Ontogenes and Chromosome Nondisjunction in the <i>D. melanogaster</i> Meiosis

Abstract

A mutation in an ontogene acts as a conditional dominant lethal: it is lethal in a certain genotype but not lethal in another. In total, 30 mutations of this type residing in the Drosophila melanogaster X chromosome have been assayed for their ability to cause meiotic nondisjunction. The level of X nondisjunction in the females heterozygous for the mutation in ontogene appears to be very high. The share of matroclinous daughters reaches 24.7% of the overall offspring and of patroclinous males, 24.9%. Neither inversion in the opposite X chromosome nor additional Y chromosome has any effect on the X nondisjunction. The balance of the XX and X0 egg cells is disturbed: exceptional daughters are prevalent in the offspring of the females with a normal opposite X chromosome and exceptional sons, in the offspring of the females with an inverted X chromosome. In addition, 12% of the matroclinous daughters of the females with a normal opposite X chromosome are homozygous for the marker of one of the maternal X chromosomes (“equational” nondisjunction). A “fading” parental effect of the mutation in ontogene on the X chromosome nondisjunction is also observed. Under experimental conditions, the mutant ontogenes reside in meiotic densely compacted X chromosomes. We infer that the ontogenes are DNA regions with controlled compaction. It is postulated that the genetic activity of ontogenes is determined by this compaction and has a biophysical (electromagnetic) nature. In a meiotic cell, ontogenes induce physical fields providing the operation of meiotic proteins. The structure of these fields is distorted in the mutants for ontogenes, thereby decreasing the efficiency of proteins and, as a consequence, causing meiotic defects.