Deletion of vp0057, a Gene Encoding a Ser/Thr Protein Kinase, Impacts the Proteome and Promotes Iron Uptake and Competitive Advantage in Vibrio parahaemolyticus.
Deletion of vp0057, a Gene Encoding a Ser/Thr Protein Kinase, Impacts the Proteome and Promotes Iron Uptake and Competitive Advantage in Vibrio parahaemolyticus.
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vp0057（编码 Ser/Thr 蛋白激酶的基因）的缺失会影响副溶血弧菌的蛋白质组并促进铁吸收和竞争优势。
DOI：
10.1021/acs.jproteome.0c00361
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发表时间：
2020-10
影响因子：
4.4
通讯作者：
Pan Jianyi
中科院分区：
文献类型：
--
作者：
Ye Chen;Ge Yongze;Zhang Yue;Zhou Lantian;Chen Wei;Zhu Xuan;Pan Jianyi
海洋细菌病原体副溶血性弧菌是食源性胃肠炎的主要原因。最近的研究结果表明，蛋白质磷酸化是调节致病细菌中许多生理过程的基础，包括细菌毒力。然而，其基本机制仍有待完全阐明。通过生物信息学分析，我们发现VP 0057可能是一个潜在的具有磷酸化活性的Ser/Thr蛋白激酶。因此，我们从野生型副溶血性弧菌血清型O3：K6中构建了vp 0057缺失突变体（Δ vp 0057），并采用基于质谱的蛋白质组学策略来表征响应于vp 0057缺失的蛋白质组变化，这是由于VP 0057在副溶血性弧菌中的潜在作用。与野生型菌株相比，Δ vp 0057菌株共鉴定出197个差异表达蛋白，其中135个蛋白表达上调，62个蛋白表达下调。对这些差异表达的蛋白质进行了详细的注释。值得注意的是，铁相关和T6 SS 1相关蛋白在Δ vp 0057菌株中上调，证实了定量PCR的结果。进一步的实验证明，vp 0057缺失促进Fe 2+和Fe 3+的吸收，并提供生长竞争优势，这分别由铁相关蛋白和T6 SS 1相关蛋白控制。虽然VP 0057在副溶血性弧菌中的调节作用和机制仍有待揭示，但我们对Δ vp 0057蛋白质谱的系统分析为深入探索VP 0057提供了一个有希望的起点。
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.
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