Amino acid replacement: ?75term.
A6471442T
K75term | mmy-PD; K75term | mmy-PB; K112term | mmy-PA
?75term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
mmyslm homozygous embryos exhibit fully penetrant defects in the longitudinal connective only after 13/14h post-fertilization, when they show narrower axon bundles of longitudinal connectives, thicker commissures, which are also closer to one another, severe axon guidance defects of posterior corner cell neurons' longitudinal tracks, namely the M track inappropriately crossing the midline, the I and L tracks collapsing onto one another,and significant decreases in the thickness of these tracks and in their distance to the midline, as compared to controls.
mmyslm has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Scer\GAL4elav.PU/robo1UAS.cKa
mmyslm has larval longitudinal connective | embryonic stage phenotype, non-suppressible by Scer\GAL4elav.PU/robo1UAS.cKa
mmyslm has symmetrical commissure | embryonic stage phenotype, non-suppressible by Scer\GAL4elav.PU/robo1UAS.cKa
mmyslm has pCC neuron | embryonic stage phenotype, non-suppressible by Scer\GAL4elav.PU/robo1UAS.cKa
mmyslm has growth cone | embryonic stage phenotype, non-suppressible by Scer\GAL4elav.PU/robo1UAS.cKa
The defects in axon medial tracts observed in late mmyslm homozygous embryos are not suppressed by the expression of robo1Scer\UAS.cKa under the control of Scer\GAL4elav.PU.
mmyslm is rescued by Scer\GAL4elav.PU/mmyUAS.cMa/Scer\GAL4sim.PU
mmyslm is partially rescued by mmyUAS.cMa/Scer\GAL4sim.PU
The severe axon guidance defects at the longitudinal connective of late mmyslm homozygous embryos are partially and fully rescued by the expression of mmyScer\UAS.cMa under the control of Scer\GAL4sim.PU alone and in combination with Scer\GAL4elav.PU, respectively.