Fukuda A, Okada Y
J Bacteriol. 1977 Jun;130(3):1199-205. doi: 10.1128/jb.130.3.1199-1205.1977.
The Caulobacter polar surface structures (flagella, pili, and the deoxyribonucleic acid phage phiCbK receptors), which are expressed at proximal sites of swarmer cells in a coordinate manner (Shapiro, Annu. Rev. Microbiol., 30:377-407, 1976) could be blocked by a single mutation. The mutant C. crescentus CB13 ple-801 did not form these surface structures when grown at 35 degrees C. Upon shift down to 25 degrees C, the mutant cells initiated the formation of the surface structures. When mitomycin C was added to the mutant culture upon shift down from 35 to 25 degrees C, phiCbK receptor formation was inhibited to a minimal level. Rifampin and chloramphenicol completely inhibited phiCbK receptor formation when added to the mutant culture upon shift down. Deoxyribonucleic acid as well as ribonucleic acid and protein synthesis seem to be required for the formation of phiCbK receptors. Penicillin V also inhibited phiCbK receptor formation, indicating the involvement of cell wall synthesis. When the mutant CB13 ple-801 cells were shifted down briefly from 35 to 25 degrees C and then shifted up to 35 degrees C, flagella and phiCbK receptors were formed even at 35 degrees C to different extents depending on how long the cells were incubated at 25 degrees C. This formation of the surface structures at 35 degrees C was inhibited by rifampin. From these results, it appears that translation, assembly, or localization processes for the formation of the surface structures are not temperature sensitive at 35 degrees C in the pleiotropic mutant CB13 ple-801. The syntheses of deoxyribonucleic acid and the cell wall do not appear to be temperature sensitive either, since the mutant grows normally at 35 degrees C. It is suggested that there exists a regulatory step that commits the cells to initiate the synthesis of requisite ribonucleic acid for the formation of the polar surface structures.
新月柄杆菌的极性表面结构(鞭毛、菌毛和脱氧核糖核酸噬菌体phiCbK受体)以协调的方式在游动细胞的近端位点表达(夏皮罗,《微生物学年评》,30:377 - 407,1976),可被单一突变阻断。突变型新月柄杆菌CB13 ple - 801在35℃生长时不形成这些表面结构。当温度降至25℃时,突变细胞开始形成表面结构。当在从35℃降至25℃时向突变培养物中添加丝裂霉素C,phiCbK受体的形成被抑制到最低水平。当在温度下降时向突变培养物中添加利福平或氯霉素,phiCbK受体的形成被完全抑制。脱氧核糖核酸以及核糖核酸和蛋白质合成似乎是phiCbK受体形成所必需的。青霉素V也抑制phiCbK受体的形成,表明细胞壁合成参与其中。当突变型CB13 ple - 801细胞从35℃短暂降至25℃,然后再升至35℃时,即使在35℃也会形成鞭毛和phiCbK受体,其形成程度不同,这取决于细胞在25℃孵育的时间长短。在35℃时表面结构的这种形成被利福平抑制。从这些结果来看,在多效性突变体CB13 ple - 801中,表面结构形成的翻译、组装或定位过程在35℃时对温度不敏感。脱氧核糖核酸和细胞壁的合成似乎对温度也不敏感,因为该突变体在35℃时生长正常。有人提出存在一个调控步骤,使细胞开始合成形成极性表面结构所需的核糖核酸。