Nucleotide substitution: C?T. Amino acid replacement: R152Y.
C9427655T
C?T
R151W | Shc-PA
R151Y
The mutation was reported as CGG to TGG, which is R to W, rather than R to Y as reported.
Mutant border cell clusters (induced as clones) migrate posteriorly, but do not migrate dorsally.
Embryos that lack maternal Shc function (derived from females carrying homozygous germ line clones) have weak terminal defects. Embryos that lack both maternal and zygotic Shc function (derived from females carrying homozygous germ line clones mated to mutant males) have a weak flb-like phenotype. Homozygous adults have rough eyes.
When mutant somatic clones are made in the border cells no effect is seen.
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.
Shc111-40/Shc[+] is a suppressor of visible | semidominant phenotype of EgfrE3
Shc111-40/Shc111-40 is a suppressor of visible phenotype of Scer\GAL4CY2, btl::Egfrλ.UAS
Shc111-40 is a non-suppressor of visible phenotype of sevS11.Tag:MYC
Shc111-40 is a non-enhancer of phenotype of Ras85DV12.sev
Shc111-40 is a non-enhancer of phenotype of Raf::tor12D.hs.sev
Shc111-40 is a suppressor of abdominal 11 anal tuft phenotype of tor13D
Shc111-40 is a suppressor of embryonic/first instar larval cuticle phenotype of tor13D
Shc111-40 is a suppressor of filzkorper phenotype of tor13D
Shc111-40/Shc111-40 is a suppressor | partially of dorsal appendage phenotype of Scer\GAL4CY2, btl::Egfrλ.UAS
Shc111-40/Shc111-40 is a suppressor of wing vein | ectopic phenotype of Scer\GAL4CY2, btl::Egfrλ.UAS
Shc111-40/Shc111-40 is a suppressor of wing phenotype of Scer\GAL4CY2, btl::Egfrλ.UAS
Shc111-40 is a non-suppressor of phenotype of Ras85DV12.sev
Shc111-40 is a non-suppressor of phenotype of Raf::tor12D.hs.sev
Shc111-40 is a non-suppressor of eye phenotype of sevS11.Tag:MYC
Shc111-40 is a non-suppressor of ommatidium phenotype of sevS11.Tag:MYC
PvrDN.UASp, Scer\GAL4slbo.2.6, Shc111-40 has border follicle cell | somatic clone phenotype
Border cells clusters that are mutant for Shc111-40 and also expressing PvrDN.Scer\UAS under the control of Scer\GAL4slbo.2.6 show severely impaired posterior migration.
Heterozygous females carrying tor13D produce embryos that produce very little cuticle. This phenotype is weakly suppressed if the females are carrying one copy of Shc111-40; 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 Shc111-40 germline clones; embryos look normal and can hatch. The eye and wing phenotypes caused by EgfrE3 are dominantly suppressed by Shc111-40. The EgfrE3 phenotype is completely suppressed if the flies are also homozygous for Shc111-40 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 Shc111-40. 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 Shc111-40; dorsal appendage material is produced around the anterior circumference of the egg.
Selected as: a mutation in which embryos derived from homozygous germ-line clones show patterning defects in the cuticle.