The enigmatic avirulence genes of phytopathogenic bacteria.

Abstract

The previous chapters have discussed how phytopathogenic bacteria can sense and respond to conditions present in a variety of microenvironments: soil, water, plant cell surfaces, and intracellular spaces. The switch from epiphyte to pathogen is apparently accompanied by fundamental reprogramming of gene activity and attendant function, as evidenced by induction of hrp genes and subsequent production of various virulence and pathogenicity factors, some of which are hostspecific, some not. This reprogramming switch between epiphytic and pathogenic growth strategies, “the pathogenic cusp” (DANGL 1994), is the point at which not only the potential pathogen but also the host first sense and respond to each other. A successful plant defense response should be based on surveillance and interdiction before the pathogen has a chance to establish production of the armory of factors which determine successful colonization of that host. It is incumbent on each potential plant host, then, to evolve mechanisms to recognize some factor, preferably one produced at this pathogenic cusp, and to base resistance strategies on early recognition. Thus, an evolutionary tug-of-war is begun: plants evolve to “recognize” a particular isolate of a particular pathogen; variants arise in the pathogen population which are no longer recognized; variants arise in the host population which recognize the new pathogen variant, and the familiar game is afoot. This scenario has apparently given rise to systems of plantpathogen interactions explained genetically by the now well established “gene-for-gene” hypothesis (reviewed in CRUTE 1985; DANGL 1992; ELLINGBOE 1981; FLOR 1971; GABRIEL and ROLFE 1990; KEEN 1990; KEEN and STASKAWICZ 1988) . During plantmicrobe interactions of this sort, the products, either direct or indirect, of pathogen avirulence (avr) genes trigger a successful host resistance reaction through the action of the product of a particular host resistance (R) gene. These interactions are thus allele-specific: each partner is defined only by the simultaneous presence of the other. The complexity of resistance loci defined genetically is astounding and the paucity of knowledge regarding their structure and function is beginning to be resolved, as evidenced by the recent cloning of the first plant resistance gene of this class (MARTIN et al. 1993) . In contrast, a plethora of avirulence genes from pseudomonads and xanthomonads have been cloned, as discussed in the remainder of this review.