The invasion of mammalian cells by intracellular bacterial pathogens reshuffles their gene expression and functions; however, we lack dynamic insight into the distinct control levels that shape the host response. Here, we have addressed the respective contribution of transcriptional and translational regulations during a time-course of infection of human intestinal epithelial cells by an epidemic strain of , using transcriptome analysis paralleled with ribosome profiling. Upregulations were dominated by early transcriptional activation of pro-inflammatory genes, whereas translation inhibition appeared as the major driver of downregulations. Instead of a widespread but transient shutoff, translation inhibition affected specifically and durably transcripts encoding components of the translation machinery harbouring a 5'-terminal oligopyrimidine motif. Pre-silencing the most repressed target gene () slowed down the intracellular multiplication of , suggesting that the infected host cell can benefit from the repression of genes involved in protein synthesis and thereby better control infection.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7549700 | PMC |
http://dx.doi.org/10.1080/15476286.2020.1777380 | DOI Listing |
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