Mesoderm invagination is delayed (mesoderm breadth is significantly reduced), posterior midgut is variably affected (the anterior movement of pole cells due to posterior midgut invagination and tissue extension is defective) and ectoderm extension is significantly reduced in cta5/cta5 embryos compared to controls.
The ab1a, ab2A, ab3A and ab1C olfactory receptor neurons respond normally to broad concentrations of odorants and CO[[2]].
cta5 mutants exhibit SNa motor axons phenotypes in 44% of hemisegments.
The mitotic pattern in early mutant embryos shows the same delay in the ventral domain as in wild-type embryos.
Egg chambers of mutant homozygotes show mild actin cytoskeleton defects.
Heat induced ectopic expression of foghs.PM has no morphological consequences. ctaGerm.Q303R, ctaGerm.R277H or ctaGerm.R277H can rescue the female sterility of mutants, few of the eggs survive to adulthood.
Defective in gonad assembly.
Embryos fail to undergo normal gastrulation: central region of ventral zone fails to undergo rapid transition to a groove. Ventral furrow remains open, embryos do not constrict enough to form shallow cup in which the pole cells sit so they remain on the outside.
Cellular blastoderm and gastrulation initiation are normal. Normal expression of twi, suggesting no abnormalities in dorsal-ventral patterning. Rapid phase of constriction is absent: many cells in midventral domain never constrict and many of the lateral twi expressing cells do not invaginate. No invagination of the posterior midgut.
Eggs derived from homozygous females cellularise normally but become abnormal at gastrulation; the posterior midgut is missing and no advancement of the germband around the posterior pole is seen. Extensive folding of the germ band is seen along the ventral side of the egg. This phenotype resembles that of fog mutants. The anterior midgut appears to form normally. The cuticle has holes at the anterior and posterior ends and there are frequent defects in the head skeleton, although the thoracic and abdominal segments appear fairly normal.
cta5/cta[+] is an enhancer of visible phenotype of RhoGEF2PX10/RhoGEF24.1
cta5/cta[+] is an enhancer of partially lethal phenotype of RhoGEF2PX10/RhoGEF24.1
cta5/cta[+] is an enhancer of visible phenotype of RhoGEF2PX6/RhoGEF24.1
cta5/cta[+] is an enhancer of partially lethal phenotype of RhoGEF2PX6/RhoGEF24.1
cta5/cta[+] is an enhancer of wing phenotype of RhoGEF2PX10/RhoGEF24.1
cta5/cta[+] is an enhancer of wing phenotype of RhoGEF2PX6/RhoGEF24.1
cta5 is an enhancer of phenotype of Rho1rev220
cta5/cta[+] is a suppressor of wing phenotype of Scer\GAL4Bx-MS1096, fogUAS.cRa
cta5/cta[+] is a suppressor of wing | male limited phenotype of Scer\GAL4Bx-MS1096, fogUAS.cRa
Abl4, cta5/Df(2L)C' has ventral midline of embryo | maternal effect phenotype
The presence of cta5 strongly suppresses the wing defects seen in male flies expressing fogScer\UAS.cRa under the control of Scer\GAL4Bx-MS1096.
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).
Egg chambers transheterozygous for Rho1rev220 and cta mutants show disruptions of the ovarian cytoskeleton and ring canals similar to that seen in females heterozygous for Rho1rev220 and RpII140wimp.