Uncle Davey wrote:
> Has anyone done any work on this topic?
>
> It seems to me as though the 'wild forms' of animals tend to have the
> dominant characteristics. When a wild boar mates with a pig, the offspring
> have more the shape of a wild boar, there is no fattening them up like a
> domesticated pig, and so the farmers hate when that happens.
>
> Can we see a general tendency that wild characteristics are dominant and
> ones bred in are nore recessive?
Dominance and recessiveness are descriptions of phenotype in the
heterozygote, not inherent properties of genes. The reason why w.t.
alleles are so often dominant to a mutant allele is that we are usually
observing the phenotypic consequences of a gene producing a protein
product that performs a function in the homozygous wild-type organism
and the phenotypic consequences of a mutant gene that either does not
produce a protein product at all or produces a profoundly defective one
in the homozygote for the mutant allele.
Only this *dramatic* difference in producing (or alternatively not
producing) a functional product produces phenotypes that are different
enough for us to notice. A mutation that reduced (or increased)
function by 10% would be 'invisible'. That is, we only notice
phenotypic differences large enough for us to see. Prior to our ability
to see DNA sequence differences, this led to a bias in observation that
meant that we were unaware of how often mutations were effectively neutral.
In the heterozygote, with one functional and one non-functional allele,
most often (but not always) the phenotype of the functional gene is the
one seen. This is in part because the functional allele is often
regulated and can compensate for the inactive allele. But it can also
be because we simply cannot 'see', given our test, a difference between
100% activity and 50% activity, but can 'see' a difference between 100%
activity and 0% activity. For example, if we are looking for growth or
no growth on a plate without histidine, the heterozygote for a gene
needed to make histidine from scratch may grow only half as fast as a
homozygote with the functional gene, but it will still be recorded as
'having grown'. OTOH, the homozygote which lacks any functional copy,
will not grow and will be clearly distinguished from either the
heterozygote or the homozygous wild type.
Interestingly enough, sometimes two *different* recessive mutations
sometimes make a right and interact to produce a functional gene
product. This is called intragenic complementation.
In other cases, the heterozygote does not exhibit
dominance/recessiveness, but incomplete dominance or even blending.
Dominance in a mutant allele is usually a consequence of a point
mutation producing a product that modifies quaternary structure of proteins.
>
> Uncle Davey
>
>
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