Ralstonia solanacearum Pectin Methylesterase Is Required for Growth on Methylated Pectin but Not for Bacterial Wilt Virulence
Ralstonia solanacearum Pectin Methylesterase Is Required for Growth on Methylated Pectin but Not for Bacterial Wilt Virulence
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DOI：
10.1128/aem.64.12.4918-4923.1998
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发表时间：
1998-12
影响因子：
4.4
通讯作者：
J. Tans-Kersten;Y. Guan;C. Allen
中科院分区：
文献类型：
--
作者：
J. Tans-Kersten;Y. Guan;C. Allen
青枯病是一种严重危害农作物的病害。该病原体产生几种胞外植物细胞壁降解酶，包括多聚半乳糖醛酸酶（PG）和果胶甲基酯酶（Pme）。Pme从果胶中除去甲基，从而促进随后通过PG（已知的细菌性枯萎病毒力因子）分解该细胞壁组分。R.青枯菌PG不能降解93%的甲基化果胶，除非底物首先被Pme脱甲基，但随着果胶底物甲基化程度的降低，PG活性增加。从已发表的pme序列衍生的引物产生800 bp的DNA探针片段，其鉴定来自R.青枯菌基因组文库一个pmechromosomal突变体在体外没有检测到Pme活性，不再生长在93%甲基化果胶作为碳源。奇怪的是，pme突变体对高度甲基化的果胶没有检测到PG活性，对番茄、茄子和烟草的毒性与野生型菌株一样强。由于PG活性是完全毒力所必需的，因此该结果表明这些特定宿主中的果胶可能不是高度甲基化的，或者高度甲基化果胶的分解通常不是疾病过程中的重要因素。一个积极的响应调节PG生产称为PehR是不需要野生型Pme生产。然而，缺乏PhcA的突变株，这是一个全球性的几个毒力基因的调节器，没有产生可检测的Pme活性。因此，pme表达直接或间接受PhcA调节，但不受PehR调节。
ABSTRACT Ralstonia (Pseudomonas)solanacearum causes bacterial wilt, a serious disease of many crop plants. The pathogen produces several extracellular plant cell wall-degrading enzymes, including polygalacturonases (PGs) and pectin methylesterase (Pme). Pme removes methyl groups from pectin, thereby facilitating subsequent breakdown of this cell wall component by PGs, which are known bacterial wilt virulence factors. R. solanacearum PGs could not degrade 93% methylated pectin unless the substrate was first demethylated by Pme, but as the degree of methylation of the pectin substrate decreased, PG activity increased. Primers derived from a published pme sequence generated an 800-bp DNA probe fragment, which identified Pme-encoding plasmids from a R. solanacearum genomic library. A pmechromosomal mutant had no detectable Pme activity in vitro and no longer grew on 93% methylated pectin as a carbon source. Curiously, the pme mutant, which had no detectable PG activity on highly methylated pectin, was just as virulent as the wild-type strain on tomato, eggplant (aubergine), and tobacco. Since PG activity is required for full virulence, this result suggests that the pectin in these particular hosts may not be highly methylated, or that the breakdown of highly methylated pectin is not a significant factor in the disease process in general. A positive response regulator of PG production called PehR was not required for wild-type Pme production. However, a mutant strain lacking PhcA, which is a global regulator of several virulence genes, produced no detectable Pme activity. Thus,pme expression is directly or indirectly regulated by PhcA but not by PehR.