Plays a central role in chromosome cohesion during meiosis and mitosis by preventing premature dissociation of cohesin complex from centromeres after prophase, when most of cohesin complex dissociates from chromosomes arms. May act by protecting or Rad21 from cleavage by Sse/separase. Required during meiosis in both males and females.

(UniProt, Q24141)

mei-S332 is a semidominant autosomal mutation that increases nondisjunction of all chromosomes to the same extent in both sexes. Although female recombination is normal, mei-S332 causes high frequencies of equational nondisjunction in both sexes as well as chromosome loss (Davis, 1971; Goldstein, 1980). In the male germline sister chromatid associations are generally normal during prophase I and metaphase I. However, by telophase I sister chromatids have frequently undergone precocious separation (Goldstein, 1980). The equational exceptions produced by mei-S332 males and females presumably result from precociously separated sister chromatids going to the same pole at anaphase II. Goldstein (1980) has also suggested that "in the case of mei-S332, chromosomes which lag in the second meiotic division are usually lost and most of the genetically observed loss in mei-S332 occurs in the second meiotic division." The hypothesis that lagging chromatids are often lost at anaphase II is consistent with Hardy's observation that mei-S332 has micronuclei present at the early spermatid stages (Hardy, 1975). Thus mei-S332 presumably defines a function required for sister chromatid cohesion. Sandler et al. (1974) have shown that ring chromosomes are frequently converted into dominant lethals in mei-S332 females, presumably resulting from an impaired ability to resolve sister ring chromosomes at anaphase II. Baker et al. (1978) have also shown that mitotic chromosome instability is elevated in the presence of mei-S332. They suggest that the function of the mei-S332+ locus is to delay the separation of sister chromatids at all divisions. Because the sole mei-S332 allele is viable, they have further suggested that either this allele is leaky or that there are overlapping or redundant functions that can compensate for this defect.