In <3u0psr$9gt at hq.jcic.org> gloria stephens <stephens at hq.jcic.org> writes:
>1. Is there enough information contained in the 'dominant' gene that the
>recessive gene is not read at all?
It depends. Dominance is a phenotype, something we observe. There could be a
lot of different mechanisms that give that result.
>2. Is there any influence from a recessive gene?
It depends. If one allele results in a deep blue pigment while another results
in a pale green pigment, you probably won't notice the pale green one if the
deep blue one is present. You could detect it spectrographically. Does it
have any influence? I dunno. Do those metabolic pathways have any result
other than color? They might actually _do_ something, beyond provide
camouflage or mating cues or whatever we think of pigments as doing. You'd
have to look at each individual case.
>3. Are both the dominant and the recessive gene read?
It depends. When a recessive gene is recessive because it has a mutation that
prevents initiation, then it isn't read.
>4. In dealing with the recessive gene, are the genes from both
>chromosomes read? I.E. are polypetides formed from both chromosomes?
That's complicated in eucaryotes. Look at the sequence of events. An RNA copy
is made of the DNA. There's room for some sort of regulation at that level.
Then that RNA is cut up and spliced to get a much shorter version. There's
room for regulation in that process, at different times the same RNA can be
processed differently. Some of the leftover fragments might be involved in the
regulation of other processes. Then the cut-and-spliced RNA is moved out to be
translated into peptides. It could get regulated there too, at some times and
places spliced RNA might not make it out of the nucleus. Then the peptide
formation starts, and that can be regulated. The RNA gets degraded sooner or
later, more potential regulation. The peptides get transported to their proper
place in the cell, that step can be regulated too. And some proteins have
enzymatic activity regulated by chemical compounds. They get degraded or
Evolutionary processes aren't obligated to fit into neat packages that make
sense. Regulatory methods can arise every-which-way. Or maybe a few methods
_work_ so well that those tend to outcompete any others. I dunno yet. But any
regulation that results in one allele's phenotype becoming invisible when
another allele is present will look like dominance.
>Basically, are both chromosomes read or just one?
>>> If you have 2 recessive alleles, no functional gene product can be
>If this is true, then how do recessive genes work?
The recessive alleles that don't produce functional gene product (and there are
some known -- it's the simplest case and easy to observe, or at least easy to
fit as an explanation to common observations) work by failing to produce
product. Their product must be something the organism can survive without,
otherwise they're recessive lethals. So you get an organism that lacks a
pathway of some sort and has an observable difference as a result.
People with PKU lack an enzyme needed to degrade phenylalanine. So they suffer
if they get too much phenylalanine. One functional copy of the gene is enough
to avoid mental impairment and early death. Do PKU carriers have some
observable symptom? I dunno. Maybe if you looked closely enough you'd find
something. That would make the "recessive" gene not totally 100% recessive.
There are a variety of hemoglobin problems that result in a changed hemoglobin.
Get one normal copy and you have a much different phenotype than with two
changed copies. We tend to call it recessive even though the heterozygous form
has its own special results.
"Dominance" is an old-fashioned concept. It's easy to observe and explain, so
it lingers. Some new more-precise terminology will replace it, but I haven't
heard the new stuff yet.