Expression of the mutated cDNA is driven by an Hsp70 promoter.
Embryos expressing Rac1N17.hs show a failure of dorsal closure. This phenotype is suppressed by Rac1V12.Scer\UAS expressed under the control of Scer\GAL4hs.PB.
Heat induced expression causes border cell migration to halted in 98% egg chambers. The actin cage that normally surrounds stage 11 nurse cell nuclei is absent resulting in ring canals becoming obstructed by the nuclei and failure to complete cytoplasm transfer.
Heat shock at intervals from 4-5 hours to 9-10 AEL produces high frequency of defects in dorsal closure due to disruption of cell shape changes in the lateral epidermis, accompanied by disruption of a localised accumulation of actin and myosin thought to be driving epidermal cell shape change. Embryos also exhibit defects in germband retraction and head involution.
Cdc42N17.UAS, Rac1N17.hs, Scer\GAL4hs.PB has embryonic/first instar larval cuticle | dorsal phenotype
Cdc42V12.UAS, Rac1N17.hs, Scer\GAL4hs.PB has embryonic/first instar larval cuticle | dorsal phenotype
Cdc42V12.UAS, Rac1N17.hs, Scer\GAL4hs.PB has embryonic/first instar larval cuticle phenotype
The dorsal closure defects of embryos co-expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB and Rac1N17.hs (using heat shock) 4 to 8 hours after egg laying are more severe than the defects produced by expression of either Rac1N17.hs or Cdc42N17.Scer\UAS alone. In contrast, the defects produced by co-expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB and Rac1N17.hs (using heat shock) 8 to 12 hours after egg laying are weaker than Rac1N17.hs expressed alone, but stronger than Cdc42N17.Scer\UAS expressed alone. When Rac1N17.hs is co-expressed with Cdc42V12.Scer\UAS under the control of Scer\GAL4hs.PB most cuticles are extremely disrupted. There is evidence of some rescue of the Rac1N17.hs phenotype by Cdc42V12.Scer\UAS expressed under the control of Scer\GAL4hs.PB, as there are greater numbers of wild-type and mild dorsal closure defective embryos than seen with the expression of Rac1N17.hs alone.
Dominant inhibitory form of Rac1.