<p>The natural context in which CRISPR–Cas systems are active in Enterobacteriaceae has remained enigmatic. Here we find that the <i>Citrobacter rodentium</i> type I-E CRISPR–Cas system is activated by the oxygen-responsive transcriptional regulator Fnr in the anoxic environment of the mouse intestine. Since Fnr-dependent regulation is predicted in ~41% of Enterobacteriaceae <i>cas3</i> orthologues, we propose that anoxic regulation of CRISPR–Cas immunity is an adaptation that protects Enterobacteriaceae against threats from foreign DNA within the intestinal microbiome.</p>

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Anoxia activates CRISPR–Cas immunity in the mouse intestine

  • Ian W. Campbell,
  • David W. Basta,
  • Franz G. Zingl,
  • Emily J. Sullivan,
  • Sudhir Doranga,
  • Matthew K. Waldor

摘要

The natural context in which CRISPR–Cas systems are active in Enterobacteriaceae has remained enigmatic. Here we find that the Citrobacter rodentium type I-E CRISPR–Cas system is activated by the oxygen-responsive transcriptional regulator Fnr in the anoxic environment of the mouse intestine. Since Fnr-dependent regulation is predicted in ~41% of Enterobacteriaceae cas3 orthologues, we propose that anoxic regulation of CRISPR–Cas immunity is an adaptation that protects Enterobacteriaceae against threats from foreign DNA within the intestinal microbiome.