Amino acid replacement: R409term.
G24743584A
R409Q | tok-PA; R409Q | tok-PB; R409Q | tok-PC
R409term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
larval neuromuscular junction & abdominal dorsal acute muscle 1 (with tokD427)
larval neuromuscular junction & abdominal dorsal acute muscle 2 (with tokD427)
larval neuromuscular junction & abdominal dorsal oblique muscle 1 (with tokD427)
larval neuromuscular junction & abdominal dorsal oblique muscle 2 (with tokD427)
larval neuromuscular junction & abdominal lateral transverse muscle 1 (with tokD427)
larval neuromuscular junction & abdominal lateral transverse muscle 2 (with tokD427)
larval neuromuscular junction & abdominal lateral transverse muscle 3 (with tokD427)
larval neuromuscular junction & abdominal lateral transverse muscle 4 (with tokD427)
larval neuromuscular junction & abdominal ventral acute muscle 1 (with tokD427)
larval neuromuscular junction & abdominal ventral acute muscle 2 (with tokD427)
larval neuromuscular junction & abdominal ventral acute muscle 3 (with tokD427)
larval neuromuscular junction & abdominal ventral longitudinal muscle 1 (with tokD427)
larval neuromuscular junction & abdominal ventral longitudinal muscle 2 (with tokD427)
larval neuromuscular junction & abdominal ventral longitudinal muscle 3 (with tokD427)
larval neuromuscular junction & abdominal ventral longitudinal muscle 4 (with tokD427)
larval neuromuscular junction & abdominal ventral oblique muscle 4 (with tokD427)
larval neuromuscular junction & abdominal ventral oblique muscle 5 (with tokD427)
larval neuromuscular junction & abdominal ventral oblique muscle 6 (with tokD427)
The ISN motor nerve of tokK788/tokD427 third instar larvae shows innervation defects at the neuromuscular junction on a number of muscles (percentage of hemisegments with defects on the indicated muscle is listed); 38.1% (muscle 1), 25.0% (muscle 9), 7.1% (muscle 2), 3.6% (muscle 10).
The SNa motor nerve of tokK788/tokD427 third instar larvae shows innervation defects at the neuromuscular junction on a number of muscles (percentage of hemisegments with defects on the indicated muscle is listed); 8.4% (muscle 21), 1.2% (muscle 22), 1.2% (muscle 23), 34.5% (muscle 24).
The ISNb motor nerve of tokK788/tokD427 third instar larvae shows innervation defects at the neuromuscular junction on a number of muscles (percentage of hemisegments with defects on the indicated muscle is listed); 64.3% (muscle 12), 56.0% (muscle 13), 23.9% (muscle 6), 34.6% (muscle 7).
The SNc motor nerve of tokK788/tokD427 third instar larvae shows innervation defects at the neuromuscular junction on a number of muscles (percentage of hemisegments with defects on the indicated muscle is listed); 21.7% (muscle 26), 74.7% (muscle 27), 71.1% (muscle 29).
The ISNd motor nerve of tokK788/tokD427 third instar larvae shows innervation defects at the neuromuscular junction on a number of muscles (percentage of hemisegments with defects on the indicated muscle is listed); 83.4% (muscle 15), 27.4% (muscle 16), 34.6% (muscle 17).
In tokK788/tokD427 third instar larvae, muscles 12 and 13 are often innervated via a dorsoventral projection of the ISN or SNa nerves, which induces the formation of neuromuscular junctions at ectopic sites (in wild-type larvae these muscles are innervated by a ventrodorsal projection of the ISNb pathway).
The ISNb nerve frequently remains attached to the ISN in tokK788/tokD427 larvae, sometimes as a separately identifiable axon bundle, and reaches its target muscles via irregular routes. Defasciculation defects are also seen in the SN pathway, with the SNa nerve often growing more posteriorly than normal as it defasciculates too late.
The branch points of the ISN appear underdeveloped in tokK788/tokD427 embryos, and/or the ISN is stalled at the second branch point and barely reaches the position of the third branch point. 51.2% of hemisegments have SNa defects in these embryos, including two dorsal branches of the SNa. The ISNb fails to defasciculate from the ISN in 96.2% of hemisegments. It is either tightly attached to the ISN or forms a separate parallel nerve bundle. Defasciculation defects are also see in Fas2-expressing nerve tracts in the embryonic central nervous system.
tokK788/tokD427 has abnormal neuroanatomy phenotype, non-suppressible by tldUAS.cHa/Scer\GAL4elav.PLu
tokK788/tokD427 has abnormal neuroanatomy phenotype, non-suppressible by kuzUAS.cFa/Scer\GAL4elav.PLu
tokK788/tokD427 has embryonic/larval neuromuscular junction phenotype, non-suppressible by tldUAS.cHa/Scer\GAL4elav.PLu
tokK788/tokD427 has embryonic/larval neuromuscular junction phenotype, non-suppressible by kuzUAS.cFa/Scer\GAL4elav.PLu
tokK788 sideC137/tokD427 sideC137 double mutant larvae show a strong enhancement of each single mutant phenotype; double mutant larvae lack virtually all neuromuscular junctions on all ventral muscles in all abdominal hemisegments. Dorsal and lateral muscles also show an increase in innervation errors compared to single mutants.
tokK788/tokD427 is rescued by tokUAS.cSa.Tag:HA/Scer\GAL4hs.PB
tokK788/tokD427 is rescued by Scer\GAL4G14/tokUAS.cSa.Tag:HA
tokK788/tokD427 is rescued by tokUAS.cSa.Tag:HA/Scer\GAL4elav.PLu
tokK788/tokD427 is rescued by Scer\GAL4srp/tokUAS.cSa.Tag:HA
tokK788/tokD427 is rescued by tokUAS.cSa.Tag:HA/Scer\GAL4ppl.PP
tokK788/tokD427 is not rescued by tokUAS.cSa.Tag:HA/Scer\GAL4ChAT.7.4
Selected as: A mutation affecting the structure of the neuromuscular junction.