Amino acid replacement: G92R.
Nucleotide substitution: G?A.
G8544920A
G?A
G92R | Nrg-PA; G92R | Nrg-PB; G92R | Nrg-PC; G92R | Nrg-PD; G92R | Nrg-PE; G92R | Nrg-PF; G92R | Nrg-PG; G92R | Nrg-PH; G92R | Nrg-PI
G92R
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
The mating frequency of homozygous females mated to wild-type males is markedly reduced (23%) relative to wild-type (97%) and heterozygous (86%) controls.
Homozygous females have defects in the mushroom bodies, central complex (especially the ellipsoid body) and antennal lobe. The mushroom body lobes are either reduced in size or completely missing and an abnormal whorl of neuronal processes is seen just ventral to the calyces. The ellipsoid body fails to fuse into a single structure (as occurs in wild type). These defects are seen in both males and females.
Homozygous males show defects in courtship behaviour relative to wild-type controls when mated to wild-type females. The mean latency is not significantly different from wild type, but they show significantly extended mating speeds. Once they are courting a female, the mutant males tend to have more breaks in their courtship than normal.
Homozygous and hemizygous mutant flies are fertile except for a few never-mating females. The mating frequency of homozygous females is reduced about 4-fold compared to wild-type levels, for virgins aged between 1 to 12 days. The largest difference from wild type occurs at 3 days of age, when the mating frequency of homozygous females averages 21% versus 88% of wild-type controls. The changes in receptivity with age are similar in homozygous and wild-type females. The mutation does not appear to be temperature sensitive (in terms of temperature of development). The sex appeal of homozygous females (measured as minutes of wing vibration directed towards the female by a male in a 5 minute test) is indistinguishable from that of wild-type females. Homozygous females show rejection behaviour (such as decamping, wing flicking, kicking, fending and ovipositor extrusion) in response to male courtship more frequently than control females. General locomotor activity of homozygous females, during courtship with wild-type males, is not different from wild type. Mutant males do not differ significantly in any component of courtship, except that mutant males give significantly more bouts of abdomen bending than wild-type males. The mating success of mutant males is not significantly different from that of wild-type males. The egg-to-adult viability of homozygotes and the progeny of a cross between homozygotes and wild type is normal. Ovarian development of homozygous females is normal. Attraction to ethanol and avoidance of 3-octanol is normal in mutant males and females, and photobehaviour is normal. The heart rate and rhythmicity of heartbeat of homozygous pupae is not significantly different wild type. Treatment with methoprene results in more mating in homozygous females.
No sperm is stored in hemizygous females.
Lays eggs. No sperm stored in hemizygous female.
Nrgibx is partially rescued by Nrg167.UAS/Scer\GAL4c316
Nrgibx is partially rescued by Nrg167.UAS/Scer\GAL4Mef2.247
Nrgibx is partially rescued by Nrg180.I.UAS/Scer\GAL4c316
Nrgibx is partially rescued by Nrg180.I.UAS/Scer\GAL4Mef2.247
Nrgibx is partially rescued by Nrg180.I.UAS/Scer\GAL430Y
Nrgibx is not rescued by Nrg167.UAS/Scer\GAL430Y
Nrgibx is not rescued by Nrg167.UAS/Scer\GAL4Tab2-201Y
Nrgibx is not rescued by Nrg180.I.UAS/Scer\GAL4Tab2-201Y
The reduced female receptivity phenotype of Nrgibx is complemented by Nrg849, Nrgl7, NrgBG01674, NrgG00305 and Nrg849.
Nrgibx and Nrg892 complement each other with respect to the reduced female receptivity phenotype seen in each homozygote.
Nrgl4, Df(1)KA14, Df(1)RA2, NrgG0099, NrgG0413 and NrgG0488b each fail to complement the reduced female receptivity phenotype of Nrgibx.
Nrgl10 complements the reduced female receptivity phenotype of Nrgibx at 18 and 25[o]C, but fails to complement this phenotype at 29[o]C. Nrgibx complements the lethality of Nrgl10 seen at 25[o]C.
The reduced female receptivity phenotype of Nrgibx is complemented by gg2, lawcEF520, otu7, ptg7, Df(1)Desi-S3, Df(1)Sxl-bt, fs(1)M1121, In(1)S, In(1)sc7, l(1)7Ed1, l(1)ESHS381, IntS4G0095, l(1)G0178G0178, sdtXN, P{GT1}BG02451 and P{NM}8A.
Expression of Nrg167.Scer\UAS under the control of Scer\GAL4c316 results in substantial rescue of the Nrgibx central brain phenotype.
Expression of Nrg167.Scer\UAS under the control of either Scer\GAL4Mef2.247, Scer\GAL430Y or Scer\GAL4Tab2-201Y does not appear to rescue the Nrgibx central brain phenotype.
Expression of Nrg167.Scer\UAS under the control of either Scer\GAL4Mef2.247 or Scer\GAL4c316 results in a significant increase in the sexual receptivity of Nrgibx females, while expression under the control of Scer\GAL4Tab2-201Y has no significant effect.
Expression of Nrg167.Scer\UAS under the control of Scer\GAL430Y results in a small but significant decrease in the sexual receptivity of Nrgibx females.
Expression of Nrg180.I.Scer\UAS under the control of either Scer\GAL4Mef2.247, Scer\GAL430Y, Scer\GAL4Tab2-201Y or Scer\GAL4c316 does not result in any clear evidence of rescue the Nrgibx central brain phenotype.
Expression of Nrg180.I.Scer\UAS under the control of either Scer\GAL4Mef2.247, Scer\GAL430Y or Scer\GAL4c316 results in a small but significant increase in the sexual receptivity of Nrgibx females, while expression under the control of Scer\GAL4Tab2-201Y has no significant effect.
Complements: otu5. Complements: otu7. Complements: Nrgl7. Complements: Nrgl10. Complements: Nrgunspecified. Complements: pt3. Complements: l(1)7Fc1. Complements: l(1)7Fd2. Complements: gg2. Complements: oc9. Complements: l(1)8Aa8. Complements: l(1)8Ad1.