news:c1vn2m$cn2$1@hood.uits.indiana.edu...
>
>
> 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.
I take it that this has all been discovered in the last twenty five years,
because they never taught me anything like this in school.
Uncle Davey
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