Leigh J A, Coplin D L
Department of Microbiology, University of Washington, Seattle 98195.
Annu Rev Microbiol. 1992;46:307-46. doi: 10.1146/annurev.mi.46.100192.001515.
Rhizobial plant symbionts and bacterial plant pathogens produce exopolysaccharides that often play essential roles in the plant interaction. Many of these exopolysaccharides are acidic heteropolysaccharides that have repeating subunit structures with carbohydrate and noncarbohydrate substituents, while others are homopolysaccharides such as alginate, levan, cellulose, and glucan. While the homopolysaccharides are synthesized by mechanisms that vary with the particular polysaccharide, the heteropolysaccharides as a rule are synthesized by subunit assembly from nucleotide diphosphate-sugar precursors on a membrane-bound lipid carrier followed by polymerization and secretion. Many mutants in exopolysaccharide synthesis have been isolated, and in several cases this has led to the identification of genes that function in particular steps of biosynthesis, as well as in regulation of exopolysaccharide biosynthesis. The genetic regulation of exopolysaccharide synthesis in many plant pathogens is complex, perhaps reflecting the various niches, free living and in planta, in which exopolysaccharides function. In some cases, exopolysaccharide synthesis is regulated coordinately with other virulence factors, and in other cases separately. Regulatory genes that have homology to the two-component sensor and transcriptional effector systems are a common motif. In Rhizobium species, exopolysaccharide synthesis is regulated by transcriptional as well as posttranslational mechanisms. Exopolysaccharides function differently in the root-nodule symbiosis versus plant pathogenesis. Specific Rhizobium exopolysaccharide structures promote nodule development and invasion in legumes that form indeterminate nodules. In plant pathogenesis, less specific mechanisms of pathogenesis occur: exopolysaccharides cause wilting by blocking xylem vessels, are partly responsible for water-soaked lesions, and may also aid in invasion, growth, and survival in plant tissues.
根瘤菌植物共生体和植物病原细菌会产生胞外多糖，这些胞外多糖在与植物的相互作用中常常发挥着至关重要的作用。其中许多胞外多糖是酸性杂多糖，具有带有碳水化合物和非碳水化合物取代基的重复亚基结构，而其他的则是同多糖，如藻酸盐、果聚糖、纤维素和葡聚糖。虽然同多糖的合成机制因特定多糖而异，但杂多糖通常是通过在膜结合脂质载体上由二磷酸核苷糖前体进行亚基组装，随后进行聚合和分泌来合成的。已经分离出许多胞外多糖合成的突变体，在一些情况下，这导致了对在生物合成特定步骤以及胞外多糖生物合成调控中起作用的基因的鉴定。许多植物病原体中胞外多糖合成的遗传调控很复杂，这可能反映了胞外多糖发挥作用的各种生态位，包括自由生活和在植物体内的生态位。在某些情况下，胞外多糖的合成与其他毒力因子协同调控，而在其他情况下则单独调控。与双组分传感器和转录效应器系统具有同源性的调控基因是一个常见的基序。在根瘤菌属中，胞外多糖的合成受转录以及翻译后机制的调控。胞外多糖在根瘤共生与植物发病机制中的功能不同。特定的根瘤菌胞外多糖结构促进形成不定根瘤的豆科植物中的根瘤发育和侵染。在植物发病机制中，发病机制不那么特异：胞外多糖通过阻塞木质部导管导致萎蔫，部分导致水渍状病斑，还可能有助于在植物组织中的侵染、生长和存活。
