Inhibition of Lgl PM targeting by hypoxia is modulated by HIF pathway but is independent of phosphorylation events. (A) Lgl::GFP showed normal subcellular relocalization in sima mutant embryos under hypoxia and reoxygenation (air). In fatiga mutant embryos, Lgl::GFP showed no significant diffusion at 60 min of hypoxia treatment, and only become diffused at 120 min of hypoxia. Lgl::GFP showed complete diffusion in fatiga sima double mutant embryos at 60 min of hypoxia and recovered normally during reoxygenation (n = 6). (B) Lgl::GFP show normal subcellular redistribution under hypoxia in either par-6 or aPKC mutant follicular epithelial cell clones (n = 4). Mutant cells of par-6 are marked by the absence of nuclear GFP, whereas aPKC mutant cells are marked by the absence of nuclear His2Av::RFP. (C) PM targeting of Lgl^S5A::GFP is acutely and reversibly inhibited under hypoxia in follicular epithelial cells. Loss of RFP marks lg^S5A::GFP clones, whereas wild-type lgl::GFP twin clones are labeled by increased expression of RFP (indicated by white asterisks). **, P < 0.01; ***, P < 0.001. Bars, 5 µm. Error bars represent means ± SEM.