Insertion of a transposable element into an intronic region between exons B and C of N.
flea at -11.9 to -11.2
Nfa-g62 mutant eyes do not display interommatidial pigment cell death.
Loss of primary pigment cell development and programmed cell death. Ablation of cone cells in four adjacent developing ommatidia at 20 hrs APF causes death of interommatidial precursor cells in wild type. This IPC death is blocked by Nfa-g62 or Ras85DV12.hs.
Interommatidial cells appear similar in shape to secondary pigment cells and are not sorted.
Retina defects are not associated with optic lobe defects in 65.2% of homozygous Nfa-g62 retina clones generated by somatic recombination. The arrangement of ommatidia is severely disrupted, the number of ommatidia is reduced and they appear shorter than normal in homozygous clones in the retina. A disruption of the fenestrated zone, laminar cortex and neuropil can be seen in the underlying optic lobe if it is defective. Homozygous late pupae have normal optic lobe morphology, but the lamina neuropil is severely disrupted, containing large vacuoles, and the medulla neuropil contains small vacuoles in homozygous adults.
Nfa-g62 is a suppressor of increased cell death phenotype of Chc4
Nfa-g62 is a suppressor of secondary pigment cell phenotype of Chc4
Nfa-g62 is a suppressor of tertiary pigment cell phenotype of Chc4
The P{MGIIa} construct fails to rescue.
Ives.
Removes N activity specifically in pigment cells.
Nfa-g62 appears to act cell autonomously.