Disease relevance of mei-S332

• Sterility is not due to aneuploid gametes--no significant second chromosome nondisjunction was found in matings to attached-2 and mei-S332 females [1].

High impact information on mei-S332

• Vertebrate shugoshin links sister centromere cohesion and kinetochore microtubule stability in mitosis [2].
• Drosophila MEI-S332 and fungal Sgo1 genes are essential for sister centromere cohesion in meiosis I [2].
• Mutations in the Drosophila mei-S332 gene cause premature separation of the sister chromatids in late anaphase of meiosis I [3].
• Therefore, the mei-S332 protein was postulated to hold the centromere regions of sister chromatids together until anaphase II [3].
• A fusion of mei-S332 to the green fluorescent protein (GFP) is fully functional and localizes specifically to the centromere region of meiotic chromosomes [3].

Biological context of mei-S332

• Previously isolated mutations in Drosophila specifically affect meiosis either in females or males, with the exception of the mei-S332 and ord genes which are required for proper sister-chromatid cohesion [4].
• Analysis of sex chromosome segregation in the double mutant indicates that ord is epistatic to mei-S332 [5].
• In mei-S332 mutants the ratio of metaphase to anaphase figures is lower than wild type, but it is higher if MEI-S332 is overexpressed [6].
• Sister chromatid associations in mei-S332 are generally normal during prophase I and metaphare I [7].
• All of the alleles are fully viable when in trans to a deficiency, thus mei-S332 is not essential for mitosis [8].

Anatomical context of mei-S332

• Two disjunction defective meiotic mutants, ord and mei-S332, each of which disrupts meiosis in both male and female Drosophila melanogaster, were analyzed cytologically and genetically in the male germ-line [7].
• MEI-S332 interacts with itself in the yeast two-hybrid assay and in immunoprecipitates from Drosophila oocyte and embryo extracts [9].
• We find that MEI-S332 is first detectable on chromosomes during prometaphase, and this localization is independent of microtubules [9].

Physical interactions of mei-S332

• INCENP binds to the cohesion protector protein MEI-S332, which is also an excellent in vitro substrate for Aurora B kinase [10].

Enzymatic interactions of mei-S332

• A MEI-S332 mutant that is only poorly phosphorylated by Aurora B is defective in localization to centromeres [10].

Regulatory relationships of mei-S332

• INCENP and Aurora B promote meiotic sister chromatid cohesion through localization of the Shugoshin MEI-S332 in Drosophila [10].

Other interactions of mei-S332

• Although overexpression of either protein in a wild-type background does not interfere with normal meiotic chromosome segregation, extra ORD+ protein in mei-S332 mutant males enhances nondisjunction at meiosis II [5].
• Both proteins remain in the centromere until metaphase, colocalizing at the centromere pairing domain that extends along the entire heterochromatin; the centromeric cohesion protein MEI-S332 is nonetheless reported in a distinct centromere domain [11].

References