Nuclear hormone receptor regulation of microRNAs controls innate immune responses in C. elegans

PLoS Pathog. 2013;9(8):e1003545. doi: 10.1371/journal.ppat.1003545. Epub 2013 Aug 22.

Abstract

Nuclear hormone receptors respond to small molecules such as retinoids or steroids and regulate development. Signaling in the conserved p38/PMK-1 MAP kinase pathway regulates innate immunity. In this study, we show that the Caenorhabditis elegans nuclear receptor DAF-12 negatively regulates the defense against pathogens via the downstream let-7 family of microRNAs, which directly target SKN-1, a gene downstream of PMK-1. These findings identify nuclear hormone receptors as components of innate immunity that crosstalk with the p38/PMK-1 MAP kinase pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caenorhabditis elegans / genetics
  • Caenorhabditis elegans / immunology*
  • Caenorhabditis elegans Proteins / genetics
  • Caenorhabditis elegans Proteins / immunology*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / immunology
  • Immunity, Innate / physiology*
  • MAP Kinase Signaling System / genetics
  • MAP Kinase Signaling System / immunology*
  • MicroRNAs / genetics
  • MicroRNAs / immunology*
  • Mitogen-Activated Protein Kinases / genetics
  • Mitogen-Activated Protein Kinases / immunology
  • Receptors, Cytoplasmic and Nuclear / genetics
  • Receptors, Cytoplasmic and Nuclear / immunology*
  • Transcription Factors / genetics
  • Transcription Factors / immunology

Substances

  • Caenorhabditis elegans Proteins
  • DAF-12 protein, C elegans
  • DNA-Binding Proteins
  • MicroRNAs
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • let-7 microRNA, C elegans
  • skn-1 protein, C elegans
  • Mitogen-Activated Protein Kinases
  • Pmk-1 protein, C elegans

Grants and funding

This work was supported by the National Basic Research Program of China (973 Programs 2012CB578100 and 2011CB505000), the National Natural Science Foundation of China (project 31030028). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.