Table 2.
Genotype |
Percentage of abnormal ISNb pathways (n)a |
Percentage of abnormal SNa pathways (n)b |
---|---|---|
Wild type | 12.2 (254) | 4.7 (254) |
Loss of function | ||
I(3)L0090-a/I(3)L0090-a | 22.0 (303) | 36.5 (307) |
gyc76CKG03723/gyc76CKG03723 | 43.0 (144) | 64.0 (147) |
gyc76CKG03723ex33/gyc76CKG03723ex33 | 45.9 (183) | 32.2 (180) |
gyc76CKG03723ex173/gyc76CKG03723ex173 | 52.4 (208) | 37.7 (204) |
gyc76CKG03723ex33/gyc76CKG03723ex173 | 50.0 (100) | 41.8 (98) |
gyc76CKG03723ex173/Df(3)5126 | 52.1 (169) | 31.3 (166) |
gyc76CKG03723ex144/gyc76CKG03723ex144 | 8.1 (135) | 14.6 (130) |
UAS:Gyc76C, elav-Gal4/+;gyc76CKG03723ex173/gyc76CKG03723ex173 | 23.4 (184)c | 21.5 (186)c |
UAS:Gyc76CD945A, elav-Gal4/+;gyc76CKG03723ex173/gyc76CKG03723ex173 | 60.0 (130) | 50.4 (121) |
sema1aP1/sema1aP1 | 84.1 (138) | 90.0 (138) |
Df(4)C3plexA/Df(4)C3plexA | 86.0 (50) | 88.0 (50) |
Genetic interactions | ||
sema1aP1/+;I(3)L0090-a/+ | 14.0 (140) | 45.0 (174) |
sema1aP1/+;gyc76CKG03723ex173/+ | 54.1 (111) | 39.8 (103) |
gyc76CKG03723ex173/+;Df(4)C3plexA/+ | 48.6 (105) | 32.3 (102) |
gyc76CKG03723ex173/Df(3R)swp2MICAL | 56.3 (87) | 30.2 (86) |
gyc76CKG03723ex173/+ | 27.6 (362) | 10.7 (355) |
enaGC10/+;gyc76CKG03723ex173/+ | 24.6 (207) | 13.6 (206) |
Gain of function | ||
UAS:Gyc76C, elav-Gal4/UAS:Gyc76C, elav-Gal4d | 57.4 (148) | 68.0 (150) [26.0]e |
UAS:Gyc76CD945A, elav-Gal4/UAS:Gyc76CD945A, elav-Gal4f
|
59.1 (110) [11.8]g
|
56.1 (107) |
Abnormal ISNb phenotype defined as failure of ISNb axons from the RP5, V, or RP3 neurons to properly innervate ventral lateral muscles 12/13 or 6/7. Phenotypes include weak or absent innervations, target bypasses, and axon bundle stalling.
Abnormal SNa phenotype defined as failure of SNa axons to make two characteristic turns at choice points along the lateral transverse muscles 22, 23, and 24 and the failure of axons to reach muscle 24.
Statistically different from values for gyc76CKG03723ex173 homozygous mutants. Fisher's exact test using a two-by-two contingency table; p <0.0001.
Longitudinal bundles of CNS axons disrupted in 18 of 20 embryos.
Percentage of total SNa pathways that incorrectly navigate between muscles 21 and 22 instead of muscles 22 and 23.
Longitudinal bundles of CNS axons disrupted in 6 of 11 embryos.
Percentage of total hemisegments in which the RP3 axon extends an exuberant process in the cleft between muscles 6 and 7.