Remobilization of P{EPgy2}msd1EY11673 results in a deletion internal to the P-element.
Female meiotic spindles in msd1ex51 mutant embryos appear to show qualitative differences to wild-type, both in terms of apparent spindle density and/or length, and in chromosome alignment. However, bipolar spindle organization is not affected, and many msd1ex51 mutant embryos undergo a variable number of mitotic divisions, before accumulating defects and arresting prior to cellularization.
The primary defect observed in msd1ex51 mutant embryos is an increase in mitotic spindle length during metaphase, and a reduction in mitotic spindle density, when compared with wild-type spindles.
msd1ex51 mutant third-instar larvae exhibit an increased mitotic index and a decrease in the proportion of cells in anaphase, suggesting that reduction of msd1 levels results in a prolonged prometaphase/metaphase.
msd1ex51/Df(3L)bab-PG hemizygous female flies are viable but sterile. Mutant embryos laid by hemizygous mothers arrest development at an earlier stage than those laid by homozygous msd1ex51 mothers.
msd1ex51 has abnormal mitotic cell cycle phenotype, enhanceable by cnnHK21
msd1ex51 is an enhancer of abnormal mitotic cell cycle phenotype of cnnHK21
cnnHK21;msd1ex51 double mutants are homozygous lethal, dying at an early pupal stage. cnnHK21;msd1ex51 mutants show "metaphase-like" cells with weak, unorganized microtubule arrays; very few robust spindles are observed. An increased mitotic index is observed in these double mutants, greater than the increase seen in either cnnHK21 or msd1ex51 single mutants, and a dramatic increase in metaphase-to-anaphase ratio. Microtubule nucleation around chromatin in cnnHK21;msd1ex51 mutants is still observed, similar to that seen during prometaphase in cnnHK21 mutants, suggesting that nucleation of microtubules from around mitotic chromatin is insufficient for viability.
msd1ex51 is rescued by msd1UAS.GFP/Scer\GAL4VP16.mat.αTub67C