Amino acid replacement: M676K.
T6676532A
M676K | Mcm6-PA
M676K
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
female sterile (with Mcm62)
female sterile (with Mcm63)
female sterile (with Mcm64)
female sterile (with Mcm65)
Mcm6K1214 homozygous mutant animals do not exhibit any defects in their scutellar or wing-margin bristles while at oogenesis stage 10 they exhibit a small but significant decrease in nurse cell number and an almost absence of amplification of chorion gene loci (with Hoechst staining level similar to controls) when compared to controls.
Eggs laid by homozygous females are flaccid with thin, fragile eggshells (including flimsy dorsal appendages). Mutant follicle cells in mitotic and endocycles appear normal. However, most stage 10B mutant follicle cells have no detectable BrdU incorporation, while a few have faint or nearly wild-type incorporation. BrdU incorporation is mosaic among cells within an egg chamber. The dorsal-anterior cells most closely apposed to the oocyte nucleus and follicle cells in the posterior of the egg chamber most often have detectable BrdU incorporation. Inappropriate genomic BrdU incorporation is also seen in stage 10B (labelling is seen in other parts of the nucleus as well as the chorion loci). There is no significant difference in DNA content between wild-type and homozygous follicle cells.
Morphological defects: substantial underproduction and disruption of the endochorion, correlated with the underproduction of 6 major chorion protein gene products: Cp15, Cp16, Cp18, Cp19, Cp36 and Cp38.
Viability and fecundity of homozygous females reduced; sterility virtually complete, but a few progeny escape. Dorsal appendages of chorion short and thin.
Ovaries derived from homozygous females show reduced incorporation of BrdU compared to wild-type, and labeling is mosaic in intensity among the follicle cells.
All major chorion proteins underproduced owing to a defect in amplification of Cp genes on both the X and chromosome 3.