TITLE:
Ontogenes and Chromosome Nondisjunction in the D. melanogaster Meiosis
AUTHORS:
Boris F. Chadov, Nina B. Fedorova
KEYWORDS:
Conditional Mutation, Ontogene, Chromosome Nondisjunction, Meiotic Division, Drosophila
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.13 No.8,
August
12,
2022
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.