| Citation | Rohlfing AK, Miteva Y, Hannenhalli S, Lamitina T. Genetic and physiological activation of osmosensitive gene expression mimics transcriptional signatures of pathogen infection in C. elegans. PLoS One, 2010. |
| PubMed ID | 20126308 |
| Short Description | Genetic and physiological activation of osmosensitive gene expression mimics transcriptional signatures of pathogen infection in C. elegans. GEO Record: GSE19310 Platform: GPL200 Download gene-centric, log2 transformed data: WBPaper00035873.ce.mr.csv |
| # of Conditions | 30 |
Full Description
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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. Experimental Details: WBPaper00035873:N2_isotonic_1 WBPaper00035873:N2_isotonic_2 WBPaper00035873:N2_isotonic_3 WBPaper00035873:15min_N2_hypertonic_1 WBPaper00035873:15min_N2_hypertonic_2 WBPaper00035873:15min_N2_hypertonic_3 WBPaper00035873:1hr_N2_hypertonic_1 WBPaper00035873:1hr_N2_hypertonic_2 WBPaper00035873:1hr_N2_hypertonic_3 WBPaper00035873:6hr_N2_hypertonic_1 WBPaper00035873:6hr_N2_hypertonic_2 WBPaper00035873:6hr_N2_hypertonic_3 WBPaper00035873:96hr_N2_hypertonic_1 WBPaper00035873:96hr_N2_hypertonic_2 WBPaper00035873:96hr_N2_hypertonic_3 WBPaper00035873:osm-7_isotonic_1 WBPaper00035873:osm-7_isotonic_2 WBPaper00035873:osm-7_isotonic_3 WBPaper00035873:osm-8_isotonic_1 WBPaper00035873:osm-8_isotonic_2 WBPaper00035873:osm-8_isotonic_3 WBPaper00035873:osm-11_isotonic_1 WBPaper00035873:osm-11_isotonic_2 WBPaper00035873:osm-11_isotonic_3 WBPaper00035873:dpy-9_isotonic_1 WBPaper00035873:dpy-9_isotonic_2 WBPaper00035873:dpy-9_isotonic_3 WBPaper00035873:dpy-10_isotonic_1 WBPaper00035873:dpy-10_isotonic_2 WBPaper00035873:dpy-10_isotonic_3. |
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