Scer\GAL4en-e16E-mediated expression of RalaG20V.Scer\UAS causes loss of crossveins.
Expression of RalaG20V.Scer\UAS under the control of Scer\GAL4amn-c651 has no effect on body size.
Expression of RalaG20V.Scer\UAS under the control of Scer\GAL4Act5C.PP in wing disc cells results in a decrease in cell size without affecting cell cycle phasing.
Embryonic expression of RalaG20V.Scer\UAS under the control of Scer\GAL4unspecified results in lethality. In some cases, the embryonic cuticle has defects on the dorsal surface, indicating that dorsal closure is defective. Expression of RalaG20V.Scer\UAS in the leading edge under the control of Scer\GAL4pnr-MD237 or Scer\GAL4LE results in large holes in the anterior or dorsal epidermis of the embryo. Some embryos show a severe dorsal-open phenotype.
RalaG20V.UAS, Scer\GAL4ap-md544 is an enhancer of wing hair | increased number phenotype of Scer\GAL4ap-md544, trcT453A.UAS.L
Coexpression of the dominant negative RalaS25N.Scer\UAS with trcT453A.Scer\UAS, under the control of Scer\GAL4ap-md544, leads to a complete suppression of the trcT453A.Scer\UAS phenotype. In contrast, coexpression of the constitutively active RalaG20V.Scer\UAS transgene with trcT453A.Scer\UAS, under the control of Scer\GAL4ap-md544, results in a dramatic enhancement of the multiple wing hair phenotype.
Expression of RalaG20V.Scer\UAS under the control of Scer\GAL4Rala-PG69 in a RalaPG69 mutant background rescues lethality, and border cell migration.
Carried in plasmid "pUAST-DRalG20V", transfected into S2 cells and used in phosphorylation assays.