Cohesin protein complexes are a molecular glue that holds two sister chromatids together. They play an important role both in mitosis and meiosis. In mitosis, all cohesin complexes present on the chromosomes are removed before the start of the anaphase stage.
Meiosis involves two distinct rounds of chromosomal segregation and cell divisions— Meiosis I followed by Meiosis II – producing four daughter cells. Meiosis I includes the separation of homologous chromosomes, whereas Meiosis-II involves the separation of sister chromatids.
The Meiosis I cohesin complex consists of four subunits – Smc1, Smc3, Rec8 (replacing Scc1 from mitotic cohesin complex), and Scc3 – forming a ring-like structure.
During Meiosis I, entire chromosomes segregate towards the opposite poles as cohesin removal takes place only from the chromosomal arms. Cohesin is still maintained at the centromere region, allowing the sister chromatids to remain connected. During the metaphase I to anaphase I transition, the differential cohesin removal is facilitated by the separase-mediated cleavage of the Rec8 subunit of cohesins along the chromosomal arms. The centromeric Rec8 is protected from cleavage by association with a protector protein Shugoshin (Sgo1).
Cohesins contribute to the maintenance of genomic stability. Mutations in genes coding for cohesin subunits or cohesin co-factors can lead to diseases called cohesinopathies. Cornelia de Lange syndrome (CdLS) and Roberts syndrome are two best-described cohesinopathies. CdLS is a neurodevelopmental disorder causing mental retardation, facial dysmorphism, upper limb abnormalities, and growth delay. Roberts syndrome results in craniofacial abnormalities, limb reduction, and growth retardation in affected patients.
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