Amino acid replacement: Q722term.
C6375806T
Q722term | slam-PB; Q722term | slam-PC
Q722term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change. Annotated protein is 23 amino acids longer than the reported protein accounting for the difference in reported and annotated mutation location.
Mutant embryos have defects in germ cell migration; about 50% of the germ cells are lost by the end of embryogenesis. slamwaldo1/slamwaldo2 embryos derived from homozygous slamwaldo1 female germline clones (embryos lack both maternal and zygotic slam function) fail to cellularise during nuclear cycle 14. Germ cells form normally during cycle 10 in these embryos, and are later found distributed throughout an otherwise unstructured embryo. Nuclei reach the periphery normally in mutant precellularisation embryos, the primordial germ cells bud normally and the somatic nuclei continue to divide until cycle 14. The first difference from wild-type is seen during the slow phase of cellularisation; membrane invagination is delayed in the mutant embryos, so that at the time when membranes normally enclose each nucleus basally, the incompletely invaginated membranes of the mutant embryos entrap the nuclei as they pinch off basally. The mutant embryos do attempt to gastrulate, but this disrupts the incompletely formed somatic cells and the embryos appear to fall apart and fail to develop further.
slamwaldo1 is a non-suppressor of germline cell phenotype of HmgcrUAS.cvDa, Scer\GAL4elav-C155
Expression of HmgcrScer\UAS.cvDa under the control of Scer\GAL4elav-C155 can attract germ cells in embryos. This phenotype is still seen in a slamwaldo1 mutant background. The germ cell migration defects of slamwaldo1 Hmgcrclb1 double mutants are stronger than either single mutant; no germ cells move off the midgut in double mutant embryos.