Recovery from an Acute Infection in C. elegans Requires the GATA Transcription Factor ELT-2

Brian Head, Alejandro Aballay

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The mechanisms involved in the recognition of microbial pathogens and activation of the immune system have been extensively studied. However, the mechanisms involved in the recovery phase of an infection are incompletely characterized at both the cellular and physiological levels. Here, we establish a Caenorhabditis elegans-Salmonella enterica model of acute infection and antibiotic treatment for studying biological changes during the resolution phase of an infection. Using whole genome expression profiles of acutely infected animals, we found that genes that are markers of innate immunity are down-regulated upon recovery, while genes involved in xenobiotic detoxification, redox regulation, and cellular homeostasis are up-regulated. In silico analyses demonstrated that genes altered during recovery from infection were transcriptionally regulated by conserved transcription factors, including GATA/ELT-2, FOXO/DAF-16, and Nrf/SKN-1. Finally, we found that recovery from an acute bacterial infection is dependent on ELT-2 activity.

Original languageEnglish (US)
JournalPLoS Genetics
Volume10
Issue number10
DOIs
StatePublished - Jan 1 2014
Externally publishedYes

Fingerprint

GATA2 Transcription Factor
Infection
infection
GATA Transcription Factors
gene
Genes
biological treatment
Salmonella enterica
genes
Caenorhabditis elegans
Xenobiotics
xenobiotics
bacterial infections
Bacterial Infections
Innate Immunity
Computer Simulation
Oxidation-Reduction
immune system
homeostasis
Immune System

ASJC Scopus subject areas

  • Ecology, Evolution, Behavior and Systematics
  • Molecular Biology
  • Genetics
  • Genetics(clinical)
  • Cancer Research

Cite this

Recovery from an Acute Infection in C. elegans Requires the GATA Transcription Factor ELT-2. / Head, Brian; Aballay, Alejandro.

In: PLoS Genetics, Vol. 10, No. 10, 01.01.2014.

Research output: Contribution to journalArticle

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