ord^ys91/ord¹ males show 26.2% non-disjunction between the X and Y chromosomes.

Meiotic recombination is reduced but not absent. Encoded protein is able to poison the activity of ord⁴ in males and females: negative complementation. Mutation exhibits negative complementation when in combination with ord⁸ in males and females, missegregation is greater in ord⁸/ord¹ transheterozygotes than that in ord⁸ hemizygotes.

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 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 do not effect Dp(1;f)J21A transmission in males.

Level of chromosome missegregation in heterozygous females is 0%, levels in males and females significantly increase when transheterozygous with ord⁴. Also the frequency of X chromosome exchange of the transheterozygous is lower compared to ord⁴ homozygotes.

Primary spermatocytes in homozygous male flies show a high degree of aneuploidy. The pattern of ring canal inheritance in the meiocyte cysts is disrupted and the number of cells in each cyst is variable. In addition the cells occupying the cyst are very asynchronous in development in contrast to wild-type. Pycnotic cysts are common. There is also a high frequency of non-disjunction during gonial mitotic divisions, which involves the large autosomes more frequently than the sex chromosomes or chromosome 4. Homozygous males are defective in some aspect of the mechanism(s) that holds sister chromatids together during meiosis; the majority of sister kinetochores in prometaphaseI-metaphaseI primary spermatocytes are physically separated, and are smaller than wild-type. Testes of homozygous males are much smaller than wild-type.

In females homozygous for ord, exchange is strongly reduced. In both males and females, ord causes a dramatic increase in both reductional and equational nondisjunction as assayed genetically. In male meiosis, Goldstein observed abnormal sister-chromatid associations during prophase as well as precocious sister-chromatid separation, followed by random disjunction during anaphase I. 'The bulk of the first division misbehavior consists of sister chromatids' disjoining from one another, a process which normally occurs only during the second meiotic division' (Goldstein, 1980). ord also elevates the frequency of mitotic chromosome misbehavior (Baker et al., 1978). 'A substantial proportion of this mitotic instability can be accounted for by a hypothesis in which ord causes precocious sister-chromatid separation, followed by random disjunction, in somatic as well as germ-line cells' (Goldstein).