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Functional and Proteomic Analysis of Virulence Upon Loss of Its Native Cas9 Nuclease.

Authors:
Nina J Gao Mahmoud M Al-Bassam Saugat Poudel Jacob M Wozniak David J Gonzalez Joshua Olson Karsten Zengler Victor Nizet J Andrés Valderrama

Front Microbiol 2019 22;10:1967. Epub 2019 Aug 22.

Division of Host-Microbe Systems and Therapeutics, Department of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, CA, United States.

The public health impact of (group A , GAS) as a top 10 cause of infection-related mortality in humans contrasts with its benefit to biotechnology as the main natural source of Cas9 nuclease, the key component of the revolutionary CRISPR-Cas9 gene editing platform. Despite widespread knowledge acquired in the last decade on the molecular mechanisms by which GAS Cas9 achieves precise DNA targeting, the functions of Cas9 in the biology and pathogenesis of its native organism remain unknown. In this study, we generated an isogenic serotype M1 GAS mutant deficient in Cas9 protein and compared its behavior and phenotypes to the wild-type parent strain. Absence of Cas9 was linked to reduced GAS epithelial cell adherence, reduced growth in human whole blood , and attenuation of virulence in a murine necrotizing skin infection model. Virulence defects of the GAS Δ strain were explored through quantitative proteomic analysis, revealing a significant reduction in the abundance of key GAS virulence determinants. Similarly, deletion of affected the expression of several known virulence regulatory proteins, indicating that Cas9 impacts the global architecture of GAS gene regulation.

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http://dx.doi.org/10.3389/fmicb.2019.01967DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6714885PMC
August 2019

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