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. 2018 Aug 6;217(8):2911–2929. doi: 10.1083/jcb.201708091

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© 2018 Pfanzelter et al.

This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).

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Figure 6. — Arp2/3-driven actin polymerization does not promote septin loss. (A) Immunofluorescence images showing the association of SEPT7 (green) with CEV, detected with the B5 antibody before membrane permeabilization (blue) in HeLa cells infected with WR and the YdF virus, which is deficient in actin tail formation (red) at 8 h. The graph shows the percentage of CEV recruiting SEPT7 for the two different viruses. (B) Images showing the association of SEPT7 with CEV in HeLa cells infected with WR or YdF and treated with the Arp2/3 inhibitor CK666. The graph shows the percentage of CEV with SEPT7 in the presence (CK666) and absence (CTRL) of the Arp2/3 inhibitor for the two different viruses. (C) Images showing the association of SEPT7 with CEV in N-WASP parental and knockout MEFs infected with WR and YdF for 10 h. The graph shows the percentage of CEV colocalizing with SEPT7 for the indicated viruses in the presence (+/+) or absence (−/−) of N-WASP. Error bars represent SEM from three independent experiments in which 900 virus particles were analyzed across 30 cells. Bars: (A and B) 5 µm; (A and B, insets) 2 µm. ****, P < 0.0001.