AEM Accepts, published online ahead of print on 16 October 2009

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Appl. Environ. Microbiol. doi:10.1128/AEM.01603-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Polyphosphate Kinase 1 is Important for VBNC Formation, Natural Transformation and Antimicrobial Resistance in Campylobacter jejuni

Dharanesh Gangaiah, Issmat I. Kassem, Zhe Liu, and Gireesh Rajashekara^*

Food Animal Health Research Program, Ohio Agricultural Research and Development Center, Department of Veterinary Preventive Medicine, The Ohio State University, Wooster, OH 44691

^* To whom correspondence should be addressed. Email: rajashekara.2{at}osu.edu.

Campylobacter jejuni, a Gram-negative, microaerophilic bacterium, is a predominant cause of bacterial gastroenteritis in humans. Although considered fragile, fastidious and lacking many classical stress response mechanisms, C. jejuni exhibits a remarkable capacity for survival and adaptation, successfully infecting humans and persisting in the environment. Consequently, understanding the physiological and genetic properties that allow C. jejuni to survive and adapt to various stress conditions is crucial for therapeutic interventions. Of importance is polyphosphate kinase 1 (PPK1), which is a key enzyme mediating the synthesis of polyphosphate (poly P), an essential molecule for survival, mediating stress responses, host colonization and virulence in many bacteria. Therefore, we investigated the role of PPK1 in C. jejuni pathogenesis, stress survival and adaptation. Our findings demonstrate that C. jejuni ppk1 mutant was deficient in poly P accumulation, which was associated with decreased ability to form viable but non-culturable cells (VBNC) under acid stress. The ppk1 mutant also showed decreased frequency of natural transformation and increased susceptibility to various antimicrobials. Furthermore, the ppk1 mutant was characterized by a dose-dependent deficiency in chicken colonization. Complementation of the ppk1 mutant with the wildtype copy of ppk1 restored the deficient phenotypes to levels similar to those of the wildtype. Our results suggest that poly P plays an important role in stress survival and adaptation and might contribute to genome plasticity, and spread and development of antimicrobial resistance in C. jejuni. These findings highlight the potential of PPK1 as a novel target for therapeutic interventions.