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Abstract
Stress granule (SG) formation is a host cell response to stress-induced translational repression. SGs assemble with RNA-binding proteins and translationally silent mRNA. SGs have been demonstrated to be both inhibitory to viruses, as well as being subverted for viral roles. In contrast, the function of SGs during non-viral microbial infections remains largely unexplored. A handful of microbial infections have been shown to result in host SG assembly. Nevertheless, a large body of evidence suggests SG formation in hosts is a widespread response to microbial infection. Diverse stresses caused by microbes and their products can activate the integrated stress response in order to inhibit translation initiation through phosphorylation of the eukaryotic translation initiation factor 2α (eIF2α). This translational response in other contexts results in SG assembly, suggesting that SG assembly can be a general phenomenon during microbial infection. This review explores evidence for host SG formation in response to bacterial, fungal, and protozoan infection and potential functions of SGs in the host and for adaptations of the pathogen.
Highlights
Stress granules (SGs) are cytoplasmic structures that accumulate as foci in response to multiple cellular stresses
This study showed a decrease in the P-eukaryotic translation initiation factor 2α (eIF2α) to 20% of the total eIF2α after 36 h, along with a decrease in ATF4 mRNA levels over the same time frame
This study suggested that endoplasmic reticulum (ER) stress was caused by M. avium induced reactive oxygen species (ROS), which is likely to play a role in the suppression of the M. avium infection
Summary
Stress granules (SGs) are cytoplasmic structures that accumulate as foci in response to multiple cellular stresses. Evidence for elevated P-eIF2α includes activation of an upstream P-eIF2α kinase, along with downstream gene induction, and even the formation of SGs in HeLa cells upon infection, which largely occurs via the P-eIF2α pathway (Tattoli et al, 2012). Mycobacterium ulcerans, capable of causing Buruli ulcer, produces the toxin mycolactone, which was shown to induce P-eIF2α when exposed to HeLa cells, along with increased CHOP and ATF4 protein expression (Ogbechi et al, 2018).
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