Deletion of vp0057, a Gene Encoding a Ser/Thr Protein Kinase, Impacts the Proteome and Promotes Iron Uptake and Competitive Advantage in Vibrio parahaemolyticus

The marine bacterial pathogen Vibrio parahaemolyticus is a major cause of food-borne gastroenteritis. Recent findings have demonstrated that protein phosphorylation is fundamental to the regulation of many physiological processes in pathogenic bacteria, including bacterial virulence. However, the underlying mechanisms remain to be completely clarified. Using bioinformatics analysis, we found that VP0057 may be a potential Ser/Thr protein kinase with phosphorylation activity. Thus, we constructed the vp0057-deletion mutant (Delta vp0057) from the wild-type V. parahaemolyticus serotype O3:K6 and employed a mass spectrometry-based proteomic strategy to characterize proteome-wide changes in response to vp0057 deletion, owing to the potential roles of VP0057 in V. parahaemolyticus. One hundred ninety-seven differentially expressed proteins were identified in the Delta vp0057 strain compared with the wild-type strain, among which 135 proteins were upregulated and 62 proteins were downregulated. Detailed annotation of these differentially expressed proteins was conducted. Notably, iron-related and T6SS1-related proteins were upregulated in the Delta vp0057 strain, corroborating the results by quantitative PCR. Further experiments proved that vp0057 deletion promotes Fe2+ and Fe3+ uptake and provides a growth competition advantage, which is controlled by iron-related and T6SS1-related proteins, respectively. Although the regulatory roles and mechanisms of VP0057 remain to be revealed in V. parahaemolyticus, our systemic analysis of the protein profile of Delta vp0057 provides a promising starting point for the intensive exploration of VP0057.

Automated summary

The marine bacterial pathogen Vibrio parahaemolyticus is a major cause of food-borne gastroenteritis. Recent research has identified VP0057 as a potential Ser/Thr protein kinase with phosphorylation activity, leading to proteome-wide changes in response to its deletion. The deletion of VP0057 resulted in differential expression of 197 proteins, notably upregulating iron-related and T6SS1-related proteins and promoting Fe2+ and Fe3+ uptake.