Loss of co-chaperone TopJ impacts adhesin P1 presentation and terminal organelle maturation in Mycoplasma pneumoniae.
Loss of co-chaperone TopJ impacts adhesin P1 presentation and terminal organelle maturation in Mycoplasma pneumoniae.
复制标题
DOI：
10.1111/j.1365-2958.2011.07712.x
复制
发表时间：
2011-07
影响因子：
3.6
通讯作者：
Krause DC
中科院分区：
文献类型：
--
作者：
Cloward JM;Krause DC
肺炎支原体（Mycoplasma pneumoniae）是一种无壁的人类呼吸道病原体，其通过具有中央电子致密核心和聚集在末端按钮处的粘附素相关蛋白的极性末端细胞器来定殖于粘膜上皮。缺乏J结构域共伴侣TopJ的突变体是非细胞粘附和非运动的，尽管具有核心和正常水平的主要细胞粘附相关蛋白。J结构域共分子伴侣与DnaK一起催化多肽结合和随后的蛋白质折叠。在这里，我们比较了功能的topJ突变体与其他cytadherence突变体，以阐明TopJ的cytadherence功能的贡献。topJ突变体的超微结构相似的非cytadherent突变体缺乏终端细胞器蛋白B/C，包括异常的核心定位和细胞形态在薄切片，但表现出一个混合卫星生长模式的突变体的功能都有和缺乏一个核心。表达YFP与末端细胞器蛋白P41融合的支原体的延时图像表明，在没有TopJ的情况下，末端细胞器形成/定位延迟或与细胞生长协调不良。TopJ需要一个本地化核心，可能涉及HMW 1。P1胰蛋白酶对其他非cytadherent突变体的可及性显着增强野生型，但出乎意料的是减少与topJ突变细胞，这表明受损的加工，易位，和/或折叠这种粘附素。
Mycoplasma pneumoniae is a wall-less human respiratory tract pathogen that colonizes mucosal epithelium via a polar terminal organelle having a central electron-dense core and adhesin-related proteins clustered at a terminal button. A mutant lacking J-domain co-chaperone TopJ is noncytadherent and nonmotile, despite having a core and normal levels of the major cytadherence-associated proteins. J-domain co-chaperones work with DnaK to catalyze polypeptide binding and subsequent protein folding. Here we compared features of the topJ mutant with other cytadherence mutants to elucidate the contribution of TopJ to cytadherence function. The topJ mutant was similar ultrastructurally to a non-cytadherent mutant lacking terminal organelle proteins B/C, including aberrant core positioning and cell morphology in thin sections, but exhibited a hybrid satellite growth pattern with features of mutants both having and lacking a core. Time-lapse images of mycoplasmas expressing a YFP fusion with terminal organelle protein P41 suggested that terminal organelle formation/positioning was delayed or poorly coordinated with cell growth in the absence of TopJ. TopJ required a core for localization, perhaps involving HMW1. P1 trypsin accessibility on other non-cytadherent mutants was significantly enhanced over wild-type but unexpectedly was reduced with topJ mutant cells, suggesting impaired processing, translocation, and / or folding of this adhesin.
登录
查看更多内容
DOI：
10.1099/00221287-136-3-471
发表时间：
1990-03-01
期刊：
JOURNAL OF GENERAL MICROBIOLOGY
影响因子：
--
作者：
GERSTENECKER, B;JACOBS, E
通讯作者：
JACOBS, E
影响因子：
3.2
作者：
Hasselbring, BM;Jordan, JL;Krause, DC
通讯作者：
Krause, DC
DOI：
10.1099/00221287-139-1-95
发表时间：
1993-01-01
期刊：
JOURNAL OF GENERAL MICROBIOLOGY
影响因子：
--
作者：
BUKAU, B;REILLY, P;WALKER, GC
通讯作者：
WALKER, GC
DOI：
10.1073/pnas.0608051103
发表时间：
2006-10-31
影响因子：
11.1
作者：
Hasselbring, Benjamin M.;Jordan, Jarrat L.;Krause, Duncan C.
通讯作者：
Krause, Duncan C.
影响因子：
3.1
作者：
FRANZOSO, G;HU, PC;BARILE, MF
通讯作者：
BARILE, MF