In-frame deletion (codons 111-136 are deleted).
An in-frame deletion of codons G111-I136 of beat-Ia.
Cells of the Bolwig's organs (BOs) form in homozygous embryos, but the morphology of the larval visual system (LVS) is severely disrupted and increased numbers of photoreceptor cells are apparent from the earliest stages of LVS development. Extra photoreceptor cells are seen both in the normal location of the BO clusters and dispersed between the two clusters. Embryos sometimes contain three BO's and, rarely, four BO clusters are seen. Migration of the BOs appears relatively normal in some embryos, but in others it is disrupted and the BO does not achieve its proper location even though head involution appears normal, or the BO is elongated.
Motor axons exit the CNS normally but then fail to branch and enter their muscle domains once in the periphery. The SNb fails to diverge from the ISN either completely (full bypass), 41% segments, or partially (partial bypass), 41% segments, the SNc fails to diverge in 82% segments.
Defective in navigation through a specific choice point during intersegmental nerve and segmental nerve b pathfinding. CNS axon pathfinding is normal.
beat-Ia2/beat-Ia3 Rac1N17.Scer\UAS Scer\GAL4elav-C155 double mutant embryos exhibit additive, not synergistic effects on the ISNb full bypass phenotype.
In beat-Ia2/beat-Ia3 transheterozygotes the SNb fails to diverge from the ISN completely (full bypass) in 38% segments or partially (partial bypass) in 28% segments. The divergence defect can be suppressed by Fas2e76 (but not significantly suppressed by Fas2e86 or Fas2e93) and the SNc defect by ConFvex238.
beat-Ia2 is rescued by Scer\GAL4elav-C155/beat-IaUAS.cFa
Scer\GAL4elav-C155 mediated expression of beat-IaScer\UAS.cFa rescues the SNb divergence defect.