fog4, foghkb.PB exhibit motor axon defects in late stage 16 embryos, with particular problems in SNa bifurcation.
fog4 mutant embryos exhibit defects in the embryonic central nervous system. These are reduced by the presence of foghkb.PB. These embryos have near normal morphology at later stages of development. In particular, the ventrally located CNS develops normally in these embryos.
The salivary gland cells fail to internalised in mutant embryos.
Mutant embryos show defects in the apical constriction of cells seen during mesoderm invagination. They lack the normal two constriction phases seen in wild-type embryos and instead show weak, asynchronous cell shape changes.
Embryos injected with cholera toxin exhibit apical flattening. Heat induced ectopic expression of foghs.PM causes a widened ventral furrow.
Mutant embryos lack posterior midgut, Malpighian tubules and hindgut. None of the posterior gut primordia invaginate.
Ventral furrow and posterior midgut invaginations fail to form normally. The posterior midgut primordium fails to invaginate. While the first phase of constrictions near the ventral midline proceeds fairly normally, cells in more lateral regions show variable defects. Constrictions fail or are delayed, and although ventral furrow formation is on average delayed by about 4 minutes, almost all of the mesodermal precursors are eventually internalized.
Defective in gonad assembly.
Muscle pattern wild type within constraints imposed by alterations in body plan. Muscles contractile and vigorous.
Embryos fail to form a posterior midgut.
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 twi expressing cells are brought into the invagination whether or not they constrict. No invagination of the posterior midgut.
fog4 mutant embryos are normal at the cellular blastoderm stage, and gastrulation starts normally. The posterior midgut does not form, and the germband does not elongate but forms a series of transverse ventral folds. Homozygous germline clones give viable embryos.
fog4 is a suppressor of abnormal cell migration | embryonic stage phenotype of Gprk206936
fog4/fog[+] is a suppressor of abnormal cell migration | embryonic stage phenotype of Gprk206936
RhoGEF26.5/RhoGEF2[+], fog4 has visible | dominant phenotype
RhoGEF26.5, fog4/fog[+] has visible phenotype
RhoGEF24.1, fog4/fog[+] has visible phenotype
RhoGEF24.1/RhoGEF2[+], fog4 has visible | dominant phenotype
fog4 has ventral furrow phenotype, non-suppressible by Gprk206936
fog4 is a suppressor of embryo | embryonic stage 6 phenotype of Gprk206936
fog4 is a suppressor of ventral furrow phenotype of Gprk206936
fog4/fog[+] is a suppressor of embryo | embryonic stage 6 phenotype of Gprk206936
fog4/fog[+] is a suppressor of ventral furrow phenotype of Gprk206936
Gprk206936, fog4 has ventral furrow phenotype
RhoGEF26.5/RhoGEF2[+], fog4 has wing phenotype
RhoGEF26.5, fog4 has wing phenotype
RhoGEF24.1, fog4 has wing phenotype
RhoGEF24.1/RhoGEF2[+], fog4 has wing phenotype
Homozygous fog4 suppresses the gastrulation phenotype seen in Gprk206936 mutant embryos. As in fog4 mutant embryos alone, only a few apically constricting cells are seen at random positions. When only one copy of Gprk206936 is present apical constriction is substantially disorganised and asynchronous among mesodermal cells.
6% of fog4/+ ; RhoGEF24.1/+ animals have wing defects. 16% of fog4/+ ; RhoGEF26.5/+ animals have wing defects.
fog4/+ ; RhoGEF24.1/+ animals have wing defects.
Ubiquitous foghs.PM expression during the late blastoderm and early gastrula stages rescues the final cuticle phenotype of embryos. Heat shocking during stages 6 and 7 provided the greatest degree of rescue.