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Jonah Thomas JEThomas at ix.netcom.com
Wed Jul 12 15:22:55 EST 1995

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 
modified also.

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?

It depends.

>>>    If you have 2 recessive alleles, no functional gene product can be 
>>> produced.  
>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.

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