A conserved PMK-1/p38 MAPK is required in Caenorhabditis elegans tissue-specific immune response to Yersinia pestis infection

Devin D. Bolz, Jennifer L. Tenor, Alejandro Aballay

Research output: Contribution to journalArticlepeer-review

73 Scopus citations

Abstract

Yersinia pestis has acquired a variety of complex strategies that enable the bacterium to overcome defenses in different hosts and ensure its survival and successful transmission. A full-genome microarray analysis on Caenorhabditis elegans infected with Y. pestis shows enrichment in genes that are markers of innate immune responses and regulated by a conserved PMK-1/p38 MAPK. Consistent with a role in regulating expression of immune effectors, inhibition of PMK-1/p38 by mutation or RNA interference enhances susceptibility to Y. pestis. Further studies of mosaic animals where PMK-1/p38 is exclusively inhibited or overexpressed in a tissue-specific manner indicate that PMK-1/p38 controls expression of a CUB-like family of immune genes at the cell-autonomous level. Given the conserved nature of PMK-1/p38 MAPK-mediated signaling and innate immune responses, PMK-1/p38 MAPK may play a role in the immune response against Y. pestis in natural hosts.

Original languageEnglish (US)
Pages (from-to)10832-10840
Number of pages9
JournalJournal of Biological Chemistry
Volume285
Issue number14
DOIs
StatePublished - Apr 2 2010
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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