UASp regulatory sequences drive expression of the full-length cyst open reading frame. Silent mutations have been introduced at two distinct sites to confer resistance to RNAi mediated by the P{TRiP.HMS01750} transgene. The intron has also been removed.
Maternal expression of cystUASp.R under the control of Scer\GAL4VP16.mat.αTub67C leads to embryonic lethality, with the embryos displaying severe defects in head morphogenesis.
cystUASp.R, Scer\GAL4VP16.mat.αTub67C is a suppressor of embryonic epidermis | maternal effect phenotype of Rho1N19.UAS, Scer\GAL4VP16.mat.αTub67C
cystUASp.R, Scer\GAL4VP16.mat.αTub67C is a suppressor of embryonic/larval cuticle | maternal effect | embryonic stage phenotype of Rho1N19.UAS, Scer\GAL4VP16.mat.αTub67C
cystUASp.R, Scer\GAL4da.G32 is a non-suppressor of embryonic/larval cuticle | maternal effect | embryonic stage phenotype of Rac1DN.UAS.cUa, Scer\GAL4da.G32
cystUASp.R, Scer\GAL4da.G32 is a non-suppressor of embryonic/larval cuticle | maternal effect | embryonic stage phenotype of Cdc42N17.UAS, Scer\GAL4da.G32
Maternal co-expression of cystUASp.R and Rho1N19.UAS under the control of Scer\GAL4VP16.mat.αTub67C leads to embryonic cuticle defects that are similar to those induced by the expression of cystUASp.R alone, and milder than those induced by Rho1N19.UAS alone.