Interaction of bacteria and host cell walls: its relation to mechanisms of induced resistance

Abstract

Cells of avirulent (B1) and incompatible (S210) strains of Pseudomonas solanacearum attach readily to the walls of tobacco mesophyll cells. By 4 h after infiltration of tobacco leaves with 10 8 bacterial cells/ml, fibrillar and granular material extruded from the host cell walls and bound by the outer wall layer envelop the attached bacteria. At the site of attachment, the host cell wall is frequently eroded, the plasmalemma separates from the cell wall and becomes convoluted and numerous membrane-bound vesicles accumulate in the space between the plasmalemma and the cell wall. With these bacteria, a hypersensitive reaction (HR) develops by 6 to 12 h after infiltration; as a result, the host cell collapses and organelles are deranged. In contrast, virulent strains of the pathogen (K60) are not attached and remain free to multiply in the intercellular fluid, causing no visible changes in organelle structure during the first 12 h after infiltration. Saprophytic bacteria ( Bacillus subtilis, Escherichia coli) are attached and enveloped, but do not cause a visible HR. When heat-killed B1 cells are infiltrated into tobacco leaves, the dead bacteria attach in the same manner as avirulent, live cells and the initial host cell responses that envelop the bacteria are observed, but there is no cell collapse. After 24 h, challenge inoculation of the pretreated leaves with 10 8 live B1 cells/ml does not result in the HR and these bacteria do not attach to and are not enveloped by the host cell walls. Prevention of the HR appears to be related to this lack of attachment to the host cell walls.