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. Author manuscript; available in PMC: 2018 Jun 14.
Published in final edited form as: Cell Host Microbe. 2017 Jun 1;21(6):719–730.e6. doi: 10.1016/j.chom.2017.05.002

Figure 6. ClC-b facilitates lysosomal degradation of bacteria to activate PGRP-LE and Relish in macrophages.

Figure 6

(A) CFU counts from flies overexpressing PGRP-LE in macrophages (He>PGRP-LE). Values normalized to wild-type (WT) UAS-PGRP-LE. (B) Z-stack projections of confocal images of isolated larval macrophages with internalized/adhered fluorescent E. coli (red and green) from the “ex vivo sequential phagocytosis assay”. Shown are single larval ClC-b1 macrophages with (He>LE) or without (UAS-LE) PGRP-LE overexpression. (C) Quantification of data shown in (B). (D) CFU counts from ClC-b1 flies overexpressing (O.E.) PGRP-LE in macrophages. Values normalized to ClC-b1;RelE20 PGRP-LE O.E.. (E) CFU counts from ClC-b1 flies expressing N-terminal fragment of Relish (Rel68) in macrophages. Values are normalized to control (ClC-b1;UAS-Rel68/+). (F) CFU counts from flies pre-injected with PBS or TCT (16 µM) 1 day before E. coli injection. Values shown are normalized to PBS controls. All values shown represent mean ±SEM. (G) Model showing the ClC-b mediated endolysosome-Relish signaling axis in Drosophila macrophages. See also Figure S5.