4,926bp deletion, removing exons 4-8 including the translational start site.
Embryos derived from lilliXS575 germline clone eggs show posterior-specific loss of cells in embryos prior to gastrulation
Cuticle from late homozygous embryos is normal. Embryos derived from homozygous female germline clones show pair-rule segmentation defects. Two classes of phenotype are seen; 52% of embryos are missing odd numbered segments, with the remaining denticle belts often fused (44%), while the other class of embryos fail to secrete cuticle properly. These two phenotypes are similarly observed whether wild-type or heterozygous males are used to produce the embryos. The germband never extends beyond 25% of dorsal egg length in embryos derived from homozygous female germline clones (in contrast to wild-type, where germband extension reaches 60% of dorsal egg length). The formation of the cephalic furrow is also delayed. Embryos derived from homozygous female germline clones show specific defects in the maintenance of the actin network during cellularisation. The initial phase of cellularisation occurs normally. However, during the second phase of cellularisation, specific defects in the maintenance of the contractile actin network are seen, as the actin network begins to contract and the furrow tips move basally. The actin filaments become unevenly distributed between nuclei, ranging from abnormally large bundles to regions where the actin network is thin or absent, resulting in multinucleate cells. The microtubular baskets surrounding each nucleus appear largely normal, even in regions where actin filaments are unevenly distributed. At the end of cellularisation, the yolk stalks are irregular in shape and size, and large connections between cortical cells and the central yolk cell are often seen. The timing of cellularisation and membrane formation is unimpaired however, and does result in an epithelial monolayer of cells with proper apical-basal polarity in these embryos. Defects in the transport of organelles are also seen during cellularisation; the cortical clearing (as the cortical cytoplasm becomes depleted of lipid droplets) is perturbed, resulting in a "halo" of non-cleared cytoplasm around the central yolk. Yolk vesicle movement is normal during cellularisation and the general distribution of microtubule arrays is largely unaffected. Homozygous clones induced in the third larval instar eye and wing imaginal discs at either 24-36 hours or 36-48 hours after egg deposition are indistinguishable from their wild-type twinspots in terms of their size and number of cells 96 hours after induction. Homozygous clones result in smaller photoreceptor cells and wing margin bristles than normal, although other cell types in the adult eye and wing are unaffected. The size of mutant cells in clones in the developing wing and eye imaginal discs appear normal. Mutant cells in the wing disc show a normal cell cycle profile.
lilliXS575 is a suppressor of lethal phenotype of Scer\GAL4nanos.PG, runUAS.cLa
lilliXS575 is a suppressor of visible phenotype of aopACT.GMR
lilliXS575 is a suppressor of visible phenotype of phylGMR.PC
lilliXS575 is a suppressor of visible phenotype of sinaGMR.PN
lilliXS575 is a suppressor of visible phenotype of ttk88.GMR.Tag:MYC
lilliXS575 is an enhancer of phenotype of Ras85DV12.sev
lilliXS575 is an enhancer of phenotype of EgfrE1
lilliXS575 is a non-enhancer of phenotype of aopACT.sev
lilliXS575 is a non-enhancer of phenotype of Nact.sev
lilliXS575 is a non-enhancer of phenotype of rlSem.sev
lilliXS575 is a non-enhancer of phenotype of rlSem
lilliXS575 is a non-enhancer of phenotype of aopS2382
lilliXS575 is a non-enhancer of phenotype of sevS11.Tag:MYC
lilliXS575 is a non-enhancer of phenotype of phylsev.PC
lilliXS575 is a non-enhancer of phenotype of Ras85DN17.sev
lilliXS575 is a suppressor of phenotype of Ras85DV12.GMR
lilliXS575 is a suppressor of phenotype of Pi3K92EDN.GMR
lilliXS575 is a suppressor of phenotype of Rho1GMR.PH
lilliXS575 is a suppressor of ommatidium phenotype of aopACT.GMR
lilliXS575 is a suppressor of phenotype of Raf::tor12D.hs.sev
lilliXS575 is a suppressor of ommatidium phenotype of phylGMR.PC
lilliXS575 is a suppressor of phenotype of phylhs.sev
lilliXS575 is a suppressor of phenotype of rprGMR.PH
lilliXS575 is a suppressor of ommatidium phenotype of sinaGMR.PN
lilliXS575 is a suppressor of ommatidium phenotype of ttk88.GMR.Tag:MYC
lilliXS575 is a suppressor of phenotype of ttk88.hs.sev.Tag:MYC
lilliXS575 is a suppressor of phenotype of Pi3K92Ewt.GMR
lilliXS575 is a suppressor of phenotype of Pi3K92EACT.GMR
lilliXS575 is a non-suppressor of phenotype of rlSem.sev
lilliXS575 is a non-suppressor of phenotype of Nact.sev
lilliXS575 is a non-suppressor of phenotype of Ras85DN17.sev
lilliXS575 is a non-suppressor of phenotype of aopACT.sev
lilliXS575 is a non-suppressor of phenotype of aopS2382
lilliXS575 is a non-suppressor of phenotype of phylsev.PC
lilliXS575 is a non-suppressor of phenotype of rlSem
lilliXS575 is a non-suppressor of phenotype of sevS11.Tag:MYC
A lilliXS575 heterozygous background gives a dominant moderate enhancement to the ato1090/Df(3R)p13 eye phenotype at 25[o]C.
runScer\UAS.cLa (Scer\GAL4nos.PG) embryos that are also heterozygous for lilliXS575 show a significant increase in viability from approximately 3% to approximately 51%.
lilliXS575/lilliGD17 is rescued by Scer\GAL4da.G32/lilliUAS.cTa