Breakpoint between amino acids 763 and 885.
DNA rearrangement that disrupts the coding region.
Embryos derived from RhoGEF24.1 germline clones contain a variable proportion of multinucleate cells.
RhoGEF25.1/RhoGEF24.1 animals show 50% embryonic viability, 13% first larval instar viability and 0% adult viability. RhoGEF26.5/RhoGEF24.1 animals show 60% embryonic viability, 6% first larval instar viability and 0% adult viability. RhoGEF24.4/RhoGEF24.1 animals show 98% embryonic viability, 97% first larval instar viability and 0% adult viability. RhoGEF21.1/RhoGEF24.1 animals show 97% embryonic viability, 96% first larval instar viability and 0% adult viability. RhoGEF2PX6/RhoGEF24.1 animals show 27% adult viability. 70% of the adults have wing defects; wings are crumpled and/or blistered. Wing discs of mid-third-instar larvae appear buckled, rather than having the normal pattern of folding. RhoGEF2PX10/RhoGEF24.1 animals show 71% adult viability. 4% of the adults have wing defects. Salivary gland cells are not internalised in RhoGEF26.5/RhoGEF24.1 embryos, but remain on the surface (in contrast to wild-type embryos). Muscle and neuronal tissues show no significant defects in gross morphology in late-stage RhoGEF26.5/RhoGEF24.1 and RhoGEF25.1/RhoGEF24.1 embryos.
The planar polarity of hairs in RhoGEF24.1/RhoGEF2PX6 clones in the wing is normal. Ommatidial polarity is normal in homozygous clones in the eye.
Embryos derived from homozygous female germline clones have normal dorso-ventral and anterior-posterior patterning, and normal mesoderm specification. Germband extension and posterior midgut invagination appear defective. The cells of the mesectoderm fail to intercalate at the ventral midline. Gastrulation is highly disorganised and ventral furrow formation never occurs. Inappropriate lateral folds are formed. Invagination of the anterior midgut is also defective. Although cellularisation appears normal, nuclear migrations in the mesoderm precursors are not accompanied by obvious apical flattening, in contrast to wild-type, and the majority of mesodermal cells expand their apical surfaces rather than undergoing apical membrane constrictions at gastrulation.
RhoGEF2PX10/RhoGEF24.1 has visible phenotype, enhanceable by cta5/cta[+]
RhoGEF2PX10/RhoGEF24.1 has partially lethal phenotype, enhanceable by cta5/cta[+]
RhoGEF2PX6/RhoGEF24.1 has visible phenotype, enhanceable by cta5/cta[+]
RhoGEF2PX6/RhoGEF24.1 has partially lethal phenotype, enhanceable by cta5/cta[+]
RhoGEF24.1/RhoGEF2[+] is a suppressor of abnormal neuroanatomy | somatic clone phenotype of ssh1-11
RhoGEF24.1/RhoGEF2[+] is a suppressor of abnormal neuroanatomy phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107
RhoGEF24.1 is a suppressor of visible phenotype of Rho1GMR.PH
RhoGEF24.1, fog4/fog[+] has visible phenotype
RhoGEF24.1/RhoGEF2[+], fog4 has visible | dominant phenotype
Rho1E3.10, RhoGEF24.1/RhoGEF2[+] has visible phenotype
Rho112-6/Rho1[+], RhoGEF24.1 has visible phenotype
RhoGEF24.1, Sbsbd-1/Sbsbd-201 has visible phenotype
Rho1J3.8, RhoGEF24.1/RhoGEF2[+] has visible phenotype
RhoGEF24.1/RhoGEF2[+], zipEbr has visible phenotype
RhoGEF24.1/RhoGEF2[+], Sbsbd-1/Sbsbd-201 has visible phenotype
Rho112-6, RhoGEF24.1/RhoGEF2[+] has visible | dominant phenotype
Rho1E3.10/Rho1[+], RhoGEF24.1 has visible | dominant phenotype
