Figure 7. Depletion of Fimbrin rescues... | Rockefeller University Press

Figure 7.

$Figure 7. Depletion of Fimbrin rescues the bnk phenotype and gastrulation. (A–I) Confocal images of Drosophila embryos expressing the myosin-II marker Sqh::mCh in control (A–C and J), in bnk−/− (D–F and K), or in bnk−/− Fimbrin KD double mutant embryos (G–I and L). Images show top views of the basal actomyosin network at a furrow ingression depth of 5 µm (A, D, and G) and 10 min later (B, E, and H). Images in C, F, and I show sagittal sections of B, E, and H. Depletion of Fimbrin ameliorated the Bnk hypercontractility phenotype and defects in network organization. Scale bars, 20 µm. (J) Confocal cross sections of a control embryo expressing the myosin-II marker Sqh::mCherry at the onset of ventral furrow formation, after 5 min, 7 min, and 10 min. (K) Confocal cross sections of a bnk−/− mutant embryo expressing the myosin-II marker Sqh::mCherry at the onset of ventral furrow formation, after 10 min, 15 min, and 20 min. (L) Confocal cross sections of a bnk−/− Fimbrin KD double mutant embryo expressing the myosin-II marker Sqh::mCherry showing rescue of ventral furrow invagination at the onset of ventral furrow formation, after 10 min, 15 min, and 20 min. Scale bars, 10 µm. (M) Frequency of normal gastrulation (competed ventral furrow formation) in control (n = 19), Fimbrin KD (n = 12), bnk−/− (n = 9), and bnk−/− Fimbrin double mutant (n = 10) embryos. Green color indicates the fraction of embryos with normal ventral furrow, and red color indicates the fraction of embryos that initiated but did not complete ventral furrow invagination. Only a small fraction of bnk mutant embryos (11%) formed a normal ventral furrow (VF), whereas upon codepletion of Fimbrin, this fraction increased to 70%.$

Depletion of Fimbrin rescues the bnk phenotype and gastrulation. (A–I) Confocal images of Drosophila embryos expressing the myosin-II marker Sqh::mCh in control (A–C and J), in bnk^−/− (D–F and K), or in bnk^−/− Fimbrin KD double mutant embryos (G–I and L). Images show top views of the basal actomyosin network at a furrow ingression depth of 5 µm (A, D, and G) and 10 min later (B, E, and H). Images in C, F, and I show sagittal sections of B, E, and H. Depletion of Fimbrin ameliorated the Bnk hypercontractility phenotype and defects in network organization. Scale bars, 20 µm. (J) Confocal cross sections of a control embryo expressing the myosin-II marker Sqh::mCherry at the onset of ventral furrow formation, after 5 min, 7 min, and 10 min. (K) Confocal cross sections of a bnk^−/− mutant embryo expressing the myosin-II marker Sqh::mCherry at the onset of ventral furrow formation, after 10 min, 15 min, and 20 min. (L) Confocal cross sections of a bnk^−/− Fimbrin KD double mutant embryo expressing the myosin-II marker Sqh::mCherry showing rescue of ventral furrow invagination at the onset of ventral furrow formation, after 10 min, 15 min, and 20 min. Scale bars, 10 µm. (M) Frequency of normal gastrulation (competed ventral furrow formation) in control (n = 19), Fimbrin KD (n = 12), bnk^−/− (n = 9), and bnk^−/− Fimbrin double mutant (n = 10) embryos. Green color indicates the fraction of embryos with normal ventral furrow, and red color indicates the fraction of embryos that initiated but did not complete ventral furrow invagination. Only a small fraction of bnk mutant embryos (11%) formed a normal ventral furrow (VF), whereas upon codepletion of Fimbrin, this fraction increased to 70%.