Overexpression of kinesin heavy chain (KHC) and loss of KHC-mediated microtubule sliding increases wMel Wolbachia abundance at the posterior pole in 10a oocytes.

(A-F) Confocal micrographs of D. melanogaster oocytes stained with propidium iodide (PI) showing representative examples of (A) Wild-type (WT) localization of Wolbachia, and (B-D) increased posterior abundance of Wolbachia when KHC is overexpressed with (B) the native KHC promoter and (C, D) the ubiquitin (ubc) promoter, both in (C) homozygotes and (D) heterozygotes. (E) Wild-type localization of Wolbachia in in flies expressing a control transgenic construct containing an inserted wild-type KHC allele. (F) Excess posterior localization of Wolbachia in transgenic oocytes containing KHC lacking the microtubule-binding domain (see Fig 5B). (A’-F’) Magnified views of pole region in A-F, respectively. (G-J) Quantification of PI fluorescence due to Wolbachia. Plots are colored according to their genotype label colors in A-F. (G,H) Total fluorescence was plotted against the amount of fluorescence localized to the (G) oocyte posterior and (H) posterior pole. (I,J) Violin plots of the relative quantification of the proportion of Wolbachia at the (I) posterior and (J) posterior pole in each of the genotypes listed on the x-axes. Genotypes that contained significantly different posterior abundances than WT in Wilcoxon rank sum tests: * p < = 0.01; ** p < = 0.001; *** p < = 0.0001. Scale bars = 25 μm.