Simultaneous mobilisation of the two progenitor insertions, resulting in a 47908bp deletion that spans the entire trol transcription unit.
A 47,908 bp deficiency resulting from the simultaneous mobilization of P{EP}EP1619 and P{lacW}trolG0271. Site of deletion on reference sequence inferred by FlyBase curator.
trolnull cap cell clones, induced during the larval and pupal stages, result in cap cell displacement from the niche; only germaria containing 3 or more mutant cap cells showed the cap cell displacement.
Hemizygous embryos show ISNb motor axon guidance defects (59.9% of hemisegments) and SNa motor axon guidance defects (38.7% of hemisegments). ISNb axons fail to defasciculate at muscles 6 and 7 and some axons stall between muscles 6 and 13. SNa axons fail to reach their proper targets.
trolnull hemizygous embryonic hemocytes show decreased competence to undertake phagocytosis of apoptotic cells, as compared to controls.
Homozygous follicle cell clones have normal apical-basal polarity under normal food conditions.
Homozygous somatic follicle-cell clones often lose epithelial tissue organisation; about 50% of clones in stage 6-9 egg chambers show a multilayer phenotype.
trol[+]/trolnull is a suppressor of abnormal neuroanatomy | embryonic stage phenotype of Scer\GAL4P52, Sema1aUAS.cYa, Sema1ak13702
Sema1ak13702, trol[+]/trolnull has abnormal neuroanatomy | dominant | embryonic stage phenotype
Df(4)C3/+, trolnull has abnormal neuroanatomy | dominant | embryonic stage phenotype
trol[+]/trolnull is a suppressor of larval posterior commissure | embryonic stage phenotype of Scer\GAL4P52, Sema1aUAS.cYa, Sema1ak13702
Sema1ak13702, trol[+]/trolnull has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype
Sema1ak13702, trol[+]/trolnull has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype
Df(4)C3/+, trolnull has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype
Df(4)C3/+, trolnull has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype
The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is significantly suppressed if the embryos are also heterozygous for trolnull.
trolnull/+ ; Sema-1ak13702/+ double heterozygous embryos show ISNb motor axon guidance defects (51.0% of hemisegments) and SNa motor axon guidance defects (41.8% of hemisegments).
trolnull/+ ; Df(4)C3/+ double heterozygous embryos show ISNb motor axon guidance defects (51.5% of hemisegments) and SNa motor axon guidance defects (40% of hemisegments).
trolnull is partially rescued by trolUAS.RG/Scer\GAL4elav.PU
trolnull is not rescued by trolUAS.RG/Scer\GAL4twi.PU
Expression of trolScer\UAS.RG under the control of Scer\GAL4elav.PU significantly rescues the ISNb and SNa motor axon guidance defects seen in trolnull embryos. Expression under the control of Scer\GAL4repo.PU only very modestly rescues the motor axon defects, and expression under the control of Scer\GAL4twi.PU fails to rescue the motor axon defects.