Amino acid replacement: W211term.
Nucleotide substitution: G?A.
G21218167A
G?A
W211term | Ilk-PA
W211term
G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation. (exact site of mutation unspecified)
Ilk1/+ does not significantly affect resistance to ethanol-induced sedation.
Adult-generated Ilk1 homozygous mutant intestinal stem cell clones have reduced maintenance 7 days and 14 days after clone induction compared to control clones; cells in the remaining clones are either diploid cells or immature enterocytes.
Ilk1 dorsal branch terminal cell clones do not cause any detectable defects in terminal cell morphology.
Homozygotes die at the end of embryogenesis. The cuticle is completely normal in Ilk1/Df(3L)Pc-14d embryos. Midgut development is normal in mutant embryos. Stage 17 homozygous and Ilk1/Df(3L)Pc-14d embryos show defects in most of the muscles, with actin clumped together rather than extending along the length of the muscles as in wild type. Muscles where the actin has detached from the plasma membrane and the membrane remains attached at its normal position adjacent to the extracellular matrix are seen in Ilk1/Df(3L)Pc-14d embryos. Muscles where both the plasma membrane and actin have retracted are also seen, although they are still separate. Homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic Ilk function) have a modestly more severe phenotype than homozygous embryos (lacking zygotic Ilk function); they show clumping of actin in the muscles slightly earlier, at stage 16. These embryos have normal cuticles. Homozygous clones in the wing result in a wing blister. Wing blisters are associated with clones on either side of the wing blade.
Ilk[+]/Ilk1 is a suppressor of chemical resistant | adult stage phenotype of Scer\GAL4elav.PU, icsRNAi.UAS.WIZ
Ilk1/+ significantly suppresses (to wild type levels) the increased resistance to ethanol-induced sedation seen in flies with expression of icsdsRNA.Scer\UAS.WIZ driven by Scer\GAL4elav.PU.
Df(3L)Pc-14d/Ilk1 is rescued by IlkmGFP6
Df(3L)Pc-14d/Ilk1 is rescued by IlkT384A.mGFP6
Df(3L)Pc-14d/Ilk1 is rescued by IlkT384D.mGFP6
Df(3L)Pc-14d/Ilk1 is rescued by Scer\GAL4how-24B/IlkUAS.mGFP6
Df(3L)Pc-14d/Ilk1 is rescued by Scer\GAL4how-24B/IlkT384A.UAS.mGFP6
Df(3L)Pc-14d/Ilk1 is rescued by Scer\GAL4how-24B/IlkT384D.UAS.mGFP6
Df(3L)Pc-14d/Ilk1 is rescued by Scer\GAL4how-24B/IlkS176G.T180G.UAS.mGFP6
Df(3L)Pc-14d/Ilk1 is rescued by IlkS176D.T180D.UAS.mGFP6/Scer\GAL4how-24B
Df(3L)Pc-14d/Ilk1 is rescued by Scer\GAL4how-24B/IlkF436A.UAS.mGFP6
Ilk1 is rescued by IlkK219M.mGFP6
Ilk1 is rescued by IlkE359K.mGFP6
Ilk1 is rescued by IlkE359K.UAS/Scer\GAL4how-24B
Ilk1 is rescued by IlkP358S.mGFP6
Df(3L)Pc-14d/Ilk1 is rescued by Ilk+t9
Df(3L)Pc-14d/Ilk1 is rescued by IlkmGFP6
Df(3L)Pc-14d/Ilk1 is partially rescued by IlkΔ34-177.mGFP6
Df(3L)Pc-14d/Ilk1 is partially rescued by IlkR208D.R210D.mGFP6
Df(3L)Pc-14d/Ilk1 is partially rescued by IlkR208D.R210D.Δ34-177.mGFP6
Df(3L)Pc-14d/Ilk1 is partially rescued by Scer\GAL4how-24B/IlkΔ34-177.UAS.mGFP6
Df(3L)Pc-14d/Ilk1 is partially rescued by IlkR208D.R210D.UAS.mGFP6/Scer\GAL4how-24B
Df(3L)Pc-14d/Ilk1 is partially rescued by Scer\GAL4how-24B/IlkR208D.R210D.Δ34-177.UAS.mGFP6
Df(3L)Pc-14d/Ilk1 is partially rescued by Scer\GAL4how-24B/IlkUAS.cZa
Df(3L)Pc-14d/Ilk1 is not rescued by IlkΔ178-448.mGFP6
Df(3L)Pc-14d/Ilk1 is not rescued by IlkΔ34-177.mGFP6/IlkΔ178-448.mGFP6
Df(3L)Pc-14d/Ilk1 is not rescued by Scer\GAL4how-24B/IlkΔ178-448.UAS.mGFP6
Df(3L)Pc-14d/Ilk1 is not rescued by Scer\GAL4how-24B/IlkΔ34-177.UAS.mGFP6/IlkΔ178-448.UAS.mGFP6
A.T.C. Carpenter.