100kb insertion into the large intron of Fas1.
Nerve terminal arborisation onto muscles is enhanced compared to wild-type. Type 2 but not type 1 terminals are affected. The excitatory junctional currents (ejcs) of muscle fibre 12 are decreased in amplitude compared to wild-type. The distribution of spontaneous miniature ejcs is altered compared to wild-type. Fas1TE89Da larvae carrying Fas1+t23 have a similar number of nerve terminal branches and varicosities to wild-type. ejcs have a normal amplitude.
Homozygotes are viable and fertile, no gross defects in the embryonic CNS. Abl1, Fas1TE89Da and Abl2, Fas1TE89Da double mutant embryos exhibit gross defects in the developing CNS axon guidance and the morphogenesis of CNS axon tracts: an allele specific interaction.
Fas1TE89Da is an enhancer of visible | recessive phenotype of bifunspecified
Fas1TE89Da is an enhancer of eye phenotype of bifunspecified
Abl1, Fas1TE89Da has central nervous system phenotype
Abl1, Fas1TE89Da has axon phenotype
Abl2, Fas1TE89Da has axon phenotype
Enhances the bifunspecified rough eye phenotype.
Fas1TE89Da is rescued by Fas1+t23
X ray generated w revertants have wild type levels of Fas1 protein in the embryo.