Nucleotide substitution: G?T.
Amino acid replacement: E38term.
G15861885T
G?T
E38term | Gbeta13F-PA; E38term | Gbeta13F-PC; E38term | Gbeta13F-PE; E38term | Gbeta13F-PF; E38term | Gbeta13F-PG; E38term | Gbeta13F-PH
E38term
Stage 8 homozygous embryos derived from homozygous female germline clones show defects in gastrulation.
64% of telophase neuroblasts divide into two similar-sized daughter cells in homozygous embryos derived from homozygous female germline clones.
The number of EL neurons per hemisegment is reduced compared to wild type in homozygous embryos derived from homozygous female germline clones.
In mutants that are both maternally and zygotically mutant neuroblasts produce nearly equal sized daughters (in contrast to wild-type where daughters are unequal in size), though the GMC is still slightly smaller than the sibling neuroblast after the initial divisions. This abnormal division causes neuroblasts to be smaller and smaller after each successive division. By stage 14 fewer neuroblasts divide in mutants than in wild-type embryos. The number of EL neurons produced by neuroblast 3-3 is reduced from the normal 10 to 5. In mutant neuroblasts, spindle and astral microtubules develop well from both centrosomes as though both spindle halves are apical. Spindle asymmetry is also abolished in mutants. However the spindle position shifts towards the side where mira localises. These defects in neural development are rescued by a paternal supply of Gβ13F.
Gβ13Ff261 is partially rescued by Scer\GAL4pros.PMG/Gβ13FUAS.cFa