UAS regulatory sequences drive expression of a short inverted repeat.
The expression of Spc105RGL00392 under the control of Scer\GAL4VP16.mat.αTub67C does not significantly affect karyosome compaction in late-stage oocytes, as compared to controls.
Expression of Spc105RGL00392 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 in oocytes disrupts kinetochore assembly, kinetochore-microtubule attachment and interactions, a loss of co-orientation of homologous chromosomes, lack of elongation of the karyosome, lack of separation of achiasmate chromosomes, lack of centromere orientation towards the spindle pole, weak/absent prometaphase and metaphase spindles, in contrast to wild type, no defect in central spindle formation or bipolar spindle morphology at prometaphase, but exhibit disorganization of the central spindle at metaphase.
Expression of Spc105RGL00392 under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 in females results in sterility.
Scer\GAL4VP16.mat.αTub67C, Spc105RGL00392 has spindle phenotype, enhanceable by subGL00583/Scer\GAL4VP16.mat.αTub67C
Scer\GAL4VP16.mat.αTub67C, Spc105RGL00392 has oocyte phenotype, enhanceable by subGL00583/Scer\GAL4VP16.mat.αTub67C
Spc105RGL00392, Scer\GAL4VP16.mat.αTub67C is a suppressor | partially of karyosome phenotype of Klp61FGL00441, Scer\GAL4VP16.mat.αTub67C
Spc105RGL00392/Scer\GAL4VP16.mat.αTub67C is a suppressor of karyosome phenotype of Scer\GAL4VP16.mat.αTub67C, cmetGL00404
Expression of subGL00583 enhances the weak/absent spindle phenotype in prometaphase oocytes expressing Spc105RGL00392 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16.
Co-expression of Spc105RGL00392 suppresses the karyosome splitting defect of oocytes expressing cmetGL00404 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16.