GalK limits type I-F CRISPR-Cas expression in a CRP-dependent manner.

Abstract:

:CRISPR-Cas adaptive immune systems protect bacteria from phage predation, and other foreign genetic elements such as plasmids. Significant advances have been made regarding how CRISPR-Cas systems elicit immunity; however, comparatively little is known about their regulation. To study CRISPR-Cas regulation, we describe the construction of suicide lacZ-reporter plasmids with different antibiotic resistance cassettes. Through recombination into the host chromosome, single-copy expression can be achieved, thus preserving natural gene expression and maintaining a reporter expression output that reflects regulation within a normal genomic context. Previous work determined that the galactose metabolism gene galM, decreased the expression of the cas operon in Pectobacterium atrosepticum. We used the new integrative reporters to investigate galK, a gene that is located elsewhere in the genome and is responsible for the conversion of α-D-Galactose to Galactose-1-P during galactose metabolism. Deletion of galK led to elevated cas expression in a CRP-dependent manner but had no effect on CRISPR array expression. These results highlight that the metabolic status of the host cell is linked to the induction of CRISPR-Cas immunity.

journal_name

FEMS Microbiol Lett

authors

Hampton HG,Patterson AG,Chang JT,Taylor C,Fineran PC

doi

10.1093/femsle/fnz137

subject

Has Abstract

pub_date

2019-06-01 00:00:00

issue

11

eissn

0378-1097

issn

1574-6968

pii

5521891

journal_volume

366

pub_type

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