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).
In mutant embryos, the motor axons that project through the SNb peripheral nerve fail to form connections to their cognate muscles. Most commonly, SNb axons appear to "stall" somewhere between the point at which they would normally separate from the ISN and the muscle 6/13 junction. In other hemisegments, SNb axons project through the muscles field but fail to branch into the intermuscle clefts where synapses should be formed. The phenotype is slightly stronger than seen in lola1A4.
In the embryonic CNS, longitudinal connectives are interrupted and commissures fuse. In some segments the VUM neurons are born and differentiate, but fail to form a well-defined posterior root to the anterior peripheral fascicle. Intersegmental nerve shows various aberrations, failing to grow or wandering into adjacent segments, or defasciculation of ISN sensory axons. The lateral chordotonal organs are sometimes displaced dorsally from their wild type position. There is no segment specificity of these phenotypes.