Meletzus D, Bermphol A, Dreier J, Eichenlaub R
Fakultät für Biologie, Gentechnologie/Mikrobiologie, Universität Bielefeld, Germany.
J Bacteriol. 1993 Apr;175(7):2131-6. doi: 10.1128/jb.175.7.2131-2136.1993.
The tomato pathogen Clavibacter michiganensis subsp. michiganensis NCPPB382, which causes bacterial wilt, harbors two plasmids pCM1 (27.5 kb) and pCM2 (72 kb). After curing of the plasmids, bacterial derivatives were still proficient in the ability to colonize the host plant and in the production of exopolysaccharides but exhibited a reduced virulence. When one of the two plasmids is lost, there is a significant delay in the development of wilting symptoms after infection and a plasmid-free derivative is not able to induce disease symptoms. By cloning of restriction fragments of both plasmids in the plasmid-free strain CMM100, two DNA fragments which restored the virulent phenotype were identified. Further analysis suggested that a fragment of plasmid pCM1 encodes an endocellulase which is involved in the expression of the pathogenic phenotype.
番茄病原菌密歇根棒杆菌密歇根亚种NCPPB382可引发细菌性枯萎病,它含有两个质粒pCM1(27.5 kb)和pCM2(72 kb)。质粒消除后,细菌衍生物在定殖宿主植物的能力以及胞外多糖的产生方面仍表现良好,但毒力有所降低。当丢失两个质粒中的一个时,感染后枯萎症状的发展会显著延迟,且无质粒衍生物无法诱导疾病症状。通过将两个质粒的限制性片段克隆到无质粒菌株CMM100中,鉴定出了两个恢复毒力表型的DNA片段。进一步分析表明,质粒pCM1的一个片段编码一种内切纤维素酶,该酶参与致病表型的表达。