Characterization of ald, a Drosophila female meiotic mutant that causes chiasmate nondisjunction. W.D. Gilliland¹, S.M. Wayson², R.S. Hawley¹. 1) Stowers Institute, Kansas City, MO; 2) U.C. Davis, Davis, CA.

   The ald mutant was recovered by OTousa in 1982 as a hypomorphic meiotic mutant that causes ~25% achiasmate, and ~9% chiasmate, nondisjunction in female meiosis. This is of interest as chiasmata are normally sufficient to ensure accurate segregation of meiotic chromosomes, so the ald mutation must define a gene in the chiasmate segregation pathway. It was mapped to chromosome 3R, near cytological division 90C, and further determined by SNP mapping to lie within a 22Kb region which contains 6 predicted transcripts of unknown function. We are sequencing this region from the ald¹ mutant line as well as from the ncd¹ stock (another third chromosome mutant recovered in the same screen) to reduce the number of potential candidate mutations. We are generating rescue constructs to identify which of these transcripts is capable of rescuing the ald phenotype, and characterizing P element insertions in this region for their nondisjunction phenotypes, to identify which transcript is ald. We have also assayed the structure of meiotic chromosomes and spindles in ald homozygotes using deconvolution microscopy, which shows that chromsomes appear overly individualized in ald mutant females, with a possible early release of sister-chromatid cohesion. This is consistent with OTousas original conjecture that ald may be a glue protein that helps hold chiasmata together until anaphase. As loss of sister chromatid cohesion has been shown to lead to sister chromatid crossing over (e.g. in ord), we are also measuring rates of ring chromosome loss in ald homozygous females.