Amino acid replacement: Q140term.
C5202577T
Q140term | cno-PC; Q140term | cno-PD; Q140term | cno-PE; Q140term | cno-PG; Q140term | cno-PH; Q140term | cno-PI; Q140term | cno-PJ
Q140term
Site and nature of nucleotide substitution in mutant inferred by FlyBase curator based on reported amino acid change.
cno3 is an enhancer of abnormal cell polarity phenotype of S48-5
cno3 has embryonic/first instar larval cuticle | dorsal phenotype, suppressible by bskhs.PS
cno3 is an enhancer of ommatidium phenotype of S48-5
cno3 is an enhancer of phenotype of Ras85DV12.sev
cno3 is an enhancer of phenotype of Ras64BV12.sev
cno3/cno[+] is a non-enhancer of ommatidium phenotype of fafFO8/fafBX3
bsk2, cnomis1/cno3 has embryonic/first instar larval cuticle | dorsal phenotype
cnomis1/cno3, hep1 has embryonic/first instar larval cuticle | dorsal phenotype
cnomis1/cno3, hep[+]/hep1 has embryonic/first instar larval cuticle | dorsal phenotype
bsk2/bsk[+], cnomis1/cno3 has embryonic/first instar larval cuticle | dorsal phenotype
The dorsal open phenotype of cno3 homozygous embryos is partly suppressed by bskhs.PS. hep1 and bsk2 dominantly enhance the cnomis1/cno3 phenotype; hep1/+; cnomis1/cno3 and bsk2/+; cnomis1/cno3 embryos have a dorsal open phenotype. Dorsal closure proceeds normally in pucE69 cno3 double heterozygotes.
Loss of cno+ activity (cno3 or Df(3R)6-7) in Ras85DV12.sev flies does not affect overproduction of R7 cells but loss of pigment cells is more severe and supernumerary cone cells appear (these cone cells are recruited from a pool of retinal precursors that normally develop into pigment cells and from cells to be eliminated by apoptosis). The phl1 mutation completely suppresses the overproduction of cone cells triggered by the Ras85DV12.sev and cno3 interaction.