Abstract
Leaves of soybean cultivars Clark (susceptible) and Clark 63 (resistant) were inoculated by infiltration with virulent or avirulent strains of X. campestris pv. [pathovar] glycines, the causal agent of bacterial pustule disease of soybean, and with X. campestris pv. campestris, a pathogen of crucifers. Ultrastructure of infected leaves was studied at 26, 48 and 72 h after inoculation. Virulent strains of X. c. pv. glycines exhibited rapid growth in vivo and remained free in the intercellular spaces of Clark and Clark 63. The incompatible strains exhibited restricted growth, induced a moderate to strong hypersensitive response evidenced by browning of leaf laminae, and were immobilized to varying degrees by fibrillar or electron-dense amorphous material on the surface of leaf mesophyll cells. The extent of bacterial immobilization was inversely related to bacterial growth. Heat-killed cells of virulent or avirulent strains of X. c. pv. glycines were also immobilized. Other host cell responses to incompatible strains of X. campestris included invagination of host plasmalemma, accumulation of vesicles and amorphous material between host plasmalemma and cell wall, migration and disorientation of thylakoid membrane systems in chloroplasts, and host cell necrosis. Host cell responses to virulent strains of X. c. pv. glycines included dilation of endoplasmic reticulum, appearance of lucent vesicles within the cytoplasm, a change in chloroplast morphology to a more rounded shape and migration of chloroplasts away from the host plasmalemma. The results indicated that active immobilization is a primary or secondary defense response of soybean against incompatible xanthomonads.