P-element insert at codon 33 of the open reading frame.
P element inserted in the middle of the codon for amino acid 32 in the open reading frame.
abdominal lateral oblique muscle 1 & neuromuscular junction
abdominal segment border muscle & neuromuscular junction
abdominal ventral longitudinal muscle 2 & neuromuscular junction
abdominal ventral longitudinal muscle 3 & neuromuscular junction
abdominal ventral longitudinal muscle 4 & neuromuscular junction
Sema-2a03021/Df(2R)B65 mutant larvae do not display any increase in dendritic non-contacting crossing in the class IV dendritic arborizing neurons.
Approximately 9.7% of homozygous Sema-2a03021 hemisegments exhibit abnormal v'ch1 projection, with the axon mis-projecting anteriorly and joining the inter-segmental nerve instead of the segmental nerve. In most cases of v'ch1 mis-projection, the axon contacts the cell bodies and axons of nearby lateral cluster neurons, lesA and 1daA, which are located anterior and slightly internal to the v'ch1 cell body. In a small number of defective hemisegments, the v'ch1 axon bifuricates sending its axon both anteriorly to the intersegmental nerve and ventrally to join the segmental nerve. A second, less frequent defect is observed whereby one or more axons of the lateral cluster sensory neurons misproject ventrally, joining the v'ch1 axon and the segmental nerve, instead of the intersegmental nerve. Mis-projections of dorsal cluster sensory neurons are also observed in homozygous Sema-2a03021 mutants. One or more axons of dorsal cluster neurons either mis-projects posteriorly or loops anteriorly in the dorsal region before joining the intersegmental nerve in its normal position in the lateral region.
Sema-2a03021 homozygous mutant embryos exhibit normal projection of the ISN and SN axons in all hemisegments in which v'ch1 and dorsal sensory axon defects occur.
The ISNb makes normal contact with muscle 12 and then extends ectopic connections dorsally and laterally into muscle 8. Ectopic connections are also observed for the transverse nerve into ventral muscles 7, 6 or 13. The SNa stops abruptly at muscle 5, does not innervate muscle 8 but makes increased contact with muscle 5.
Eclosion of adults is greatly reduced, and eclosed adults show flightlessness and behavioral defects in drinking tests and visual orientation tests though they are not blind. They survive for only 2 days. At the gross structural level there are no abnormalities in patterning of CNS and PNS axon tracts, nor in the brain neuropil of the adult.
Sema2a03021 has abnormal neuroanatomy phenotype, enhanceable by Df(4)C3
Sema2a03021 has abnormal neuroanatomy phenotype, non-enhanceable by Sema1ak13702
Sema2a03021 has abnormal neuroanatomy phenotype, non-suppressible by Sema1ak13702
Sema2a03021 is an enhancer of abnormal neuroanatomy phenotype of PlexBKG00878
Sema2a03021 is an enhancer of visible | dominant phenotype of KrIf-1
Sema2a03021 has lch1 neuron phenotype, enhanceable by Df(4)C3
Sema2a03021 has lch1 neuron phenotype, enhanceable by PlexBKG00878
Sema2a03021 has lch1 neuron phenotype, non-enhanceable by Sema1ak13702
Sema2a03021 has lobula columnar neuron LC14 phenotype, non-enhanceable by Sema1ak13702
Sema2a03021 has lch1 neuron phenotype, non-suppressible by Sema1ak13702
Sema2a03021 has lobula columnar neuron LC14 phenotype, non-suppressible by Sema1ak13702
Sema2a03021 is an enhancer of lch1 neuron phenotype of PlexBKG00878
Sema2a03021 is an enhancer of eye phenotype of KrIf-1
Sema2a03021 is an enhancer of ommatidium phenotype of KrIf-1
Sema-1ak13702 Sema-2a03021 double mutants exhibit sensory axon mis-projections in the same frequency as Sema-2a03021 homozygotes.
Sema-2a03021;;Df(4)C3 double mutant embryos show v'ch1 mis-projections (24.5% of hemisegments) and lateral axon mis-projections (7.5% of hemisegments) at higher penetrance levels than are seen in either single homozygous mutant.
Sema-2a03021;;PlexBKG00878 double homozygotes show v'ch1 mis-projections (27.8% of hemisegments) and lateral axon mis-projections (4.2% of hemisegments) at higher levels than in either single homozygous mutant.
Sema-2a03021/+; SoxNGA1192/+ mutants are viable.
A. Spradling.
Dysgenesis-induced loss of the P element can revert the phenotype to wild type.
Complements: Cdk405428. Complements: Hmgs06214. Complements: l(2)k07127k07127. Complements: l(2)k07824k07824. Complements: l(2)k07824k07828. Complements: Ca-P60Ak08308ab. Complements: vegk17010. Complements: scbk17029a. Complements: Cdk4s4639.