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Deletion of vp0057, a Gene Encoding a Ser/Thr Protein Kinase, Impacts the Proteome and Promotes Iron Uptake and Competitive Advantage in Vibrio parahaemolyticus
Journal of Proteome Research ( IF 3.8 ) Pub Date : 2020-10-28 , DOI: 10.1021/acs.jproteome.0c00361 Chen Ye 1 , Yongze Ge 1 , Yue Zhang 1 , Lantian Zhou 1 , Wei Chen 1 , Xuan Zhu 1 , Jianyi Pan 1
Journal of Proteome Research ( IF 3.8 ) Pub Date : 2020-10-28 , DOI: 10.1021/acs.jproteome.0c00361 Chen Ye 1 , Yongze Ge 1 , Yue Zhang 1 , Lantian Zhou 1 , Wei Chen 1 , Xuan Zhu 1 , Jianyi Pan 1
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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 (Δvp0057) 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 Δvp0057 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 Δvp0057 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 Δvp0057 provides a promising starting point for the intensive exploration of VP0057.
中文翻译：
vp0057（一种编码Ser / Thr蛋白激酶的基因）的缺失会影响蛋白质组并促进铁吸收和副溶血性弧菌的竞争优势。
海洋细菌病原体副溶血弧菌是食源性胃肠炎的主要原因。最近的发现表明，蛋白质磷酸化是调节致病细菌中许多生理过程（包括细菌毒力）的基础。但是，其潜在机制仍有待完全阐明。使用生物信息学分析，我们发现VP0057可能是具有磷酸化活性的潜在Ser / Thr蛋白激酶。因此，我们从野生型副溶血弧菌血清型O3：K6构建了vp0057-缺失突变体（Δvp0057），并采用了基于质谱的蛋白质组学策略来表征响应vp0057的蛋白质组范围内的变化由于VP0057在副溶血性弧菌中的潜在作用，导致缺失。与野生型相比，在Δvp0057菌株中鉴定到了一百七十七个差异表达的蛋白质，其中135个蛋白质被上调，而62个蛋白质被下调。对这些差异表达的蛋白质进行了详细注释。值得注意的是，Δvp0057菌株中铁相关蛋白和T6SS1相关蛋白被上调，从而通过定量PCR证实了结果。进一步的实验证明，vp0057缺失可促进Fe 2+和Fe 3+摄取并提供增长竞争优势，这分别受铁相关蛋白和T6SS1相关蛋白控制。尽管VP0057的调节作用和机制在副溶血性弧菌中仍有待揭示，但我们对Δvp0057蛋白质谱的系统分析为深入探索VP0057提供了有希望的起点。
更新日期：2021-01-01
中文翻译：
vp0057（一种编码Ser / Thr蛋白激酶的基因）的缺失会影响蛋白质组并促进铁吸收和副溶血性弧菌的竞争优势。
海洋细菌病原体副溶血弧菌是食源性胃肠炎的主要原因。最近的发现表明，蛋白质磷酸化是调节致病细菌中许多生理过程（包括细菌毒力）的基础。但是，其潜在机制仍有待完全阐明。使用生物信息学分析，我们发现VP0057可能是具有磷酸化活性的潜在Ser / Thr蛋白激酶。因此，我们从野生型副溶血弧菌血清型O3：K6构建了vp0057-缺失突变体（Δvp0057），并采用了基于质谱的蛋白质组学策略来表征响应vp0057的蛋白质组范围内的变化由于VP0057在副溶血性弧菌中的潜在作用，导致缺失。与野生型相比，在Δvp0057菌株中鉴定到了一百七十七个差异表达的蛋白质，其中135个蛋白质被上调，而62个蛋白质被下调。对这些差异表达的蛋白质进行了详细注释。值得注意的是，Δvp0057菌株中铁相关蛋白和T6SS1相关蛋白被上调，从而通过定量PCR证实了结果。进一步的实验证明，vp0057缺失可促进Fe 2+和Fe 3+摄取并提供增长竞争优势，这分别受铁相关蛋白和T6SS1相关蛋白控制。尽管VP0057的调节作用和机制在副溶血性弧菌中仍有待揭示，但我们对Δvp0057蛋白质谱的系统分析为深入探索VP0057提供了有希望的起点。
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