Evolution of Sexual heterochromosomes

Only unusually few genes have been identified on sex heterochromosomes, i.e. on chromosomes that occur only in cells of the heterogametic sex. For example, in humans, the gene determining hairiness of the ear lobes was, for a long time, the only gene whose position could be localized on the Y-chromosome using genetic methods. At the end of the last century, about 20 genes were known, of which 10 were expressed in the testicles and the others affected mainly secondary sex traits (Roldan & Gomendio 1999). Thus, compared to the other chromosomes, the Y-chromosome is very poor in genes.

            This state is apparently not accidental and a number of hypotheses attempt to explain it (Graves 2000). It is assumed that this could, for example, be a form of defense of the organism against a certain category of outlaw genes. The formerly described blue-beard model (see IV.9.1 and Fig. IV.10) is a hypothetical example of such a gene. The model assumes the existence of a gene on the Y-chromosome of a (heterogametic) male. The presence of this gene causes that the male kills all (or almost all) his daughters and feed his sons with their meat. Such a gene is, of course, disadvantageous for the population and the species and its presence will almost certainly be manifested in a reduction in the size of the population. However, in the subpopulation of males, this gene will spread almost without limits, as males with a Y-chromosome containing this gene leave behind more (and better-fed) sons than males with a normal Y-chromosomes. We do not yet know of a situation in nature that would correspond directly to the blue-beard model. However, we know a great many cases where an outlaw gene achieves the same effect of influencing the behavior, not of organisms, but of individual chromosomes during meiosis, i.e. the mechanism known as meiotic drive. The organism can then produce a far greater number of progeny of one sex at the expense of the number of progeny of the other sex, which can apparently even lead to extinction of the population in some cases (Carvalho & Vaz 1999).

            Genes on the X-chromosome are not exposed to such strong pressure to “favor” the members of the homogametic sex because their copies are also present in the genomes of members of the heterogametic sex. However, the cells of members of the homogametic sex contain two specimens of these chromosomes, while the cells of the members of the heterogametic sex contain only one. As a consequence, the genes on the X-chromosomes spent two thirds of the time from their evolutionary formation in the cells of homogametic individuals and only one third of their time in the cells of heterogametic individuals. Consequently, here too female analogues of the blue-beard model can be expected to a certain extent. For example, published studies have shown that grandmothers and aunts invest far more into the children of their daughters than into the children of sons {xxx, 12148}. However, it is not clear whether this is a result of the shared X-chromosomes or the substantially greater certainty in relation to the maternity of the children of daughters than the paternity of the children of sons.

            Evolution can, of course, not foresee the possible arise of outlaw genes and take the relevant counter measures in advance. Subsequent inactivation of any formed outlaw genes by inactivation of genes on mutually nonhomologous parts of the sex chromosomes is a far more probable mechanism of defense of organisms against outlaw genes. It will certainly be interesting to study the sequence of genes and pseudogenes derived from just these parts of the genome.

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The classical Darwinian theory of evolution can explain the evolution of adaptive traits only in asexual organisms. The frozen plasticity theory is much more general: It can also explain the origin and evolution of adaptive traits in both asexual and sexual organisms Read more