Fig. 5: The UDP-glucose biosynthetic pathway is required for filamentation.
From: Bacterial filamentation as a mechanism for cell-to-cell spread within an animal host
a CLUSTAL O multiple sequence alignment of GtaB from divergent bacteria with the predicted catalytic arginine highlighted. b In vitro filamentation of LUAb7(gtaBR17C) and the complemented LUAb7 + gtaB+ as measured by bacterial length in LB and TB (n = 150, 2 independent experiments, Tukey’s plot with boxes’ lower and upper bounds representing 25th and 75th percentiles, respectively, center lines representing medians, lower whiskers representing minima and upper whiskers representing largest values less than 75th percentile plus 1.5 times interquartile range (IQR). Individual points are values that are larger than 75th percentile + 1.5 IQR). The cutoff for a filament is 4 μm (hatched line) (left), p < 0.0001 (****) or not significant (ns) by Kruskal-Wallis test followed by Dunn’s post test with multiple-comparison correction. The change in percent filaments was measured (% filaments in TB − % filaments in LB) (right). Bar graphs are presented with means and SD error bars. Each point represents value from an independent experiment. c The UDP-glucose biosynthetic pathway converting glucose (glc) to UDP-glucose (UDP-glc). d B. atropi knockouts measured for the change in percent filaments. Results are from 3 independent experiments, n > 400 bacteria per replicate, p < 0.05(*) or p = 0.0087(**) by unpaired two-tailed t-test with Welch’s correction compared to WT. Exact sample sizes for each group are provided in Source Data. Bar graphs show means with SD error bars. e Anterior to posterior (A-P) spreading of B. atropi mutants in vivo, normalized to animal length. Results are from n = 65 (WT), 67 (LUAb7), 64 (ΔopgH), and 68 (Δpgm1) animals examined over 2 independent experiments, p < 0.0001 (****) or not significant (ns) by Mann–Whitney unpaired two-tailed t-test. Error bars represent SD. f Model for B. atropi intracellular filamentation and spreading.
