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Author Topic:   Random mutations
Loudmouth
Inactive Member


Message 2 of 35 (69218)
11-25-2003 1:22 PM
Reply to: Message 1 by judge
11-25-2003 7:21 AM


quote:
As I understand it random mutations are random WRT to their effect on the fitness of the organism.
Random mutations occur in the DNA, for instance a cytosine is changed to a tyrosine. The effects of each mutation can be deleterious (bad), neutral (no change), and beneficial (good). How we determine the advantage or disadvantage of each mutation is somewhat ad hoc, but the overall agreement is that if a mutation allows an organism to reproduce at a higher rate or fill a new niche it is advantageous.
So, saying that the effect on fitness is random isn't quite accurate, rather mutations are random changes in the DNA which may or may not affect fitness. Although there are "mutational hotspots", or areas in the genome that have a slightly higher rate of mutation, whether or not the actual mutation happens is still random among individuals.
I can look up some papers for you if you wish, but suffice it to say that studies that have looked at antibiotic resistance in bacteria, for example, have not seen the same mutation occuring among all resistant bacteria. It doesn't look like there is a mechanism that allows organisms to specifically change their DNA in response to an environmental stress. Rather, mutants are selected for by the environment.
One possible way to falsify this would be to look at different mutants that have arisen in different locals and see if they are exhibiting the same exact mutation and no other mutation. It is possible that only one possible mutation is going to work and is being selected for, but this is highly unlikely. Another falsification would be the discovery of a mutational enzyme that is responsible for all mutations in the genome. This mutational enzyme would be "front-loaded", in other words the enzyme creates specific mutations to specific stimuli. So far, enzymes of this nature have not been observed (to my knowledge) and random mistakes in DNA duplication seem to be the rule.

This message is a reply to:
 Message 1 by judge, posted 11-25-2003 7:21 AM judge has replied

Replies to this message:
 Message 5 by judge, posted 11-25-2003 3:50 PM Loudmouth has not replied
 Message 6 by Rrhain, posted 11-25-2003 5:59 PM Loudmouth has replied

  
Loudmouth
Inactive Member


Message 4 of 35 (69231)
11-25-2003 2:10 PM
Reply to: Message 3 by Rei
11-25-2003 1:23 PM


wrt=with respect to

This message is a reply to:
 Message 3 by Rei, posted 11-25-2003 1:23 PM Rei has not replied

  
Loudmouth
Inactive Member


Message 7 of 35 (69262)
11-25-2003 6:24 PM
Reply to: Message 6 by Rrhain
11-25-2003 5:59 PM


quote:
It seems that selective pressures can be specific enough to result in only those organisms that acquire specific mutations.
Yes, I should have made that a little more specific. Mutations are random in themselves but selection weeds out some before they can be observed.
I was trying to find a paper on the frequency of random mutations and found this paper and abstract
---
Single sperm analysis of the trinucleotide repeats in the Huntington's disease gene: quantification of the mutation frequency spectrum
Esther P.Leeflang, Lin Zhang, Simon Tavar, Rene Hubert, Jayalakshmi Srinidhi, Marcy E.MacDonald, Richard H.Myers, Margot de Young, Nancy S.Wexler, James F.Gusella and Norman Arnheim*
*To whom correspondence should be addressed
Received April 10,1995; Revised and Accepted June 2,1995
Thee CAG triplet repeat region of the Huntington's disease gene was amplified in 923 single sperm from three affected and two normal individuals. Average-size alleles (15-18 repeats) showed only three contraction mutations among 475 sperm (0.6%). A 30 repeat normal allele showed an 11% mutation frequency. The mutation frequency of a 36 repeat intermediate allele was 53% with 8% of all gametes having expansions which brought the allele size into the HD disease range (>=38 repeats). Disease alleles (38-51 repeats) showed a very high mutation frequency (92-99%). As repeat number increased there was a marked elevation in the frequency of expansions, in the mean number of repeats added per expansion and the size of the largest observed expansion. Contraction frequencies also appeared to increase with allele size but decreased as repeat number exceeded 36. Our sperm typing data are of a discrete nature rather than consisting of smears of PCR product from pooled sperm. This allowed the observed mutation frequency spectra to be compared to the distribution calculated using discrete stochastic models based on current molecular ideas of the expansion process. An excellent fit was found when the model specified that a random number of repeats are added during the progression of the polymerase through the repeated region.
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These are PCR's of single sperm which are not put under strict selective pressure and show high levels of additional repeats (a type of mutation). The distribution of repeats among single sperm appeared to be random. This would seem to be a hotspot for repeat polymorphisms, but point mutations could be caused by mutagens in a random sense in non-selected sperm as well.
The entire paper can be found here.

This message is a reply to:
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