Principios de Taxonomia

154j 6 Biological Species as a Gene-Flow Community
something troubling scientifically becomes apparent in the history of biology:
Muller s hypothesis of X-autosomal disharmony was convincing only because of
its simplicity and plausibility and not because of experimental support for it.
Only decades later, the general validity of Haldane s Rule was disproved by new
observations and experiments. The observations and experiments were conducted
with simple methods. Initially, it was substantiated that the entire matter is far more
complex. First, Haldane s Rule affects fertility to a greater extent than vitality. The
hybrid offspring is much more likely to be sterile than to have its vitality be weakened.
Second, there is a distinct difference in whether the heterogametic hybrids are male
or female. If the sons are heterogametic (X/Y constitutions), then the decrease in
fertility is affected more significantly than if the daughters are heterogametic (Z/W
constitution) (Wu, Johnson, and Palopoli, 1998). This difference between the sexes
could not be explained by a simple understanding of Muller s explanation.
However, the universal validity of Haldane s Rule was even more powerfully
disproved by a simple experiment on Drosophila. By a genetic trick, it was possible to
produce female F1-species-hybrids that received both X chromosomes from only one
parent species. Thus, these experimentally produced homogametic daughters have
the same X-autosomal imbalance as the hetrogametic F1-sons of hybrid crosses.
Despite this scenario, the daughters were, in part, fertile, while the male offspring,
having a similar genetic constitution, were completely sterile (Wu, Johnson, and
Palopoli, 1998).
Nevertheless, the validity of Haldane s Rule has not been entirely disproved by
these observations and experiments. It is important to consider that the three
phenotypic consequences of postzygotic hybrid incompatibility are controlled
by different genes. These genes are not the same genes that regulate vitality,
the function of the male sexual organs and the function of the female sexual organs.
All three differentiation processes are regulated by different gene clusters and,
therefore, do not necessarily have to be equally affected by X-autosomal imbalance.
Indeed, it was substantiated that, especially the genes, which control male spermatogenesis,
are subject to a specific rapid evolutionary speed. The genes for male
fertility are said to be subject to a ten times faster evolutionary speed than the
genes for female fertility (Wu, Johnson, and Palopoli, 1998). Moreover, the genes
of male fertility change more rapidly than the genes for which both sexes depend
on their vitality.
Nevertheless, biologists know little about the genes that cause postzygotic allelic
incompatibilities, which are, in many cases, the first cause of speciation (Orr, 2009).
Do few or many genes mutate, when an organism adapts to a new environment? Can
the respective genes be identified? Are the same genes involved in adaptations to a
new environment, if such adaptations occur several times independently from each
other in different populations?
In recent years, approximately half a dozen genes causing sterility or a decrease in
vitality in hybrids have been identified by evolution geneticists. These genes usually
have basic and entirely different tasks, which at first appear to have nothing to do with
regulating vitality or fertility. Some of these genes code for enzymes, others for
structural proteins, and some even produce proteins that bind to the DNA and