UASt regulatory sequences drive expression of an inverted repeat.
Expression of βTub56DGD14171 under the control of Scer\GAL4insc-Mz1407 results in formation of ectopic neuroblast in both type I lineages and type II lineages in third instar larval brains.
Expression of βTub56DGD14171 (together with UAS-Dicer2 to enhance RNAi efficiency) under the control of Scer\GAL4erm.PU does not have any obvious effect on total neuroblast numbers or asymmetric protein segregation in secondary neuroblasts in third instar larval brains compared to controls.
Expression under the control of Scer\GAL4Mef2.PR results in late pupal lethality.
βTub56DGD14171, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | third instar larval stage phenotype, enhanceable by pinsP89
βTub56DGD14171, Scer\GAL4insc-Mz1407 has increased cell number | third instar larval stage phenotype, enhanceable by pinsP89
Scer\GAL4insc-Mz1407/βTub56DGD14171 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of pinsP89
Scer\GAL4insc-Mz1407/βTub56DGD14171 is a suppressor of decreased cell number | third instar larval stage phenotype of pinsP89
βTub56DGD14171, Scer\GAL4insc-Mz1407 has type I neuroblast | third instar larval stage | increased number phenotype, enhanceable by pinsP89
βTub56DGD14171, Scer\GAL4insc-Mz1407 has type II neuroblast | third instar larval stage | increased number phenotype, enhanceable by pinsP89
The increased number of brain neuroblasts observed in third instar larvae expressing βTub56DGD14171 under the control of Scer\GAL4insc-Mz1407 is increased further by combination with pinsP89 (although the pinsP89 mutants on their own display significantly lower number of brain neuroblasts compared to controls) and leads to a dramatic neuroblast overgrowth.
Expression of βTub56DGD14171 under the control of Scer\GAL4erm.PU in pinsP89 mutant background leads to severely increased number of neuroblast due to dedifferentiation of intermediate neural progenitors. The protein segregation defects observed in pinsP89 mutants during metaphase are enhanced by concomitant βTub56DGD14171 expression and perdure to telophase leading to protein mis-segregation.