Abstract:

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.

Key words: Ralstonia solanacearum, plant, pathogenic mechanism