In <914F1A35CA at mercury.uark.edu> DRHOADS at MERCURY.UARK.EDU ("Douglas Rhoads")
>> >Modifying genes that affect dominance do NOT have to be linked to the
>> >gene. Why should they?? And what point are YOU trying to make?
>> Ah, why should they be linked. OK, let's look carefully at that.
>> First, both Fisher and I suppose there is a general mechanism to affect
>> gene expression. A gene that's turned on, makes something that
>> eventually results in mRNA that produces a specific protein. A gene
>> that's turned off has that process interrupted so the protein is not
>> produced. Fisher and I both suppose that mechanisms exist which use
>> this mechanism to produce dominance. There is more here than the
>> simple model which says that recessive genes never produce a functional
>> protein. In this model a recessive gene may produce a protein when
>> it's homozygous, but that production gets shut off when the dominant
>> allele is present.
>But why look for some weird kind of interactions unless you just want
>to find out whether you can envision some form of gene interaction
>and then go out and find that it has or does occur in nature.
It's an approach to evolution that might be useful. No one really knows how
sexuality got selected. We can think of various possibilities and most of
them have subtle flaws that would keep them from working. Here we have the
other side -- something that would be selected if it happened, and we live
with the results it predicts, only we don't know that it does happen.
>dominance-recessive interactions have to do with altered proteins
>rather than RNA expression.
Are you sure? How do you know? Most dominance-recessive interactions are
assumed to be that way, and never really checked.
>> Here it comes: Could you select such a dominance-modifying gene based
>> on its effect on dominance? And the answer is, with reasonable
>> assumptions it's hard to select such a gene if it is unlinked to the
>> gene it affects. It is only selected when the version it makes
>> dominant is selected relative to the version it makes recessive. This
>> is a transient condition. When either allele is rare there isn't much
>> selection for the modifier. When the modifying gene is rare there
>> isn't much selection for the modifier. And after the dominant version
>> increases its frequency, the only way to get another pulse of selection
>> in favor of the modifier is to first select the other direction to get
>> the frequency back down. This is not an effective way to breed
>> modifying genes. It doesn't work.
>But modifying genes would either be transcription factors that
>regulate the gene or proteins that interact with the protein product
>of the gene. In my opinion the transcription factor modifiers may be
>less attractive because they will have multiple genes that they
They _may_ have multiple genes that they regulate. What if they do? Then
those multiple genes become dominant or recessive together.
>However, there could be variant transcription factors and
>therefore when these _unlinked_ genes come in contact (through a
>cross) with a particularly susceptible allele then you can have an
>altered penetrance/recessiveness. For multi-polypeptide complexes
>and their interactions in penetrance/recessiveness one would look for
>compensating (i.e. suppressor) mutants.
Sure. But if they act only on the genes they're linked to, the selection
works out better. Then the variant versions are only important to their
>> There is likewise no real-world data available to test
>> the standard Just-So story.
>So are you arguing that the sickle cell hemoglobin gene is
>dysfunctional??? On the contrary it is very functional it is just
>that in certain contexts it is considered `bad' while in other
>contexts it is good. It is a variant and has varying degrees of
>penetrance depending on the environment (high altitude vs sea level,
No, not at all. But it isn't a candidate for the kind of regulation I'm
proposing, as it has its advantage in the heterozygote state when both
alleles produce peptides.