Genetic and physiological activation of osmosensitive gene expression mimics transcriptional signatures of pathogen infection in C. elegans.
The soil-dwelling nematode C. elegans is a powerful system for comparative molecular analyses of environmental stress response mechanisms. Infection of worms with bacterial and fungal pathogens causes the activation of well-characterized innate immune transcriptional programs in pathogen-exposed hypodermal and intestinal tissues. However, the pathophysiological events that drive such transcriptional responses are not understood. Here, we show that infection-activated transcriptional responses are, in large part, recapitulated by either physiological or genetic activation of the osmotic stress response. Microarray profiling of wild type worms exposed to non-lethal hypertonicity identified a suite of genes that were also regulated by infection. Expression profiles of five different osmotic stress resistant (osr) mutants under isotonic conditions reiterated the wild type transcriptional response to osmotic stress and also showed substantial similarity to infection-induced gene expression under isotonic conditions. Computational, transgenic, and functional approaches revealed that two GATA transcription factors previously implicated in infection-induced transcriptional responses, elt-2 and elt-3, are also essential for coordinated tissue-specific activation of osmosensitive gene expression and promote survival under osmotically stressful conditions. Together, our data suggest infection and osmotic adaptation share previously unappreciated transcriptional similarities which might be controlled via regulation of tissue-specific GATA transcription factors.
Rohlfing
Anne-Katrin
AK
Department of Physiology, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Miteva
Yana
Y
Hannenhalli
Sridhar
S
Lamitina
Todd
T
D000192:Actinomycetales / Q000502:physiology; D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000382:microbiology / Q000502:physiology; D029742:Caenorhabditis elegans Proteins / Q000235:genetics*; D016000:Cluster Analysis; D050980:GATA Transcription Factors / Q000235:genetics; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics*; D054884:Host-Pathogen Interactions; D020411:Oligonucleotide Array Sequence Analysis; D009995:Osmosis; D034622:RNA Interference; D020133:Reverse Transcriptase Polymerase Chain Reaction; D055049:Salt Tolerance / Q000235:genetics; D012965:Sodium Chloride / Q000494:pharmacology
D029742:Caenorhabditis elegans Proteins; C094134:ELT-2 protein, C elegans; D050980:GATA Transcription Factors; C118721:elt-3 protein, C elegans; D012965:Sodium Chloride