A deletion removes a 2347bp segment that includes the minimal promoter and 5' transcribed leader sequence.
In mutant embryos, most embryos within longitudinal connectives fail to project across segmental boundaries and frequently terminate in tangles at or near the boundaries. In addition, both the anterior and posterior commissures of each segment fail to develop properly. Also the overall fascicle organisation and apparent axon density of the ventral commissures is affected. The motor neuron nerve tracts and the axon patterning of the peripheral nervous system appears normal. In mutant embryos the pCC interneurons fail to send their axons anteriorly and instead project their axons either in a lateral or posterior direction, and any of the posterior projecting pCC axons cross the ventral midline in adjacent posterior segments. By stage 14, all pCC interneurons have misguided axons and many of these axons have extensive side branches. The overall development and patterning of the aCC and RP2 motorneuron axon tracts do not appear to be adversely affected.
nerfin-154 has larval longitudinal connective phenotype, enhanceable by prosIl3
nerfin-154 is an enhancer of larval longitudinal connective phenotype of prosIl3
nerfin-154 is rescued by nerfin-1+t11.154
nerfin-154 is partially rescued by Scer\GAL4elav-C155/nerfin-1UAS.cKa
Created as a consequence of the "ends in" homologous recombination gene knockout technique. The deletion was most likely caused by exonuclease digestion of the targeting vector after the SceI exonuclease induced double strand break but before its integration into the nerfin-1 chromosomal locus. The deletion was detected after the allelic substitution step and are most likely the result of illegitimate recombination between micro-homologies present in the minimal promoter of one copy of the nerfin-1 duplication and the transcribed region of the tandem copy.