Evolutionary Rewiring

[Wolfhnd]

Strong selective pressure can lead to rapid and reproducible evolution in bacteria.

 

"Bacteria that lack a vital protein for growing flagella—tail-like structures that enable the microbes to swim—can attain flagella in as little as four days given enough pressure to evolve, according to a paper published in Science today (February 26). Furthermore, this fast fix evolves in nearly the same way in each independent strain: through the repurposing of a distantly related protein.

“This is a fascinating set of evolution experiments,” wrote evolutionary biologist Richard Lenski of Michigan State University in an e-mail to The Scientist. “Their experiments show how a biological function—in this case, flagellar motility in Pseudomonas fluorescens—can re-evolve after the deletion of a seemingly critical gene. The bacteria regained motility not by reacquiring the lost gene . . . but instead by mutations in other genes that put their products to new uses.” "

http://www.the-scientist.com/?articles.view/articleNo/42284/title/Evolutionary-Rewiring/

I'm really lost as to what to think about this finding. It could be that it is just the law of large numbers and every conceivable mutation was available for selection. It could also be that the repair mechanism are more complex than imaginable. The third possibility is a little of both. Opinions?

Edited February 27, 2015 by Wolfhnd

[CharonY]

It is in some way far easier. What was mutated was not the flagellum itself but a central regulator. Loss of it stops the bacterium from initiating motility. However, there are homologs (related genes with similar sequences) that were able to have a similar role (i.e. initiate motility) once the right mutation(s) hit. In this case only two steps were needed. One, to increase the expresssion of the homolog and a second to allow it bind the regulatory sequence of the flagellar system.

 

This goes into the larger (known) aspect that regulatory mechanisms are a the main source of rapid changes as few mutations can result in far reaching physiological changes. If the whole flagellar operon (i.e. the genes that actually synthesize the flagellum) was lost, it would have taken much longer.

Edited February 27, 2015 by CharonY

[starlarvae]

It is in some way far easier. What was mutated was not the flagellum itself but a central regulator. Loss of it stops the bacterium from initiating motility. However, there are homologs (related genes with similar sequences) that were able to have a similar role (i.e. initiate motility) once the right mutation(s) hit. In this case only two steps were needed. One, to increase the expresssion of the homolog and a second to allow it bind the regulatory sequence of the flagellar system.

 

This goes into the larger (known) aspect that regulatory mechanisms are a the main source of rapid changes as few mutations can result in far reaching physiological changes. If the whole flagellar operon (i.e. the genes that actually synthesize the flagellum) was lost, it would have taken much longer.

 

Does it strain credulity to assert that the necessary two mutations, which repurpose a distantly related protein, occur predictably in each independent strain?

 

That's one heck of a coincidence. Lucky flagellates.

[overtone]

 

 

Does it strain credulity to assert that the necessary two mutations, which repurpose a distantly related protein, occur predictably in each independent strain?

No.

That's one heck of a coincidence

It's probably almost an inevitability - from the evidence. Not much luck involved at all.

Edited February 28, 2015 by overtone

[CharonY]

Not at all, the buggers accumulate massive amounts of mutations under routine cultivation conditions. In fact selection for new resistant strains or other reverting auxotroph mutants is something we are often do as in low-level microbio courses.

It is actually quite a bit of a problem for cases where you create mutations to investigate stress-related responses. Sometimes they are only sensitive for a few generation and then somehow regain a wildtype phenotype. In the olden days that was it, but nowadays sequencing has become so (relatively) cheap that you could look at where the mutations are.

I envy the kids nowadays.

Edited February 28, 2015 by CharonY

[Wolfhnd]

I read that human cells on average have between 500 and 1000 mutations per day. Does anyone know the guess at what the mutation rate for Bacteria is?

[Robittybob1]

I read that human cells on average have between 500 and 1000 mutations per day. Does anyone know the guess at what the mutation rate for Bacteria is?

Where did you read that?

[Wolfhnd]

Where did you read that?

 

Most get repaired so it's not alarming and it could be that it was simply wrong or I misread it.

 

I suppose the more interesting figure is covered in this article.

 

 

Human mutation rate revealed

 

"Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome."

 

http://www.nature.com/news/2009/090827/full/news.2009.864.html

 

 

Here is an article on Rates of Spontaneous Mutation

 

http://www.genetics.org/content/148/4/1667.full

[Robittybob1]

 

Most get repaired so it's not alarming and it could be that it was simply wrong or I misread it.

 

I suppose the more interesting figure is covered in this article.

 

 

Human mutation rate revealed

 

"Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome."

 

http://www.nature.com/news/2009/090827/full/news.2009.864.html

 

 

Here is an article on Rates of Spontaneous Mutation

 

http://www.genetics.org/content/148/4/1667.full

Thanks I'll check them out later.

[Wolfhnd]

Does it strain credulity to assert that the necessary two mutations, which repurpose a distantly related protein, occur predictably in each independent strain?

That's one heck of a coincidence. Lucky flagellates.

