Actin is dispersed and mitotic furrows do not form in divisions 10-13 of syncytial blastoderm embryos derived from homozygous females. Microtubules from individual spindle poles often interact with chromosomes on neighbouring spindles, forming microtubule bridges. Small actin caps form during interphase. The processes of pole cell formation, blastoderm cellularisation and postcellularisation mitotic divisions appear to be unaffected in these mutant embryos.
Embryos derived from sced1 mutant females show severe mitotic defects during divisions 11 to 13.
50% of embryos from homozygous mothers have uneven nuclear migration in nuclear cycles 9 and 10 and all undergo abnormal cortical nuclear divisions prior to cellularization. Affected embryos cellularize with fewer cortical nuclei and an excess of interior nuclei. Affected embryos develop distinct defects in the cortical cytoskeleton.
sced[+]/sced1 is a suppressor of aster | embryonic cycle 5 phenotype of CycB+t10
sced[+]/sced1 is a suppressor of aster | embryonic cycle 6 phenotype of CycB+t10
sced[+]/sced1 is a suppressor of aster | embryonic cycle 7 phenotype of CycB+t10
sced[+]/sced1 is a suppressor of mitotic domain 1 | embryonic cycle 10 phenotype of CycB+t10
sced[+]/sced1 is a suppressor of mitotic domain 1 | embryonic cycle 14 phenotype of CycB+t10
Excision of the P-element can revert the mutant phenotype.
Revertant analysis confirmed that maternal effect is caused by the P-element. The same phenotype is observed in embryos derived from homozygous or hemizygous females.