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. 2020 Jan 15;219(3):e201905228. doi: 10.1083/jcb.201905228

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© 2020 Edwards-Jorquera et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 7. — The role of Trpml in phagocytic processing is independent of Myo-II activity. (A) Representative images of LifeAct-GFP–expressing hemocytes cultured during 1 h with fluorescently labeled bacteria and LysoTracker probe. Evaluated conditions are Myo-II deficiency by expressing sqh RNAi, Myo-II overactivation by expressing mypt75D^F117A in a control, and trpml¹ genetic background. Scale bar: 5 µm. Note that the bar is smaller in sqh-deficient hemocytes, as the cells present defects in cytokinesis and are larger. (B) Phagocytic processing quantified as the percentage of hemocytes containing bacteria within at least two acidic vesicles after 1 h of culture (n = 3 independent cultures, n ≥ 20 hemocytes/condition). Data are presented as scatter dot plot, indicating mean ± SD, one-way ANOVA with Tukey's multiple comparisons post hoc test. Mean values are indicated as “+”; statistically equivalent values are represented with the same letter (P value < 0.05). Cg, collagen Gal4 driver.