Females containing homozygous germline clones show defects in stage 14 egg chambers, including dumpless egg chambers (egg chambers in which the nurse cells have failed to transfer their cytoplasmic contents to the oocyte, have intact nuclei and do not appear to be undergoing programmed cell death) and egg chambers with persisting nurse cell nuclei (egg chambers in which nurse cells have transferred their cytoplasmic contents to the oocyte, but their nuclei have failed to undergo programmed cell death including nuclear condensation).
Mutants have a strong mutant neuronal phenotype.
lola[+]/lola00642 is a suppressor of lethal phenotype of JIL-1EP3657
SoxNGA1192, lola[+]/lola00642 has partially lethal phenotype
lola[+]/lola00642 is a suppressor of chaeta | increased number phenotype of gcmPyx
SoxNGA1192, lola[+]/lola00642 has larval longitudinal connective phenotype
SoxNGA1192, lola[+]/lola00642 has axon phenotype
SoxNGA1192, lola[+]/lola00642 has larval anterior commissure phenotype
SoxNGA1192, lola[+]/lola00642 has larval posterior commissure phenotype
lola00642/+, SoxNGA1192/+ double heterozygous embryos show defects in axon scaffolding, such as fusion of commissures, axonal tangles, disruption and/or reduction of longitudinal connectives. This phenotype is not seen in either single mutant heterozygote.
The hatch rate of lola00642/+ ; JIL-1EP3657/JIL-1EP3657 embryos is 20%.
A. Spradling.