Mutations

[UTEOTW]

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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http://www.baptistboard.com/ubb/ultimatebb.php/topic/66/21.html

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.

 

[Helen]

I have to get dinner, but I do have one comment to make on the initial part of the post. If none of the bacteria were resistant in the first place, none of them would have survived. So it is not a matter of evolution. It is a matter of part of the population having a natural resistance.

I had mentioned in another thread -- I think here, but if not then now -- that bacteria are known to mutate back and forth at hot spots. A to B to A to B etc. It is not A to B to C to D and so on. So with the various combinations that regularly occur in each population or colony, you will find some which have resistance to this or that and some that don't. In the presence of a this or a that, those which already have the resistance make it and those which don't are killed off. But the sub-population which does have resistance grows and they continue to have the hot spot variations until once again they are ready to take on, as a population, any number of threats and have some survive.

The other information you gave is really interesting. I need a much closer look that I have the time for at this moment. I will honestly try to get back to it later. On a personal side, I'm due at the hospital all day tomorrow to learn more about my diabetes in two half-day sessions. One general info and the other with a dietician. So tomorrow is basically a loss. I have a paper to edit tonight after dinner, so the soonest I can be back is Thursday.

With my apologies and thanks for the links to some interesting stuff.

 

[UTEOTW]

"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.

 

[Helen]

Please go study a bit on bacteria, OK? They were DESIGNED to mutate back and forth in a number of hot spots. If not, they would all be wiped out by now, which means we would be dead, too, as well as most living things. Not because we evolved from them, but because we depend on them.

Your lack of knowledge about something this basic also tells me that your material above was either fed to you or cut and pasted and that you don't know much about any of it anyway.

Which also means I needn't waste my time with it.
G'night.

 

[The Galatian]

We know, for example, that the ability to utilize nylon (a material that never appeared in nature until humans fabricated it) was not inherent in any bacterium.

We know exactly how that new information evolved. It occurred by a frameshift mutation in a plasmid.

 

[UTEOTW]

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.

Their VanA elements were compared with the prototype element, Tn1546, by an overlapping PCR method. Three related isolates contained resistance elements indistinguishable from Tn1546 [designated Greek type I]. The other five isolates all contained identical elements that differed from Tn1546 by the presence of IS1251 between vanS and vanH, by a point mutation [G <- T] at nucleotide position 8234 within vanX and by a partial loss of transposition gene orf1 [designated Greek type II ].

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.

 

[The Galatian]

One of my degrees, BTW, is in Bacteriology, so I do have some understanding of the subject.

 

[Helen]

Galatian, to repeat myself, an enzyme's ability to degrade nylon is simply the result of a reduction of specificity for that enzyme, enabling it to use a substrate it previously could not use.

A reduction in specificity. A step downhill, not uphill.

By the way, since Barry is sick, I'm home today so will be here sporadically during breaks.

 

[The Galatian]

There was no other enzyme, Helen. This one did not replace existing enzymes, which were still functional. Rather a plasmid (a small amount of extrachromosomal DNA) had a frameshift mutation (which shifts the code one letter) that produced an entirely new enyzme.

This is only one way new information evolves without losing the old. Gene duplication, followed by mutation of one of the copies is another. That way, the organism has information for the old protein and the new one.

Which by anyone's measure, is an increase in information.

BTW, tell Barry, I hope he will be feeling better soon.

 

[Magnetic Poles]

Originally posted by Helen:
Your lack of knowledge about something this basic also tells me that your material above was either fed to you or cut and pasted and that you don't know much about any of it anyway.

Which also means I needn't waste my time with it.
G'night.

Nice Dodge!

"It contradicts my baseless assertions, so I won't address it."

 

[Helen]

It's not a dodge. I think you can see from this page that I don't dodge things. However I am not going to try to discuss a subject with someone who actually knows nothing about it but is trying to declare that he is right anyway. That is definitely a waste of time. I have spent too many years on the internet not to know that.

 

[The Galatian]

This is where evidence comes in.

Barbarian asserts:
It is a waste of time to argue by assertion.

 

[Helen]

That's what you do mostly, Galatian. If you follow your own statement there your posts will become much shorter and fewer

 

[The Galatian]

See above. I provided you with some evidence concerning how the new information evolved. Would you like more detail?

 

[Magnetic Poles]

Pseudoscientists and self-proclaimed authorities with their life invested in fallacious pet theories won't change their views regardless of evidence to the contrary. This so much reminds me of Pons & Fleischman's cold fusion. May as well beat your head against the wall.

What next? A "scientist" who wants to change lead into gold?

 

[UTEOTW]

"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.