Heat shock proteins IbpA and IbpB are required for NlpI-participated cell division in Escherichia coli.-猫眼课题宝

热休克蛋白 IbpA 和 IbpB 是 NlpI 参与大肠杆菌细胞分裂所必需的

DOI：

10.3389/fmicb.2015.00051

发表时间：

2015

期刊：

Frontiers in microbiology

影响因子：

5.2

通讯作者：

中科院分区：

生物学2区

文献类型：

作者：

Tao J;Sang Y;Teng Q;Ni J;Yang Y;Tsui SK;Yao YF

来源链接：

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4316790/?report=classic

大肠杆菌的脂蛋白 NlpI 参与细胞分裂、毒力以及细菌与真核宿主细胞的相互作用。为了阐明 NlpI 的功能机制，我们研究了 NlpI 如何影响细胞分裂，发现 NlpI 的诱导会抑制类核分裂并停止细胞生长。与这些结果一致，细胞分裂蛋白 FtsZ 未能定位于隔膜，而是扩散到细胞质中。 NlpI 表达的升高增强了热休克蛋白 IbpA 和 IbpB 的转录和外膜定位。 ibpA 或 ibpB 的缺失消除了 NlpI 诱导的作用，这种作用可以通过互补来恢复。 NlpI 的 C 末端对于增强 IbpA 和 IbpB 的产生至关重要，而 NlpI 的 N 末端对于 NlpI、IbpA 和 IbpB 的外膜定位是必需的。此外，NlpI 与 IbpB 发生物理相互作用。这些结果表明，NlpI 的过表达可以中断由 IbpA/IbpB 介导的类核分裂和 FtsZ 在隔膜处的组装，表明 NlpI/IbpA/IbpB 复合物在细胞分裂中的作用。

Lipoprotein NlpI of Escherichia coli is involved in the cell division, virulence, and bacterial interaction with eukaryotic host cells. To elucidate the functional mechanism of NlpI, we examined how NlpI affects cell division and found that induction of NlpI inhibits nucleoid division and halts cell growth. Consistent with these results, the cell division protein FtsZ failed to localize at the septum but diffused in the cytosol. Elevation of NlpI expression enhanced the transcription and the outer membrane localization of the heat shock protein IbpA and IbpB. Deletion of either ibpA or ibpB abolished the effects of NlpI induction, which could be restored by complementation. The C-terminus of NlpI is critical for the enhancement in IbpA and IbpB production, and the N-terminus of NlpI is required for the outer membrane localization of NlpI, IbpA, and IbpB. Furthermore, NlpI physically interacts with IbpB. These results indicate that over-expression of NlpI can interrupt the nucleoids division and the assembly of FtsZ at the septum, mediated by IbpA/IbpB, suggesting a role of the NlpI/IbpA/IbpB complex in the cell division.