Alteration in the splice acceptor site of exon seven inducing a frame shift of -1 that results in D376T and a premature stop codon after seven additional amino acids (GISQRVS).
Inferred alteration at the splice acceptor of side exon 7 (1bp deletion) leads to a frameshift that results in a D376T mutation and early translation termination after the addition of seven novel amino acids (GISQRVS).
abnormal neuroanatomy | embryonic stage (with sideI1563), with Scer\GAL4btl.PS, sideUAS.cSa
abnormal neuroanatomy | embryonic stage (with sideI1563), with Scer\GAL4srp, sideUAS.cSa
growth cone & intersegmental nerve (with sideI1563)
larval intersegmental nerve (with sideI1563), with Scer\GAL4btl.PS, sideUAS.cSa
larval neuromuscular junction & abdominal dorsal acute muscle 1 (with sideI1563)
larval neuromuscular junction & abdominal dorsal acute muscle 2 (with sideI1563)
larval neuromuscular junction & abdominal dorsal oblique muscle 1 (with sideI1563)
larval neuromuscular junction & abdominal dorsal oblique muscle 2 (with sideI1563)
larval neuromuscular junction & abdominal lateral transverse muscle 1 (with sideI1563)
larval neuromuscular junction & abdominal lateral transverse muscle 2 (with sideI1563)
larval neuromuscular junction & abdominal lateral transverse muscle 3 (with sideI1563)
larval neuromuscular junction & abdominal lateral transverse muscle 4 (with sideI1563)
larval neuromuscular junction & abdominal ventral acute muscle 1 (with sideI1563)
larval neuromuscular junction & abdominal ventral acute muscle 2 (with sideI1563)
larval neuromuscular junction & abdominal ventral acute muscle 3 (with sideI1563)
larval neuromuscular junction & abdominal ventral longitudinal muscle 1 (with sideI1563)
larval neuromuscular junction & abdominal ventral longitudinal muscle 2 (with sideI1563)
larval neuromuscular junction & abdominal ventral longitudinal muscle 3 (with sideI1563)
larval neuromuscular junction & abdominal ventral longitudinal muscle 4 (with sideI1563)
larval neuromuscular junction & abdominal ventral oblique muscle 4 (with sideI1563)
larval neuromuscular junction & abdominal ventral oblique muscle 5 (with sideI1563)
larval neuromuscular junction & abdominal ventral oblique muscle 6 (with sideI1563)
49% of hemisegments show detachment of ISN motor axons from sensory nerves of the anterior fascicle in sideC137/sideI1563 embryos.
sideC137/sideI1563 embryos show severe delays in the dorsal migration of the ISN compared to wild type. Growth cones do eventually manage to cross the dorsal trunk, but a subset lag behind. The average growth rate of the mutant nerve is 15.2 +/- 4.6 mm/h compared to 31.9 +/- 13.4 mm/h for wild-type nerves. A small fraction of mutant ISN growth cones show highly disoriented directionality, extending in abnormal directions over the course of axonal growth.
Most, if not all, ISN growth cones are tightly attached to tracheal branches in sideC137/sideI1563 embryos expressing sideScer\UAS.cSa in the trachea under the control of Scer\GAL4btl.PS. The ISN follows the tracheal substrate in these embryos and crosses and re-crosses the transverse connective.
Most, if not all, ISN growth cones are attached to hemocytes in sideC137/sideI1563 embryos expressing sideScer\UAS.cSa in the hemocytes under the control of Scer\GAL4srp (this does not occur in wild-type embryos). Filopodial extensions of both cell membranes are tightly interdigitated.
sideC137/sideI1563 third instar larvae often lack neuromuscular junctions (NMJs) on dorsal muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 1 (19%), muscle 9 (24%), muscle 2 (11%), muscle 10 (9%).
sideC137/sideI1563 third instar larvae often lack neuromuscular junctions (NMJs) on ventral muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 12 (58%), muscle 13 (75%), muscle 6 (77%), muscle 7 (85%).
The ISN motor nerve of sideC137/sideI1563 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); 25.0% (muscle 1), 35.0% (muscle 9), 16.7% (muscle 2), 11.7% (muscle 10).
The SNa motor nerve of sideC137/sideI1563 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); 41.7% (muscle 21), 3.4% (muscle 22), 3.3% (muscle 23), 51.7% (muscle 24).
The ISNb motor nerve of sideC137/sideI1563 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); 75.0% (muscle 12), 75.0% (muscle 13), 83.3% (muscle 6), 85.0% (muscle 7).
The SNc motor nerve of sideC137/sideI1563 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); 61.7% (muscle 26), 86.7% (muscle 27), 66.7% (muscle 29).
The ISNd motor nerve of sideC137/sideI1563 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); 78.3% (muscle 15), 63.3% (muscle 16), 98.4% (muscle 17).
Homozygous embryos show defective pathfinding of the ISNb in 83.8% of hemisegments. ISN, SNa, SNc and ISNd nerves also show innervation defects in these embryos.
sideC137/Df(3R)Tl-P embryos show defects in all of the motor axon projection branches; 85% of hemisegments lack the ISNd branch, 85% lack the SNc branch, 86% lack the ISNb branch at the M6/7 muscle cleft, 70% lack the ISNb branch at the M13 muscle cleft, 84% lack the ISNb branch at the M12 muscle cleft, 3% lack the dorsal SNa branch, 8% lack the lateral SNa branch, 2% lack the first branch of the ISN, 6% lack the second branch of the ISN, 28% lack the third branch of the ISN and 8% of hemisegments show crossing of the segment boundary by the ISN.
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.
Selected as: A mutation affecting the structure of the neuromuscular junction.
