Mutations

On another thread that got out of hand, Helen suggested "you start a new thread with this one, UTE. This thread is for the birds."

So, we'll split the off topic material off.

Helen said:

"The mutation of bacteria to resist antibacterial agents involves a change in the folding of the protein where the original substrate is lost.

MP, what evidence do you have that any mutation causes a new function?"

And I responded:

Let's look specifically at the evolution of resistance to the antibiotic vancomycin.

Vancomycin works by attacking the D-alanyl-D-alanine in the cell wall of the bacterium. There are two genes, VanR and VanS, whose job is to make proteins to detect the presence of vancomycin. When detected, a cascade of other enzymes are created to protect the cell. VanH starts by converting precursor materials into D-lactate. VanA then joins the D-lactate with D-alanyl to make D-alanyl-D-lactate, instead of D-alanyl-D-alanine which is usually used in the cell wall. VanX hydrolyzes the D-alanyl-D-alanine that is still being made before it can be used in the cell wall.

This is the usual process, but there are variations. Some bacteria have VanB instead of VanA to make D-alanyl-D-lactate. Some bacteria replace the D-alanyl instead and make D-serine-D-alanine component instead of D-alanyl-D-lactate.

Once the resistance evolved, it was spread through plasmids.

So, why do you think that bacteria would be carrying around a gene such as VanX that hydrolyzes its own cell wall? What is the loss of function in this cascade? Which of these enzymes was produced by hotspots? Which of these is the loss due to a new folding of the protein?

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There are several examples. Some include...

"Selective sweep of a newly evolved sperm-specific gene in Drosophila," Nurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL, Nature. 1998 Dec 10;396(6711):572-5.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9859991&dopt=Abstract

You have two genes that are beside each other. They get duplicated. In one of the copies, some of the sequence between the two genes gets deleted. This allows the genes to combine into one chimeric gene. You have the two original genes intact and you have a new gene.


"Adaptive evolution after gene duplication," Hughes AL, Trends Genetics, 2002 Sep.18(9):433-4.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12175796&dopt=Abstract

In this case a gene, RNASE1, was duplicated such that we had a new gene, RNASE1B. These genes occur in the colobine monkey, douc langur and make pancreatic ribonuclease. Through a change in diet, the conditions within the digestive tract of the monkey were altered. Through delective pressure, the B copy of the gene mutated until it was adapted to digest single stranded bacterial RNA.

Again, we have new information. The original gene still exists to perform its original function. The gene was duplicated. When the copy mutated, then there was information that was not there previously, namely the new DNA sequence. The second copy eventually mutated until it performed a new digestive process.


"Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis," Mi S, Lee X, Li X, Veldman GM, Finnerty H, Racie L, LaVallie E, Tang XY, Edouard P, Howes S, Keith JC Jr, McCoy JM, Nature 2000 Feb 17;403(6771):785-9.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=20155476&dopt=Abstract

In this case, a retrovirus inserted a section of DNA into the genome. In this case, humans have co-opted the gene to serve an important role in the area of human placental morphogenesis. The purpose of the original gene was as the envelope gene of the virus. So humans gained a gene and a function which they previously did not have. The information of the human genome was thus increased.

 

"It is a matter of part of the population having a natural resistance."

They reproduce asexually. Somewhere there were mutations that made the difference. THis is not evolution? How can that be? For that matter, are you telling me that God made these bacteria in their original form vancomycin resistent? That does not seem very nice. Otherwise, the ability evolved.

I believe that this touches upon one of the aspects of punctuated equilibrium. During periods of stasis, neutral mutations can accumulate. When conditions change, some of these formerly neutral variations may provide an advantage. This built in genetic variation can allow some relativelt rapid evolution. Even if all of the pieces were in place before the arrival of vancomycin, this fits in with PE.

 

I think that all of us have our material given to us by someone else unless there is a PhD Evolutionary Biologists lurking among us.

Perhaps you can explain to me just what you mean about this being nothing but hotspots. Lets just take a look at the vancomycin resistance that I brought up above.

E. DEMERTZI, M-F.I. PALEPOU, M.E. KAUFMANN, A. AVLAMIS and N. WOODFORD, Characterisation of VanA and VanB elements from glycopeptide-resistant Enterococcus faecium from Greece, J. Med. Microbiol. -- Vol. 50 (2001), 682-687.

So their VanA elements were different from the original gene by a new insert, a point mutation, and a deletion. How does this fit into you hotspot idea? My understanding was that the hotspots were locations where point mutations were more favorable. This is significantly more involved than that.

 

"They were DESIGNED to mutate back and forth in a number of hot spots."

I'd still like to know how changes that involve insertions and deletions in combination with point mutations can be said to be simply hotspots that mutate back and forth? Those insertions just appear and dissappear? More importatnly, do the deletions just pop back into existance? I'd like to know how a real world example fits your claims.