Since the beginning of resistance breeding, protection of plants against pathogens has relied on specific resistance genes encoding rapid tissue death. Our work has demonstrated in different host–pathogen relationships that plants can defend themselves against pathogens by cell growth and cell division. We first demonstrated this general defence response (GDR) in plants by identifying the gds gene in pepper. Subsequently, the existence of a genetic system for tissue defence became apparent and we set the goal to analyse it. The gdr 1 + 2 genes, which operate the complete GDR system, protect plant tissues from pathogens in a direcessive homozygous state in both host and non-host relationships. The inheritance pattern of the two genes follows a 12:3:1 cleavage of the dominant epistasis. With the knowledge of the gds and gdr 1 + 2 genes, the role of tissue-preserving (GDR) and tissue-destructive (HR) pathways in disease development and their relationship was determined. The genes encoding the general defence response have a low stimulus threshold and are not tissue-destructive and pathogen-specific. They are able to fulfil the role of the plant immune system by providing a general response to various specific stresses. This broad-spectrum general defence system is the most effective in the plant kingdom.

Pepper (Capsicum annuum L.) carrying the gds (corresponding to bs5) gene can prevent the development of bacterial leaf spot disease without HR. However, little is known regarding the development of the resistance mechanism encoded by gds, especially its influence on the bacterium. Here, the effect of gds was compared with pattern-triggered immunity (PTI), another form of asymptomatic resistance, to reveal the interactions and differences between these two defense mechanisms. The level of resistance was examined by its effect on the bacterial growth and in planta expression of the stress and pathogenicity genes of Xanthomonas euvesicatoria. PTI, which was activated with a Pseudomonas syringae hrcC mutant pretreatment, inhibited the growth of Xanthomonas euvesicatoria to a greater extent than gds, and the effect was additive when PTI was activated in gds plants. The stronger influence of PTI was further supported by the expression pattern of the dpsA bacterial stress gene, which reached its highest expression level in PTI-induced plants. PTI inhibited the hrp/hrc expression, but unexpectedly, in gds plant leaves, the hrp/hrc genes were generally expressed at a higher level than in the susceptible one. These results imply that different mechanisms underlie the gds and PTI to perform the symptomless defense reaction.