Fig. 3: Screening for surface factors identifies the lipoprotein Blr as essential for BBB crossing in Drosophila.
a Schematic representation of GBS surface structures and tested virulence factors with corresponding mutants. a’ Schematic structure of Blr lipoprotein. b, c Screening of GBS surface structures and virulence factors at b 24 h and c 6 h post-infection identified GBS surface lipoproteins, and in particular Blr, as crucial for BBB crossing. A Kruskal–Wallis test followed by Dunn’s multiple comparisons test generated adjusted p-values. b WT GBS (n = 31) is compared to Δlgt (p = 0.0124, n = 12), Δlsp (p = 0.0022, n = 8), Δlgt/lsp (p < 10−10, n = 43), Δblr (p = 9.77 * 10−7, n = 45), Δblr + blr (p > 0.9999, n = 13), and + blr (p > 0.9999, n = 15). c WT GBS (n = 19) is compared to Δlgt/lsp (p = 1.27 * 10−8, n = 22), Δblr (p = 0.0029, n = 16). Results are presented as box and whisker plots: whiskers mark the minimum and maximum, the box includes the 25th–75th percentile, and the line in the box is the median. n represents the number of larvae analysed. *p ≤ 0.05; **p ≤ 0.01; ****p ≤ 0.0001; ns, not significant. d SEM pictures of WT GBS and Δblr GBS attached to the brain surface, without or with HEPES. Colourisations show biofilm-type matrix (yellow) present at the surface of the bacteria. e Close-up of confocal images of brain infected with Δblr, with and without acidosis, showing the SPG membrane (mdr65-mtd-tomato, red) and septate junctions (Lachesin::GFP, green) at 6 h post-infection. Septate junctions are strongly affected under Δblr infection without HEPES and partially rescued with HEPES (compare to Fig. 2e). SPG membranes are still damaged under Δblr infection with HEPES (6 h post-infection). Dashed lines outline SPG damages. Source data are provided as a Source Data file for b, c.
