The endo-beta-1,4-glucanase CelA of Clavibacter michiganensis subsp. michiganensis is a pathogenicity determinant required for induction of bacterial wilt of tomato.
The endo-beta-1,4-glucanase CelA of Clavibacter michiganensis subsp. michiganensis is a pathogenicity determinant required for induction of bacterial wilt of tomato.
复制标题
密歇根棒状杆菌亚种的内切 β-1,4-葡聚糖酶 CelA。
DOI：
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发表时间：
2000
影响因子：
3.5
通讯作者：
R. Eichenlaub
中科院分区：
文献类型：
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作者：
H. Jahr;J. Dreier;D. Meletzus;R. Bahro;R. Eichenlaub
植物病原细菌Clavibacter michiganensis subsp. michiganensisNCPPB 382含有两个质粒pCM 1（27.35kb）和pCM 2（72 kb），分别编码与番茄青枯病和溃疡病有关的毒力基因（D. Meletzus，A. Bempohl，J. Dreier，and R. Eichenlaub，1993，J. Bacteriol. 175：2131-2136; J. Dreier，D. Meletzus，和R. Eichenlaub，1997，Mol.植物-微生物相互作用10：195-206）。通过缺失分析和互补分析，定位了携带内切葡聚糖酶基因celA的pCM 1区域。RNA杂交鉴定了celA结构基因的2.4-knt（kilobenzide）转录本，并绘制了转录起始位点。celA基因编码CelA，CelA是一种78 kDa（746个氨基酸）的蛋白质，与A1家族纤维素酶的内切-β-1，4-葡聚糖酶相似。CelA具有催化结构域、IIa型纤维素结合结构域和C末端结构域的三结构域结构。我们目前的证据表明，CelA在致病性中起着重要作用，因为枯萎病诱导能力是通过在无质粒，无毒力菌株中表达内切葡聚糖酶和通过CelA基因置换突变体CMM-H4与野生型celA基因互补获得的。
The phytopathogenic bacterium Clavibacter michiganensis subsp. michiganensis NCPPB382, which causes bacterial wilt and canker of tomato, harbors two plasmids, pCM1 (27.35 kb) and pCM2 (72 kb), encoding genes involved in virulence (D. Meletzus, A. Bermpohl, J. Dreier, and R. Eichenlaub, 1993, J. Bacteriol. 175:2131-2136; J. Dreier, D. Meletzus, and R. Eichenlaub, 1997, Mol. Plant-Microbe Interact. 10:195-206). The region of pCM1 carrying the endoglucanase gene celA was mapped by deletion analysis and complementation. RNA hybridization identified a 2.4-knt (kilonucleotide) transcript of the celA structural gene and the transcriptional initiation site was mapped. The celA gene encodes CelA, a protein of 78 kDa (746 amino acids) with similarity to endo-beta-1,4-glucanases of family A1 cellulases. CelA has a three-domain structure with a catalytic domain, a type IIa-like cellulose-binding domain, and a C-terminal domain. We present evidence that CelA plays a major role in pathogenicity, since wilt induction capability is obtained by endoglucanase expression in plasmid-free, nonvirulent strains and by complementation of the CelA- gene-replacement mutant CMM-H4 with the wild-type celA gene.