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Updated: Jan 13, 2026

Investigating Target Gene Function in a CD40 Agonistic Antibody-induced Colitis Model using CRISPR/Cas9-based Technologies
Published on: June 2, 2021
Anoxia activates CRISPR-Cas immunity in the mouse intestine
Ian W Campbell1,2, David W Basta3, Franz G Zingl4,5
1Division of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA. icampbell3@bwh.harvard.edu.
None:
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.
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