Nucleotide substitution: C?A. Nucleotide substitution: A?T. Amino acid replacement: T297N. Above mutation followed by insertion of two C nucleotides, resulting in a frameshift at the N-terminal end of the SH2 domain and a subsequent stop codon at position 337.
A two base substitution in Shc codon 297 and a two base insertion in codon 298 results in a net two base insertion, a frameshift, and early translation termination.
ATGCC
ShcBG homozygous clones in the dorsal air sac primordium are found at the tip of the primordium at a significantly lower frequency than wild-type clones.
Embryos derived from homozygous female germ-line clones display terminal defects. Most embryos fail to hatch and show a reduction of posterior Filzkorper and the 8th abdominal segment as well as mild defects in the anterior head skeleton. Malpighian tubules are always absent. Embryos lacking both maternal and zygotic Shc function show defects in germband retraction and a variable reduction of ventral denticle belts not seen in paternally rescued embryos. 70% of homozygotes die during the late pupal stage. Females that survive to adulthood do not lay eggs. Homozygous adult survivors are delayed in development and show defects in the eye, wing and ovary. The eyes are reduced in size and slightly roughened. The severity of the phenotype is graded in an anterior to posterior fashion, with the anterior side being more disorganised than the posterior. The ommatidia in the posterior region of the eye appear essentially normal and contain the full complement of photoreceptors, whereas in the anterior part of the eye, several ommatidia lack one or more outer photoreceptors. These mutant ommatidia do contain small central R7-like photoreceptors. In some ommatidia, the photoreceptors show rotated planar polarity. There is a partially penetrant loss of wing vein material in the distal part of the L4 vein. Homozygous females contain mature oocytes surrounded by a weakly ventralised chorion (as indicated by the fusion of the dorsal appendages).
ShcBG/Shc[+] is a suppressor of visible | semidominant phenotype of EgfrE3
ShcBG/ShcBG is a suppressor of visible phenotype of Scer\GAL4CY2, btl::Egfrλ.UAS
ShcBG is a non-suppressor of visible phenotype of sevS11.Tag:MYC
ShcBG is a non-enhancer of phenotype of Ras85DV12.sev
ShcBG is a non-enhancer of phenotype of Raf::tor12D.hs.sev
ShcBG is a suppressor of abdominal 11 anal tuft phenotype of tor13D
ShcBG is a suppressor of embryonic/first instar larval cuticle phenotype of tor13D
ShcBG is a suppressor of filzkorper phenotype of tor13D
ShcBG/ShcBG is a suppressor | partially of dorsal appendage phenotype of Scer\GAL4CY2, btl::Egfrλ.UAS
ShcBG/ShcBG is a suppressor of wing vein | ectopic phenotype of Scer\GAL4CY2, btl::Egfrλ.UAS
ShcBG/ShcBG is a suppressor of wing phenotype of Scer\GAL4CY2, btl::Egfrλ.UAS
ShcBG is a non-suppressor of phenotype of Ras85DV12.sev
ShcBG is a non-suppressor of phenotype of Raf::tor12D.hs.sev
ShcBG is a non-suppressor of eye phenotype of sevS11.Tag:MYC
ShcBG is a non-suppressor of ommatidium phenotype of sevS11.Tag:MYC
ShcBG, dosP115 has cephalopharyngeal skeleton | germline clone phenotype
ShcBG, dosP115 has embryonic abdominal segment 8 | germline clone phenotype
Heterozygous females carrying tor13D produce embryos that produce very little cuticle. This phenotype is weakly suppressed if the females are carrying one copy of ShcBG; the embryos develop more cuticle and show posterior structures such as Filzkorper and Tuft structures. The phenotype is completely suppressed if the tor13D/+ females also carry homozygous ShcBG germline clones; embryos look normal and can hatch. The eye and wing phenotypes caused by EgfrE3 are dominantly suppressed by ShcBG. The EgfrE3 phenotype is completely suppressed if the flies are also homozygous for ShcBG and the viability of these flies is restored. Expression of btl::EgfrScer\UAS.T:λ\cI-DD under the control of Scer\GAL4CY2 results in the formation of ectopic wing vein material at multiple sites on the wing. This phenotype is completely suppressed if the flies are also homozygous for ShcBG. Females expressing btl::EgfrScer\UAS.T:λ\cI-DD under the control of Scer\GAL4CY2 produce strongly dorsalised eggs with no dorsal appendages. This phenotype is partially suppressed if the females are also homozygous for ShcBG; dorsal appendage material is produced around the anterior circumference of the egg. 85% of embryos derived from dosP115 ShcBG double mutant female germline clones lack all structures posterior to segment A7 and have reduced head skeletons. The remaining 15% retain segment A8 but no structures posterior to it. Embryos derived from ShcBG drkΔP24 double mutant female germline clones have a stronger phenotype than embryos derived from either single mutant female germline clone.
Selected as: a dominant enhancer of the haploinsufficient dl mutant phenotype.