Rho1J3.8/Rho1[+], RhoGEF24.1 has visible | dominant phenotype
RhoGEF24.1, zip[+]/zipEbr has visible | dominant phenotype
RhoGEF24.1, zipEbr has visible | dominant phenotype
RhoGEF2PX10/RhoGEF24.1 has wing phenotype, enhanceable by cta5/cta[+]
RhoGEF2PX6/RhoGEF24.1 has wing phenotype, enhanceable by cta5/cta[+]
RhoGEF24.1/RhoGEF2[+] is a suppressor of adult mushroom body | somatic clone phenotype of ssh1-11
RhoGEF24.1/RhoGEF2[+] is a suppressor of adult mushroom body phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107
RhoGEF24.1 is a suppressor of eye phenotype of Rho1GMR.PH
RhoGEF24.1 is a suppressor of embryonic head | dorsal phenotype of foghkb.PB
RhoGEF24.1, fog4 has wing phenotype
RhoGEF24.1/RhoGEF2[+], fog4 has wing phenotype
Rho1E3.10, RhoGEF24.1 has wing phenotype
RhoGEF24.1, Sbsbd-1/Sbsbd-201 has leg phenotype
Rho1E3.10, RhoGEF24.1 has leg phenotype
Rho112-6, RhoGEF24.1 has leg phenotype
RhoGEF24.1/RhoGEF2[+], Sbsbd-1/Sbsbd-201 has leg phenotype
Rho112-6, RhoGEF24.1/RhoGEF2[+] has leg phenotype
Rho1J3.8, RhoGEF24.1 has leg phenotype
Rho1E3.10/Rho1[+], RhoGEF24.1 has wing phenotype
Rho1E3.10/Rho1[+], RhoGEF24.1 has leg phenotype
Rho1J3.8/Rho1[+], RhoGEF24.1 has leg phenotype
RhoGEF24.1, zip[+]/zipEbr has leg phenotype
RhoGEF24.1, zipEbr has leg phenotype
RhoGEF24.1, zip[+]/zipEbr has wing phenotype
RhoGEF24.1, zip[+]/zipEbr has femur phenotype
RhoGEF24.1, zip[+]/zipEbr has tibia phenotype
RhoGEF24.1, zipEbr has wing phenotype
RhoGEF24.1, zipEbr has femur phenotype
RhoGEF24.1, zipEbr has tibia phenotype
RhoGEF2PX6/cta5 RhoGEF24.1 animals show 8% adult viability. The frequency of wing defects in these animals is 92% (compared to 70% in RhoGEF2PX6/RhoGEF24.1 adults). RhoGEF2PX10/cta5 RhoGEF24.1 animals show 28% adult viability. The frequency of wing defects in these animals is 35% (compared to 4% in RhoGEF2PX10/RhoGEF24.1 adults). 6% of fog4/+ ; RhoGEF24.1/+ animals have wing defects.
fog4/+ ; RhoGEF24.1/+ animals have wing defects.
RhoGEF24.1 shows a moderate interaction (25-49% of double heterozygotes have at least one malformed leg) with the following mutations: Rho112-6. br1 fails to show a significant genetic interaction (assayed in terms of a malformed leg phenotype) with RhoGEF24.1. RhoGEF24.1 shows a moderate interaction (25-49% of double heterozygotes have at least one malformed wing) with the following mutations: Rho1E3.10. Sbsbd-201/Sbsbd-1 shows a weak interaction (5-24% of double mutants have at least one malformed leg) with the following mutations: RhoGEF24.1/+.
27% of RhoGEF24.1/zipEbr double heterozygotes have a malformed leg phenotype, which shows variable expressivity. In less severe cases, there is a dent in the femur or tibia. Flies with malformed legs often also show wing defects. Weak phenotypes include a broadening of the wing blade and folding back of the distal portion of the wing blade. In the most severe cases, wings are greatly reduced in size.
Dominantly suppresses the Rho1GMR.PH rough eye phenotype. The transient depression in the dorsal head region seen in embryos carrying foghkb.PB in a wild-type background is not seen in embryos carrying foghkb.PB which are derived from homozygous RhoGEF24.1 female germline clones.
Isolated as a dominant suppressor of the Rho1GMR.PH rough eye phenotype.