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CccS 和 CccP 参与构建集胞藻 PCC 6803 细胞表面成分。

CccS and CccP are involved in construction of cell surface components in the cyanobacterium Synechocystis sp. strain PCC 6803.

机构信息

Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo. 153-8902 Japan.

出版信息

Plant Cell Physiol. 2010 Jul;51(7):1163-72. doi: 10.1093/pcp/pcq081. Epub 2010 Jun 10.

Abstract

We have previously identified two target genes (slr1667 and slr1668) for transcriptional regulation by a cAMP receptor protein, SYCRP1, in a cAMP-dependent manner. For this study we investigated the localizations of products of slr1667 and slr1668 (designated cccS and cccP, respectively) biochemically and immunocytochemically, and examined the phenotypes of their disruptants. CccS protein was detected in the culture medium and the acid-soluble fraction containing proteins derived from outside the outer membrane. Disruptants of cccS and cccP showed a more or less similar pleiotropic phenotype. Several proteins secreted into the culture medium or retained on the outside of the outer membrane were greatly reduced in both disruptants compared with the wild type. Electron microscopy revealed that the cccS disruptant lacked the thick pili responsible for motility and that the cccP disruptant had almost no discernible thick pili on its cell surface. Both disruptants largely secreted far greater amounts of yellow pigments into the culture medium than did the wild type. Furthermore, the disruptions reduced the amount of UV-absorbing compound(s) extractable from the exopolysaccharide layer. These results suggest that the cccS and cccP genes are involved in the construction of cell surface components in Synechocystis sp. strain PCC 6803.

摘要

我们之前已经确定了两个靶基因(slr1667 和 slr1668),它们可以通过 cAMP 受体蛋白 SYCRP1 以 cAMP 依赖性的方式进行转录调控。在这项研究中,我们通过生物化学和免疫细胞化学的方法研究了 slr1667 和 slr1668 产物(分别命名为 cccS 和 cccP)的定位,并检测了它们的缺失突变体的表型。CccS 蛋白被检测到在培养基和酸可溶部分中,该部分含有来源于外膜之外的蛋白质。cccS 和 cccP 的缺失突变体表现出或多或少相似的表型。与野生型相比,这两种缺失突变体中分泌到培养基中的几种蛋白质或保留在外膜外的蛋白质大大减少。电子显微镜显示,cccS 缺失突变体缺乏负责运动的厚鞭毛,而 cccP 缺失突变体在其细胞表面几乎没有可识别的厚鞭毛。这两种缺失突变体在培养基中分泌的黄色素量大大超过了野生型。此外,缺失突变降低了从胞外多糖层中提取的紫外线吸收化合物的量。这些结果表明,cccS 和 cccP 基因参与了 Synechocystis sp. PCC 6803 细胞表面成分的构建。

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