In article <57270p$t73 at scotsman.ed.ac.uk>, rhi at tattoo.ed.ac.uk (Rhiannon
> > Sounds like natural selection, can you expound on that. How do I know
> > there weren't a small percent of insects that were resistant to
> > the insecticide to begin with.
> But where did this small percent come from in the first place?
Many insecticide resistance mutations involve a minor (minor in the sense
of requiring only a small point mutation) alteration in amino acid sequence
of a particular receptor protein which renders the particular pesticide
ineffective. A classic example is the _Rdl_ mutation of a GABA receptor
subunit in Drosophila (homologue of which have since been found in a wide
range of other insect species). A single amino acid change in the protein
ends up conferring thousandfold resistance to an array of cyclodiene
insecticides which, were it not for this mutation, would have been able to
block a crucial nerve cell ion channel.
Due to the kind of commonplace errors in DNA replication that are one of
many possible sources of mutation in eukaryotes, it is a relatively simple
manner to produce mutant haplotypes which differ from wild-type by a single
nucleotide, especially if normal function of a particular protein is not
significantly altered. Such mutant haplotypes exist naturally, albeit in
very low frequency, in natural populations and are not "recognized" as
beneficial until the proper kind of selective force comes along . . . in
this case, humans and their insecticide arsenals.
There may be many mutations that occur in natural populations that end up
conferring a selective advantage completely by accident. The most recent
example in humans is a group of individuals who seemingly cannot contract
AIDS despite frequent exposure to HIV. The reason? Certain of their immune
cells lack a receptor protein that the virus particle latches on to in
order to enter the cell.
The point of these examples is to illustrate just how effective seemingly
random and minor alterations in DNA can lead to large selective advantages.