A novel function for the competence inducing peptide, XIP, as a cell death effector of Streptococcus mutans.
A novel function for the competence inducing peptide, XIP, as a cell death effector of Streptococcus mutans.
复制标题
诱导肽XIP作为链球菌突变的细胞死亡效应的能力的新功能。
DOI：
10.1111/j.1574-6968.2012.02660.x
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发表时间：
2012-11
影响因子：
2.1
通讯作者：
Senadheera DB
中科院分区：
文献类型：
--
作者：
Wenderska IB;Lukenda N;Cordova M;Magarvey N;Cvitkovitch DG;Senadheera DB
在变形链球菌中，ComX（一种替代的西格玛因子）驱动遗传转化所需的“晚期能力基因”的转录。 ComX 活性由来自 ComDE 和 ComRS 两个信号通路的输入调节，这两个信号通路分别响应能力刺激肽 (CSP) 和 SigX 诱导肽 (XIP)。特别是，编码 ComR 调节蛋白和 XIP 的 ComS 前体的 comRS，充当 ComX 激活的近端调节系统。在这里，我们研究了 CSP 和 XIP 对变形链球菌遗传转化和细胞杀伤的单独和组合影响。我们的转化结果证实了 Mashburn-Warren 等人最近的报告。和德赛等人。 XIP 在化学成分确定的培养基 (CDM) 中发挥最佳作用，而当细胞在复杂培养基中生长时，其活性会受到抑制。使用串联质谱 (MS/MS) 裂解，观察到 ComX 缺陷培养物中 XIP 水平急剧降低，这表明 ComX 介导的 XIP 合成正反馈机制。我们对 10μM XIP 存在下的细胞活力进行评估，结果导致近 82% 的细胞死亡。显示杀伤活性取决于 comR/S 和 comX 的存在。这些结果表明 XIP 作为细胞死亡的引人注目的效应物具有新的作用。这是第一份证明 XIP 在细胞杀伤中作用的报告。
In Streptococcus mutans, ComX, an alternative sigma factor, drives the transcription of the “late-competence genes” required for genetic transformation. ComX activity is modulated by inputs from two signaling pathways, ComDE and ComRS, that respond to the competence stimulating peptide (CSP) and the SigX-inducing peptide (XIP), respectively. In particular, the comRS, encoding the ComR regulatory protein and the ComS precursor to XIP, functions as the proximal regulatory system for ComX activation. Here, we investigated the individual and combinatorial effects of CSP and XIP on genetic transformation and cell killing of S. mutans. Our transformation results confirm the recent reports by Mashburn-Warren et al. and Desai et al. that XIP functions optimally in a chemically defined medium (CDM), whereas its activity is inhibited when cells are grown in complex medium. Using tandem mass spectrometry (MS/MS) fragmentation, a drastic reduction in XIP levels in ComX-deficient cultures were observed, suggesting a ComX-mediated positive feedback mechanism for XIP synthesis. Our evaluation of cell viability in the presence of 10μM XIP resulted in the killing nearly 82% of the population. The killing activity was shown to be dependent on the presence of comR/S and comX. These results suggest a novel role for XIP as a compelling effector of cell death. This is the first report that demonstrates a role for XIP in cell killing.