Proximity-dependent proteomics of the Chlamydia trachomatis inclusion membrane reveals functional interactions with endoplasmic reticulum exit sites
Fig 9
RNAi depletion of ERES regulatory proteins Sec12 and cTAGE5 disrupt Chlamydia growth.
(A) Cells were treated with siRNA oligonucleotides and incubated for 48 hours, then infected with C. trachomatis L2. At 48 hpi, cells were lysed and infectious Chlamydia EB from each sample group were tested for IFU by infecting new cells. IFU values were compared to scramble siRNA treated, infected cells. Significance determined by one-way ANOVA with Dunnett’s multiple comparisons test, compared to control IFU. Bars, mean (SD);***, p < 0.001; ****, p < 0.0001; n ≥ 3. (B) Sec12 (anti-Sec12, green in merge) colocalizes with Sec31 (anti-Sec31A, purple in merge) in infected cells. Representative deconvolved merged z-series image. Scale bar = 16 μm. (C) Sec12 (anti-Sec12, green in merge) overlaps with IncA (anti-IncA, purple in merge) in a similar manner to Sec16 or Sec31. Single plane from deconvolved z-series image. Scale bar = 16 μm.