I know this is rather belated but I was looking for another thread on mutation and came across this post which I never got round to addressing.
Are there any that can't be considered 'mutations' and if so what do you call them what are they and how do they operate? I'm curious because of the "all change is mutation" crowd here.
Many people only consider genetic mutation to be mutation proper, i.e. changes in the amount and base composition of the DNA. There are other heritable states based upon chemical and structural changes in the DNA such as methylation of DNA or methylation and acetylation of histones, which are sometimes termed epigenetic mutations. These epigentic mutations are sometimes not as stable as genetic mutations and their roles are much better studied in cell populations, as in tumorigenesis, than in transgenerational studies of organisms. This is changing however and there are a number of heritable phenotypes associated with apparently stable epigenetic mutations.
These aren't mutations anyone is likely to come across much until studying at an undergraduate level, although epigenetics has a higher profile now than it used to due to the importance of epigenetic factors in nuclear reprogramming and its relevance to cloning and stem cell production.
Bad news for the 'half' that misses a critical one, but extra material to play with for the other.
It can easily be bad news for both. Extra chromosomes are often associated with genetic or developmental defects leading to infertility or sterility.
Do we know of any mechanism that control the rates of changes, and how do these impact the picture?
There are a number of different mechanisms. One is the development of a mutator phenotype, in some cases this is merely due to the loss of a proofreading enzyme which relaxes the error checking during DNA synthesis. There are a number of well studied bacterial mutator phenotypes and they are one of the explanations for apparently adaptive mutations, another possible mechanism is mutation leading to a decrease in activity of cell membrane transport proteins which act to export mutagenic metabolites.
Conversely there are mechanisms considered more truly adaptive, although they are still similar in mechanism, such as one described in a recent paper where stress caused a bacterium to actively switch from a high fidelity to an error prone mechanism of double strand break repair, the double strand break repair mechanism leads to a localisation of mutations to regions where breaks occur which limits the number of possible mutations but doesn't specifically target any specific gene
per se (
Ponder, et al., 2005).
TTFN,
WK