mei-S332¹/Df(2R)BSC597 mutants do not display any significant loss of co-orientation of homologous chromosomes, as compared with wild type.

Transmission rate of Dp(1;f)J21A through females to progeny is 28%, mei-S332¹ ord¹ double mutant causes a mild reduction in transmission, mei-S332¹ mutation alone has no effect on transmission. mei-S332¹ ord¹ double mutant also decreases transmission of Dp(1;f)1B, Dp(1;f)25A and Dp(1;f)10B. mei-S332¹ ord¹ double mutant has no effect Dp(1;f)J21A transmission in males.

Mutants exhibit premature sister chromatid separation. mei-S332¹ mutation does not rescue the meiotic defects of grau or cort mutants as shown by the double mutant phenotype.

High levels of nondisjunction in males and females.

Defects in sister chromatid cohesion. 20--30% total non-disjunction, hemizygotes exhibited a small increase in total nondisjunction. Nondisjunction of chromosomes 2 and 3 in males and females.

mei-S332¹ results in high X and 4th chromosome nondisjunction in both sexes. The incidence of nondisjunction in males and females is approximately the same and nonhomologs are independent. Nondisjunction occurs predominantly at the second meiotic division.

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 germ-line 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.