11  Homeotic genes
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Homeotic genes are control genes that set in motion the entire developmental cascade of embryonic development. They are very similar over a wide systematic range, from the fly, mouse, chicken, right up to the human being. The great similarity of these embryo-developmental control genes initially led one to think of them as key genes of macro evolution. This expectation, however, remained unfulfilled.


Some decades ago, a biologist at the University of Denver, in the course of a public debate, proclaimed an example of a “beneficial” mutation. It concerned the bithorax gene that produces four wings in the fruit fly. This, however, reduces its capacity to fly. Possibly the control program in the brain for flying with four wings is lacking. Such insects would rapidly be selected out by natural selection (1).
 
“Control genes, like homeotic genes may be the target of mutations that would conceivably change phenotypes, but one must remember that, the more central one makes changes in a complex system, the more severe the peripheral consequences become. Homeotic changes induced in drosophila genes have only led to monstrosities,” the evolutionist Schwabe admits (2).

In view of the ingenious way in which these main switch genes direct the subordinate genes of the morphogenesis (form creation) in a precise spatial and temporal pattern (3), it is difficult to attribute the origin of this symphony to random development over a long period of time. One false note, for instance one protein DNA interaction disrupted by a mutation, can, at any time (or with a temporal delay where there is buffering capacity), means the failure of the orchestra, (i.e., a maldevelopment or dysplasia) and thereby reduced health of both the individual and the species.

 Every positive homeotic mutation, which is supposed to lead to a “higher” appearance, must be followed by a large number of small positive mutations in the target genes lower in the hierarchy of control. In purely mathematical terms, this brings about a multiplication of positive mutation probabilities. This drastically reduces the probability of realizing a new higher design process or phenotype by means of random mutations.


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References:

(1) Jane B. Reece und Neil A. Campbell, Biology, Benjamin/Cummings, 1999, page 460.
(2) C. Schwabe, Theoretical limitations of molecular phylogenetics and the evolution of relaxins, Comp. Biochem. Physiol., 107B, 1994, pages 167–177.
(3) Walter J. Gehring, Wie Gene die Entwicklung steuern, Birkhäuser Verlag, 2001.
 
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