as a whole.
He’s talking about a news article in Nature from February summarising two papers investigating how differing choices in codons that code for the same amino acid can affect the efficiency of the (here, circadian rhythm-related) proteins that they create, one studying a type of fungus and the other a bacterium. Continue reading →
On June 9, 2008, the New Scientist published an article describing preliminary results of a long-running experiment started by Lenski [ED:link]. Lenski and his team had taken a single strain of the bacterium E. coli, separated its descendants into twelve populations, and proceeded to observe their mutations over the course of twenty years (a process discussed on Lenski’s website). The E. coli were fed a measured amount of glucose every day. At one point, one of the populations exploded far beyond the parameters of the experiment. Lenski eventually discovered that this population had evolved the ability to “eat” citrate, an organic molecule which was part of the solution the E. coli lived in, but which E. coli cannot normally digest. Thus, evolution had been visibly observed, with an exquisite amount of evidence establishing the timeline along the way. Not only that, but the experiment was repeatable; Lenski started new experiments with the frozen “archives” of the population which exploded, and found that beyond a certain point, that particular population of E. coli were highly likely to evolve the ability to digest citrate. The paper also highlighted the role of historical contingency in evolution and the role of potentiating mutations.
There is an additional, less commonly known but still important fact to note: your average E. coli can already metabolise citrate, just not in the presence of oxygen. Indeed, not doing so is a defining characteristic of the species* – does this experiment then qualify as the creation of a new “kind” of organism, I wonder?
Anyway, that’s what we already knew. While the appearance of citrate metabolism was well-documented, with huge quantities of data to wade through only now (with a new paper in Nature) do we have an insight into the changes at the genetic level that allowed the phenotypic changes be observed. Perhaps in a desire to become the next Schlafly, Brian Thomas writes Bacterial ‘Evolution’ Is Actually Design in Action. Continue reading →
This fortnight we have the question of antibiotic resistance, in “Evolving Bacteria”:
With all the bad bacteria out there, scientists are working hard to develop new antibiotics to combat them. But these microbes often mutate when they reproduce, making some of them resistant to medicine. Is this process “evolution in action”?
The ICR obviously thinks the answer to that is a ‘no.’
Commensalism is a relationship between organisms in which one organism benefits and the other is unaffected. Today’s Daily (pseudo)Science Update – Bacteria Share Light Spectrum with Plant Leaves – boils down to Mr Thomas asserting that such a relationship could not have evolved.
I haven’t done anything on yesterday’s DpSU – while it’s certainly wrong, it would take more time for me to go over why exactly that is than I presently have available. Today’s DpSU – The Ingenious Way That Bacteria Resist Aging – presents no such problem. It also counts as biology revision, which is a minor plus.
Here’s the situation: Binary fission in a bacterial cell produces two identical cells. The old, worn out machinery of the original cell is divvied up between the daughter cells. But this presents the problem of ageing – do bacterial cells age?
An additional problem with this is that observations conflict. Some people have reported yes, others no. The study that this DpSU is based on works out a way to explain this by arguing that the older material is biased in going to one cell or the other. That is, one daughter gets a better inheritance than the other. The press release ends like so:
“There must be an active transport system within the bacterial cell that puts the non-genetic damage into one of the daughter cells,” said Chao. “We think evolution drove this asymmetry. If bacteria were symmetrical, there would be no aging. But because you have this asymmetry, one daughter by having more damage has aged, while the other daughter gets a rejuvenated start with less damage.”