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. 2019 Jun 14;16(2):334–346. doi: 10.1080/15548627.2019.1628539

Figure 5.

Figure 5.

GAS inhibits ATG14 recruitment to GcAVs. (a) MTORC1 activity is decreased by GAS infection. HeLa cells were treated with rapamycin (100 nM) or infected with GAS JRS4 wild-type for the indicated times. The phosphorylation states at Thr389 of endogenous RPS6KB1, and at Ser757 of endogenous ULK1 in cell lysate were analyzed by western blot. (b) BECN1 and ATG14 are activated during GAS infection. HeLa cells were treated with rapamycin (100 nM) or infected with GAS strains for indicated times. The phosphorylation states at Ser29 of endogenous ATG14 and at Ser15 of endogenous BECN1 in cell lysate were analyzed by western blot. (c) HeLa cells expressing GFP-LC3 and mCherry-ATG14 were infected with GAS WT and Δnga for 2 or 4 h. Representative images of ATG14 localization to GAS at 2 h (c) and quantification of ATG14-positive GAS (d). Scale bars: 10 μm. Data in (d) were tested by two-tailed Student’s t-test: ***P < 0.001.