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dc.contributor.authorBaxt, Leigh A.en_US
dc.contributor.authorGoldberg, Marcia B.en_US
dc.date.accessioned2014-05-06T16:16:08Z
dc.date.issued2014en_US
dc.identifier.citationBaxt, Leigh A., and Marcia B. Goldberg. 2014. “Host and Bacterial Proteins That Repress Recruitment of LC3 to Shigella Early during Infection.” PLoS ONE 9 (4): e94653. doi:10.1371/journal.pone.0094653. http://dx.doi.org/10.1371/journal.pone.0094653.en
dc.identifier.issn1932-6203en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:12152839
dc.description.abstractShigella spp. are intracytosolic gram-negative pathogens that cause disease by invasion and spread through the colonic mucosa, utilizing host cytoskeletal components to form propulsive actin tails. We have previously identified the host factor Toca-1 as being recruited to intracellular S. flexneri and being required for efficient bacterial actin tail formation. We show that at early times during infection (40 min.), the type three-secreted effector protein IcsB recruits Toca-1 to intracellular bacteria and that recruitment of Toca-1 is associated with repression of recruitment of LC3, as well as with repression of recruitment of the autophagy marker NDP52, around these intracellular bacteria. LC3 is best characterized as a marker of autophagosomes, but also marks phagosomal membranes in the process LC3-associated phagocytosis. IcsB has previously been demonstrated to be required for S. flexneri evasion of autophagy at late times during infection (4–6 hr) by inhibiting binding of the autophagy protein Atg5 to the Shigella surface protein IcsA (VirG). Our results suggest that IcsB and Toca-1 modulation of LC3 recruitment restricts LC3-associated phagocytosis and/or LC3 recruitment to vacuolar membrane remnants. Together with published results, our findings suggest that IcsB inhibits innate immune responses in two distinct ways, first, by inhibiting LC3-associated phagocytosis and/or LC3 recruitment to vacuolar membrane remnants early during infection, and second, by inhibiting autophagy late during infection.en
dc.language.isoen_USen
dc.publisherPublic Library of Scienceen
dc.relation.isversionofdoi:10.1371/journal.pone.0094653en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3983221/pdf/en
dash.licenseLAAen_US
dc.subjectBiology and Life Sciencesen
dc.subjectImmunologyen
dc.subjectImmune Systemen
dc.subjectInnate Immune Systemen
dc.subjectImmunityen
dc.subjectMicrobiologyen
dc.subjectBacteriologyen
dc.subjectGram Negativeen
dc.subjectMedical Microbiologyen
dc.subjectMicrobial Pathogensen
dc.subjectBacterial Pathogensen
dc.subjectMedicine and Health Sciencesen
dc.subjectInfectious Diseasesen
dc.subjectPathology and Laboratory Medicineen
dc.subjectPathogenesisen
dc.subjectHost-Pathogen Interactionsen
dc.titleHost and Bacterial Proteins That Repress Recruitment of LC3 to Shigella Early during Infectionen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalPLoS ONEen
dash.depositing.authorGoldberg, Marcia B.en_US
dc.date.available2014-05-06T16:16:08Z
dc.identifier.doi10.1371/journal.pone.0094653*
dash.contributor.affiliatedGoldberg, Marcia


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