Deletion of nucleotides 1581-1749, which results in a frameshift after amino acid residue 446 (the protein produced contains 14 novel amino acid residues, which are RTWPRRSPRSTTTS).
169 bp deletion that causes a frameshift followed immediately by a stop codon. This produces a truncated protein lacking the C-terminal 384 amino acids, including the pros binding domain.
A 169bp deletion causes a frameshift, followed by a stop codon
The transplantation of miraZZ176 larval neuroblast clones into the abdomen of adult hosts causes tumor growth, with clones growing to 100 times their original size thereby severely damaging and displacing the host's organs. Although genome stability is not grossly affected shortly after transplantation, 40-day-old tumors show karyotype defects such as segmental aneuploidy. Additionally, 15-20% of cells within the tumors have supernumerary centrosomes and these cells tend to be hyperploid.
Mutant embryos have a variable phenotype in the NGB 6-4T lineage, showing reduced, normal or extra NGB 6-4T-derived glia. Neuronal progeny of the NGB 6-4T lineage are completely absent in 46% of hemisegments but may be normal in other hemisegments.
Axon tracts of embryos are grossly defective, longitudinal connectives are generally broken or severely reduced in width and commissures are partially or completely fused.
miraZZ176 is not rescued by Scer\GAL4unspecified/mira5A.UAS.Tag:HA
mira5A.Scer\UAS.T:Ivir\HA1 expression is not able to rescue embryonic lethality of miraZZ176 animals.
One of a group of six alleles isolated in the same screen.