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鼠疫耶尔森氏菌热休克和冷休克刺激物的DNA微阵列分析

DNA microarray analysis of the heat- and cold-shock stimulons in Yersinia pestis.

作者信息

Han Yanping, Zhou Dongsheng, Pang Xin, Zhang Ling, Song Yajun, Tong Zongzhong, Bao Jingyue, Dai Erhei, Wang Jin, Guo Zhaobiao, Zhai Junhui, Du Zongmin, Wang Xiaoyi, Wang Jian, Huang Peitang, Yang Ruifu

机构信息

Laboratory of Analytical Microbiology, National Center for Biomedical Analysis, Army Center for Microbial Detection and Research, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS), Beijing 100071, China.

出版信息

Microbes Infect. 2005 Mar;7(3):335-48. doi: 10.1016/j.micinf.2004.11.005. Epub 2005 Feb 10.

Abstract

DNA microarray was used as a tool to define the heat- and cold-shock stimulons in Yersinia pestis. Heat shock dramatically enhanced the transcription of genes encoding major heat-shock proteins (MHSPs) that are important for cell survival against the heat. Many other genes were also greatly up-regulated, but their roles in heat-shock response need to be elucidated. Meanwhile, heat shock retarded most of the metabolic processes, i.e. RNA transcription, protein translation, aerobic respiration, energy metabolism, small molecule metabolism, peptidoglycan biosynthesis, sulfate uptake and cysteine biosynthesis. In response to cold shock, Y. pestis has evolved complex adaptive mechanisms by elevating the transcription of a specific set of genes whose protein products are designed to prevent or eliminate cold-induced DNA or RNA structuring, to remodel cell membrane components for maintenance of normal functions, to elevate the energy generation for ensuring ATP-dependent responses during cold adaptation and to synthesize or transport compatible solutes such as cryoprotectants, and at the same time, by repressing the mRNA level of certain genes whose protein products are not needed for bacterial growth at low temperatures, such as the MHSPs. These results provide a set of new candidate genes for hypothesis-based investigations of their roles in stress response, host adaptation and pathogenicity of this deadly pathogen.

摘要

DNA微阵列被用作一种工具来定义鼠疫耶尔森菌中的热休克和冷休克刺激子。热休克显著增强了编码主要热休克蛋白(MHSPs)的基因的转录,这些蛋白对于细胞在热应激下的存活至关重要。许多其他基因也被大幅上调,但其在热休克反应中的作用有待阐明。同时,热休克阻碍了大多数代谢过程,即RNA转录、蛋白质翻译、有氧呼吸、能量代谢、小分子代谢、肽聚糖生物合成、硫酸盐摄取和半胱氨酸生物合成。响应冷休克时,鼠疫耶尔森菌通过提高一组特定基因的转录来进化出复杂的适应性机制,这些基因的蛋白质产物旨在防止或消除冷诱导的DNA或RNA结构形成、重塑细胞膜成分以维持正常功能、提高能量生成以确保在冷适应过程中依赖ATP的反应以及合成或运输相容性溶质如低温保护剂,同时,通过抑制某些基因的mRNA水平,这些基因的蛋白质产物在低温下对细菌生长并非必需,例如MHSPs。这些结果为基于假设研究它们在这种致命病原体的应激反应、宿主适应和致病性中的作用提供了一组新的候选基因。

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