Speaker
Description
Humans have 23 pairs of chromosomes, one of each pair from each parent, obtained by the
process of reductional cell division called meiosis. But before we get one chromosome from
a pair from each parent, there is recombination and shuffling between each pair. This
introduces variation to ensure that we aren’t identical half copies of each parent. From one
species to another, from one chromosome to another, from one region in the chromosome to
another, the rate of recombination can vary. In some species like humans and mice, but not
all, recombination is absolutely required, both for introducing variation but also for ensuring
that one chromosome from each pair is segreated properly during meiosis into the gametes,
to maintain fertility, avoid sterility and disorders resulting from improper segregation of
chromosomes like down syndrome. We explore genetic and epigenetic regulators of meiotic
recombination in mammals, which are working in tandem. We carry out in silico analysis to
characterize the variation and evolution of the proposed putative meiotic recombination
regulators using genomic, transcriptomic, and epigenetic data with the overarching aim to
uncover genetic factors affecting genome stability by dictating proper recombination and
repair. We envision a comprehensive evolutionary description of the nature and dynamics of
the putative meiotic recombination regulators in the context of diversity, population structure,
hybrid sterility, and speciation. Further, there is medical potential to study the association
between variation in the different meiotic recombination drivers and the disease states in
which meiotic segregation and recombination errors manifest such as aneuploidy, pregnancy
failure, sterility, congenital disorders.
