Nucleotide substitution: C?T.
Amino acid replacement: ?133term.
Amino acid replacement: Q133term.
C8826890T
C?T
Q133term | SoxN-PA; Q133term | SoxN-PB
Q133term
Mutant embryos show a moderate loss of denticles.
Virtually all thoracic and abdominal eg- and ems-expressing neurons and glia are missing from the central nervous system of homozygous embryos. The embryos show a substantial reduction in the longitudinal axon tracts; 60% of hemisegments show complete loss of longitudinal tracts. The commissures fail to separate in 52% of segments and are absent in 2%. The regular axonal fasciculation pattern is disrupted and many axons inappropriately cross the midline. There appears to be no difference in phenotype along the anteroposterior axis. The embryos have no segmentation defects. Within the central nervous system, the spacing between two segments in the middle of the embryo (most often A3 and A4) is greatly increased, while spacing in the neighbouring segments is reduced. In extreme cases there are gaps in the neuroectoderm, however, no segments are lost. A small number of embryos (less than 5%) fail to complete germband retraction. Loss of neuroblasts is seen, with S1 neuroblasts (NBs) in the intermediate and lateral columns being more affected that those in the medial column. Later born intermediate and lateral NBs are more affected than S1 NBs. Loss of S1 neuroblasts is seen; NB1-1 is missing in 12% of hemisegments, MP2 is missing in 5%, NB5-2 is missing in 38%, NB7-1 is missing in 4%, NB5-3 is missing in 52% of hemisegments, NB2-5 is missing in 36%, NB5-6 is missing in 69%, NB7-4 is missing in 23% and NB3-5 is missing in 56%. 100% of NB6-4 S3 neuroblasts are missing, and NB2-4 (S4 neuroblast), NB3-3 (S4 neuroblast), NB4-4 (S4 neuroblast) and NB7-3 (S5 neuroblast) are nearly always missing. A number of eve-expressing neurons are missing; the CQ neurons are missing in 3% of hemisegments, RP2 neurons are missing in 96% and the eve lateral cluster (ELC) is missing in 100%, however, 0% of aCC/pCC neurons are missing.
SoxNU6-35 has abnormal neuroanatomy phenotype, enhanceable by Dr72
SoxNU6-35 is an enhancer of abnormal neuroanatomy phenotype of Dr72
SoxNU6-35 has neuroblast NB5-3 phenotype, enhanceable by Dr72
SoxNU6-35 is an enhancer of neuroblast NB5-3 phenotype of Dr72
Dr72, SoxNU6-35 has larval longitudinal connective phenotype
Dr72, SoxNU6-35 has pCC neuron phenotype
Dr72, SoxNU6-35 has symmetrical commissure phenotype
Dr72, SoxNU6-35 has presumptive embryonic/larval central nervous system phenotype
Dr72, SoxNU6-35 has larval DA1 motor neuron phenotype
wgl-17; SoxNU6-35 double mutant embryos have cuticles with few or no ectopic denticles.
SoxNU6-35/+ partially suppresses the formation of ectopic denticles seen in pan2 mutant larvae, while pan2 ; SoxNU6-35 double mutants have the same cuticle phenotype as SoxNU6-35 single mutants.
Dr72/+ strongly enhances the loss of denticle phenotype seen in SoxNU6-35 embryos, such that denticle formation is almost completely abolished.
Dr72 SoxNU6-35 double mutant embryos show severe disruption in the organisation and structure of the central nervous system. There is a complete loss of longitudinal axons in many segments and frequent gaps in the neuropil. Commissures are often absent, and those that do form are virtually never separated. The aCC/pCC and CQ neurons are missing in at least 15% of hemisegments. RP2 neurons are missing in 94% of hemisegments and eve lateral cluster neurons are missing in 99% of hemisegments. Neuroblast NB5-3 is missing in 79% of hemisegments.
SoxNU6-35 is partially rescued by Scer\GAL4Kr.PM/SoxNUAS.cOa
