Abstract:
Cohesins are ring-shaped protein complexes critical for keeping sister-chromatids
together, which are conserved from simple to complex organisms. They are also
important for chromosomal segregation, meiotic recombination events and in the
maintenance of chromosomal morphology. There are distinct cohesin complexes in
mitosis and meiosis. More interestingly, different cohesin complexes can localize to
different regions on the same chromosome making cohesin loading context-dependent.
In Schizosaccharomyces pombe, the meiotic chromosomes have different cohesin
complexes containing Rec8-Psc3 at the pericentric regions and Rec8-Rec11 in the
chromosomal arms. Earlier studies have shown that Rec8 is important for reductional
division in meiosis. Rec11 has been shown to activate recombination machinery in the
chromosomal arm regions, hence facilitating crossover events. Biochemical studies of
the mammalian cohesin complexes have shown biases in the interaction among the
different cohesin subunits. In many types of cancer cells, an aberrant expression of
meiotic cohesin genes has been reported. Overexpression of meiotic cohesins in mitotic
cells has been shown to affect growth and chromosomal segregation fidelity. Hence, it
becomes important to analyze the properties of these non-canonical complexes that can
be formed when the paralogs of these cohesins are untimely expressed in cells. In this
study, we generate yeast strains that express different combinations of mitotic and
meiotic cohesin complexes in cells. We did not observe a significant difference in the
growth rate of cells expressing different combinations of cohesins in mitosis except for a
few genotypes. During meiosis, both the meiotic cohesin subunits Rec8 and Rec11 are
essential to facilitate recombination events and these functions can not be substituted
by their mitotic counterparts Rad21 and Psc3, respectively. Interestingly, we also
observe a strong effect on the viability of cells when expressing certain combinations of
mitotic and meiotic cohesin subunits, suggesting improper formation or functioning of
certain cohesin complexes inside cells. We test multiple scenarios to explain this
observation and discuss our results. This study provides insights into why and how all
the theoretically possible cohesin complexes cannot be formed during cell division and
give possible clues on the rules for the formation of cohesin complexes inside cells.
