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Coxiella burnetii inhibits host immunity by a protein phosphatase adapted from glycolysis.


ABSTRACT: Coxiella burnetii is a bacterial pathogen that replicates within host cells by establishing a membrane-bound niche called the Coxiella-containing vacuole. Biogenesis of this compartment requires effectors of its Dot/Icm type IV secretion system. A large cohort of such effectors has been identified, but the function of most of them remain elusive. Here, by a cell-based functional screening, we identified the effector Cbu0513 (designated as CinF) as an inhibitor of NF-κB signaling. CinF is highly similar to a fructose-1,6-bisphosphate (FBP) aldolase/phosphatase present in diverse bacteria. Further study reveals that unlike its ortholog from Sulfolobus tokodaii, CinF does not exhibit FBP phosphatase activity. Instead, it functions as a protein phosphatase that specifically dephosphorylates and stabilizes IκBα. The IκBα phosphatase activity is essential for the role of CinF in C. burnetii virulence. Our results establish that C. burnetii utilizes a protein adapted from sugar metabolism to subvert host immunity.

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC8740755 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature

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<i>Coxiella burnetii</i> inhibits host immunity by a protein phosphatase adapted from glycolysis.

Zhang Yong Y   Fu Jiaqi J   Liu Shuxin S   Wang Lidong L   Qiu Jiazhang J   van Schaik Erin J EJ   Samuel James E JE   Song Lei L   Luo Zhao-Qing ZQ  

Proceedings of the National Academy of Sciences of the United States of America 20220101 1


<i>Coxiella burnetii</i> is a bacterial pathogen that replicates within host cells by establishing a membrane-bound niche called the <i>Coxiella</i>-containing vacuole. Biogenesis of this compartment requires effectors of its Dot/Icm type IV secretion system. A large cohort of such effectors has been identified, but the function of most of them remain elusive. Here, by a cell-based functional screening, we identified the effector Cbu0513 (designated as CinF) as an inhibitor of NF-κB signaling. C  ...[more]

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