caps05121 embryos show discontinuous dorsal trunk formation.
73% of homozygous embryos fail to hatch, though all those that do hatch develop into normal looking larvae. Very few (3%) survive to adulthood. In homozygous mutant embryos, the SNb enters the ventral muscle field and the RP neurons defasciculate normally. Furthermore, RP1, RP3 and RP4 properly synapse with their respective target muscles, whereas the RP5 axons stall, show enlarged growth cone like structures and fail to contact the target muscle. Instead the RP5 axons are split and found also in direct contact with the transversal nerve.
KrmCD, Kr1/+, caps05121/+ embryos show a SNb nerve phenotype, without affecting the ISN and SNa. In about 1/3 of cases the SNb stops along the ventral longitudinal muscles, ending with a large growth cone structure. In addition properly defasciculated RP axons fail to continue along their normal paths, a portion of them elongate and stall along their normal paths; a portion of them elongate and stall either in a position close to the transversal nerve or are directly connected to it. Kr1, caps05121 double homozygotes (that also carry KrmCD) develop an even stronger phenotype; the SNb is absent in most of the double mutants analysed or do not extend beyond its second choice point close to muscle 28. In only a few cases the SNb stalls in the ventral muscle field.
A. Spradling.
Excision of the P{PZ} element reverts the phenotype to wild-type.
Complements: stv00543. Complements: l(3)0422004220.