In-frame translation termination codon at amino acid 131.
Imprecise excision of P element results in an in-frame stop codon at amino acid 131.
adult thorax | dorsal & chaeta | somatic clone
mechanosensory chaeta & adult abdomen | somatic clone
mechanosensory chaeta | supernumerary & adult abdomen | somatic clone
socket & adult abdomen | somatic clone
Snr1R3 mutant MARCM somatic clone in the third instar larval wing disc display increased levels of apoptosis and are much smaller compared to control clones.
The frequency and size of homozygous clones is reduced relative to control clones, indicating that Snr1 is important for cell viability. Homozygous clones in the abdomen result in duplicated, fused or malformed (stunted, twisted or bent) mechanosensory bristles. Within the clones, patches of tissue that lack bristles and/or bristle sockets are seen. Cuticle defects are also seen, including fusion of adjacent segments within clones, loss of pigmentation and cuticle disruptions. Homozygous clones on the dorsal thorax show only minor shortening of bristles within the clone. Homozygous clones in the eye disc result in only slightly reduced eye sizes, with no significant morphological defects. Few homozygous clones are recovered in the head region. Homozygous clones in the leg occur at a similar frequency to control clones and no not result in any obvious mutant phenotype. Females containing homozygous germline clones are infertile and do not produce any eggs. Expression of Snr1cdel.3.Scer\UAS under the control of Scer\GAL4e22c in a Snr1R3/+ background results in lethality at 29oC, and significant cuticle disruption, including incomplete fusion of the abdominal tergites along the dorsal midline. More than 70% of females expressing Snr1cdel.3.Scer\UAS under the control of Scer\GAL4Act5C.PI in a Snr1R3 background are sterile. Scer\GAL4Act5C.PI/Snr1cdel.3.Scer\UAS;Snr1R3 adults show a rapid decrease in viability following eclosion, with the effect being more pronounced among males.
Heterozygotes are phenotypically normal.
Snr1R3/Snr1[+] is an enhancer of visible phenotype of Scer\GAL4ey.PH, brmK804R.UAS.Tag:HA
HDAC104556, Snr1R3/Snr1[+] has visible | dominant phenotype
HDAC104556/Rpd3[+], Snr1R3 has visible phenotype
Snr1R3 has adult abdomen | somatic clone phenotype, enhanceable by brm[+]/brm2
Snr1R3/Snr1[+] is an enhancer of eye phenotype of Scer\GAL4ey.PH, brmK804R.UAS.Tag:HA
Snr1R3/Snr1[+] is an enhancer of ommatidium phenotype of Scer\GAL4ey.PH, brmK804R.UAS.Tag:HA
Snr1R3/Snr1[+] is a suppressor of wing vein phenotype of Scer\GAL469B, brmK804R.UAS.Tag:HA
Snr1R3/Snr1E1 is a suppressor of wing vein L5 phenotype of rhove-1
Snr1R3, Snr1cdel.3.UAS, Scer\GAL469B is a suppressor of wing vein L5 phenotype of CycEJP
Snr1R3, Scer\GAL4Act5C.PI, Snr1cdel.3.UAS is a suppressor of wing vein L5 phenotype of CycEJP
Snr1R3, Snr1cdel.3.UAS, Scer\GAL469B is a suppressor of wing phenotype of CycEJP
Snr1R3, Scer\GAL4Act5C.PI, Snr1cdel.3.UAS is a suppressor of wing phenotype of CycEJP
HDAC104556, Snr1R3/Snr1[+] has wing phenotype
HDAC104556, Snr1R3/Snr1[+] has wing vein | ectopic phenotype
HDAC104556, Snr1R3 has wing phenotype
HDAC104556, Snr1R3 has wing vein | ectopic phenotype
Snr1R3/Snr1[+], brm2 has postpronotum phenotype
Snr1R3/Snr1[+], brm2 has adult prothoracic segment phenotype
Snr1R3, brm2 has postpronotum phenotype
The loss of wing veins seen in animals expressing brmK804R.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL469B is suppressed by Snr1R3. The Dl9P thick vein phenotype is enhanced by Snr1E1/Snr1R3. dpps1/dpps1 Snr1E1/Snr1R3 animals show suppression of the Snr1 extra wing vein phenotype and enhancement of the dpp loss of vein phenotype in L5. Snr1E1/Snr1R3 suppresses the loss of wing vein L5 seen in rhove-1 homozygotes and rhove-1 suppresses the Snr1E1/Snr1R3 extra wing vein phenotype.
Rpd304556/Snr1R3 double heterozygotes have wing vein defects; 32% have normal wings, 38% have an ectopic vein emanating from the posterior crossvein and 30% have ectopic veins emanating from the posterior crossvein and posterior to the L5 longitudinal vein. The ectopic wing vein phenotype seen in Rpd304556/Snr1R3 double heterozygotes at 29oC is partially suppressed by brm2/+.
Homozygous Snr1R3 clones induced in a brm2/+ background are less frequently observed and are smaller in size compared to both brm+ and control clones induced at similar stages, suggesting an additive effect between brm and Snr1. The presence of brm2/+ enhances the Snr1R3 clone phenotype in the abdomen. The AntpNs/+ antenna to leg transformation is suppressed about 50% by Snr1R3.