innominatetwice asks:

>I ask this question with two purposes:
>
>1) to obtain a clear explanation of the meaning of "recessive genes".

This is a question that befuddled biologists for nearly 70 years as well, but
the answer now seems clear and amazingly simple.

Genes encode two kinds of proteins: structural and catalytic. We call the
second catalytic form of proteins "enzymes." For the most part,
you have two
copies of every gene. If one of the two copies is defective (it no longer
specifies a properly functioning protein) and the gene encodes a catalytic
enzyme, it often doesn't matter much. Enzyme activity is regulated by an upper
level control circuitry. If you don't have enough of the necessary enzyme at
any particular moment, the control circuitry just asks the functioning
alternate translation circuit to crank up and build more of the necessary
enzyme. Clearly the functioning copy has to work twice as hard in this
situation, but it often can with no ill effects to the individual phenotype.

In this case, the defective copy of the enzyme's gene is
"recessive" and you
wouldn't notice the problem with the defective copy unless you inherited two
defective copies, one on each chromosome (and they don't even need to be the
same defect, btw). In this latter case, there would be no properly functioning
catalytic enzymes for this particular function and the absence of this function
will almost certainly be seen in the phenotype as some form of congenital
illness.

The problem of a defective copy is generally more severe for a structural
protein (kerogen, collagen, etc.) however. In this case, both copies of the
gene are generally translated into protein, but the admixture of the two (a
good copy of the protein and a less good one) often result in a pretty poorly
working structure. In this case, the defect is called "dominant." If it's
present, it's pretty much guaranteed to screw things up.

The only good news in this second scenario is that these forms of defects are
fairly rapidly scrubbed from a population, but at the cost of course of the
death or exclusion of the non-competitive phenotypes from the breeding
population.


>2) To understand how the inter-mixture of two groups (with differing
>sets of recessive genes) might benefit from their mutual exchange.

Mixing "recessive" defects from various populations won't make
much difference
in reality. As mentioned above, it doesn't matter if the defects are identical
on both chromosomes or are different. What matters is that you have at least
one good working copy if you hope to have a marginally working metabolism.

Wirt Atmar
---
þ RIMEGate(tm)/RGXPost V1.14 at BBSWORLD * Info{at}bbsworld.com

---
 * RIMEGate(tm)V10.2áÿ* RelayNet(tm) NNTP Gateway * MoonDog BBS
 * RgateImp.MoonDog.BBS at 12/12/04 6:22:57 AM