Molecular mechanism for the functional divergence between cohesin paralogs during meiosis
The key features of meiosis that enhance evolutionary success compared to mitosis are the processes of recombination and independent assortment during chromosome segregation, which help cells adapt to changing environments. Cohesins play critical roles in both these processes and have evolved specialized paralogs that are essential for meiotic chromosome dynamics. Studies so far have elucidated the roles of these meiotic cohesins but it is still unclear why the original mitotic proteins could not serve these evolved functions. In this study, we identify the mechanistic steps that are lost during meiosis when the mitotic counterparts replace the meiotic cohesins in Schizosaccharomyces pombe. The meiotic cohesin subunit Rec8REC8 has evolved multiple unique features that differentiate it from its mitotic paralog Rad21RAD21. Although ectopic expression of Rad21 in meiosis allows its chromatin enrichment, it fails to support reductional separation of chromosomes, initiation of recombination and protection of cohesion in anaphase I, resulting in catastrophic segregation errors. In contrast, the meiotic cohesin regulatory subunit Rec11STAG3, has only one major function of initiation of recombination, which is expectedly hampered in its absence. We show that although the mitotic paralog Psc3STAG1/2 is highly enriched at the cohesin-rich chromosomal axes, it is unable to recruit the downstream activators required for the induction of double-strand breaks. Our work systematically demonstrates the minimal functions that were necessary for the molecular evolution of these paralogs and explains the mechanisms that led to these adaptations.