青枯菌对植物的致病机制及其调节

青枯菌引起许多植物及林木青枯病。该菌侵染植物根部,首先在根皮层细胞间隙等处定殖,然后入侵维管束,在木质部导管内扩展危害;细菌在导管及相邻组织内迅猛增殖和广泛散布,由此产生输水管道的阻塞和破坏并最终导致植物枯萎。胞外多糖(EPSI)、细胞壁分解酶(主要是果胶质酶和纤维素酶)、Ⅲ型Hrp分泌系统产物是主要的致病因子,其中EPSI尤为突出,它在保护细菌、促进细菌移动和定殖以及堵塞和破坏寄主导管方面都起着重要作用。而上述致病因子的协调作用则由一复杂的调节系统控制,这一系统由随细菌密度变化而变化的3 -羟基棕榈酸甲基酯水平作为信号,以PhcA调节基因的启动和转录为核心,自动而精密地调节病菌有关致病基因的表达及关闭,并由此控制细菌的生长状态。

The Mechanism of Pathogenicity and Its Regulation of Ralstonia solanacearum to Plants

Ralstonia solanacearum caused bacterial wilt on a variety of plants and trees. The pathogenic bacteria first invaded roots of hosts, aggregated in the intercellular spaces of cortex tissues, and then ingressed into vascular bundles and spread in xylem vessels to induce the wilt symptom. The rapid dispersal and extensive colonization of plant water conducting element which lead to the occlusion and rupture of the vessels, were the main reasons of wilting of plants. Extrapolysaccharide (EPSI), cell wall degrading enzymes such as pectinolytic and cellalolytic enzymes, products of type hrp III section system and the mobility of bacteria constituted the major factors for the pathogenicity. Among these, EPSI was particularly important. It acted to protect the bacteria from host defense reaction, facilitate the movement and colonization of bacteria, occlude and break xylem vessels of hosts. The coordinated functioning of these pathogenic factors was controlled by a sophisticated auto_regulation system initiated by 3-OH palmitic acid methyl ester whose concentration varies according to the density of bacteria. The system used PhcA concentration as a core to regulate the expression of pathogenic factors, and thus the growth state of bacteria.