 

 

This is highly controversial. See "Arguments against a mutator phenotype" in this paper Do mutator mutations fuel tumorigenesis? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987827/. I have seen experiments that suggest normal mutation and selection can account for variable mutation rates. However there does seem to be an unexpectedly low lethal mutagenesis. Evolution at a High Imposed Mutation Rate: Adaptation Obscures the Load in Phage T7 http://www.genetics.org/content/184/1/221.abstract

 

I think the answer to your question is no one knows for sure.

Edited February 28, 2015 by Wolfhnd

[Delta1212]

 

Does it strain credulity to assert that the necessary two mutations, which repurpose a distantly related protein, occur predictably in each independent strain?

 

That's one heck of a coincidence. Lucky flagellates.

If there is a strong selection pressure and only one (easy) path to a flagella, then any situation where the flagella evolves is likely to be the result of the same mutations. These mutations, given enough time, will occur anyway, but without the selection pressure, they are exceedingly unlikely to be retained and lead to widespread reemergence of a flagella structure. Under the selection pressure, the newly reformed flagella is likely to propagate very quickly.

 

It's less a mark able coincidence and more that it's a fairly simple mutation and the only such mutation that is likely to lead to the reemergence of a highly favorable trait. Given enough time, you would reasonably expect most any population under a strong selection pressure for that trait to wind up having that mutation be widespread.

[CharonY]

 

Does it strain credulity to assert that the necessary two mutations, which repurpose a distantly related protein, occur predictably in each independent strain?

That's one heck of a coincidence. Lucky flagellates.

 

 

This is highly controversial. See "Arguments against a mutator phenotype" in this paper Do mutator mutations fuel tumorigenesis? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987827/. I have seen experiments that suggest normal mutation and selection can account for variable mutation rates. However there does seem to be an unexpectedly low lethal mutagenesis. Evolution at a High Imposed Mutation Rate: Adaptation Obscures the Load in Phage T7 http://www.genetics.org/content/184/1/221.abstract

 

I think the answer to your question is no one knows for sure.

 

 

It seems to me you are conflating two very different systems, multicellular organisms and unicellular ones. The effects are vastly different. A clonal cell population can undergo high-risk events (read up on SOS-response) where they increase mutation rate for example. Even if a large amount of the cells die, they will still have a largely clonal pool in the next generation. This is not true for more complex organisms.

And to reiterate, the mutation are fairly minor as they are on the regulatory side. They did not create new flagella, they just restarted the their regulation.

Even in eukaryotes small mutations in central regulators are known to be able to result in massive phenotypic changes (the HOM genes being prime examples).

[Wolfhnd]

"fleQ appears to be the highest-level activator in the hierarchical regulatory cascade involved in the flagellar biogenesis pathway. It is essential for flagellar motility as an fleQ mutant does not assemble a flagellum nor does it synthesize detectable amounts of flagellin."

[CharonY]

Precisely as I stated, or is something unclear to you about that?

[Wolfhnd]

Oh sorry I was going to make a reply and got distracted.

[starlarvae]

Commentary from the dark side, but what do you think? Is this a fair criticism of the conclusions drawn by the researchers? Or, where does this critic go wrong?

 

http://www.evolutionnews.org/2015/03/resurrected_fla094081.html

[Strange]

Commentary from the dark side, but what do you think? Is this a fair criticism of the conclusions drawn by the researchers? Or, where does this critic go wrong?

 

http://www.evolutionnews.org/2015/03/resurrected_fla094081.html

 

Why am I not surprised to find you quoting Behe ...

[starlarvae]

 

Why am I not surprised to find you quoting Behe ...

Guilt by association?

 

More importantly, what do you make of his assessment?

[CharonY]

The part that it was not a new flagellum was basically what what the lead author described (and what I mentioned) and which got blown out of proportion by media (as usual). The rest is his usual drivel and mix of bad analogies and agenda. Basically he is attacking a straw man that was partially assisted by media exaggeration (which is why I dislike certain types of simplification, it gives people with an agenda the material to build bogus arguments).

 

What is relevant which Behe conveniently forgets (which to some point may also apply to posters here) is that the paper describes dynamics of regulation and the fact that small changes in regulatory mechanisms can have large physiological impact. Many laymen assume that you need genes for everything and are confused why there is so little variation between bacterium and elephant. Truth is that the coding genes are only part of the story, but for the actual activity their expression and the coordination of expression reigns supreme (well and quite a few other interactions but at some point the catchy phrase turns into an essay).

Edited March 5, 2015 by CharonY

[Strange]

Guilt by association?

 

Not really. Just more confirmation of your agenda.

 

More importantly, what do you make of his assessment?

 

CharonY said what I would have said, pretty much word for word.

[CharonY]

Minus typos and liberal use of grammar, I hope.

[Wolfhnd]

Creationist aside it's still an interesting article

[CharonY]

What is silly is that it is a report on a report on a scientific article. And now we are discussing this, instead of the original research.

[Strange]

Creationist aside it's still an interesting article

 

Agreed. It provides some interesting insights.