Turnip crinkle virus (TCV) inoculation onto TCV-resistant Arabidopsis leads to a hypersensitive response (HR) controlled by the dominant gene HRT . HRT is a member of the class of resistance ( R ) genes that contain a leucine zipper, a nucleotide binding site, and leucine-rich repeats. The chromosomal position of HRT and its homology to resistance gene RPP8 and two RPP8 homologs indicate that unequal crossing over and gene conversion may have contributed to HRT evolution. RPP8 confers resistance to an oomycete pathogen, Peronospora parasitica . Despite very strong similarities within the HRT/RPP8 family, HRT and RPP8 are specific for the respective pathogens they detect. Hence, the HRT/ RPP8 family provides molecular evidence that sequence changes between closely related members of multigene families can generate novel specificities for radically different pathogens. Transgenic plants expressing HRT developed an HR but generally remained susceptible to TCV because of a second gene, RRT , that regulates resistance to TCV. However, several transgenic plants that overexpressed HRT produced micro-HRs or no HR when inoculated with TCV and were resistant to infection. Expression of the TCV coat protein gene in seedlings containing HRT resulted in massive necrosis and death, indicating that the avirulence factor detected by the HRT -encoded protein is the TCV coat protein.
INTRODUCTIONTo survive, plants must defend themselves against numerous pathogens. Some defenses are constitutive, such as various preformed antimicrobial compounds (Osbourn, 1996), whereas others are activated by recognition of pathogens (Hammond-Kosack and Jones, 1996;Yang et al., 1997). The key players in this recognition process include the product of a dominant or semidominant resistance ( R ) gene present in the plant and the corresponding dominant avirulence (Avr) factor encoded by or derived from the pathogen. Recognition of the Avr factor by the host plant initiates one or more signal transduction pathways that activate various plant defenses and thus compromise the ability of the pathogen to colonize the plant. In this gene-for-gene interaction, the prevailing thought is that the R protein either acts directly as the receptor of the Avr factor (Ellingboe, 1980; Bent, 1996;Yang et al., 1997) or recognizes the Avr factor indirectly through a coreceptor (Dixon et al., 1998). To date, direct interaction between an R protein and an Avr factor has been demonstrated only for the tomato Pto and the Pseudomonas syringae AvrPto proteins (Scofield et al., 1996;Tang et al., 1996) and between the rice Pi-ta and the Magnaporthe grisea AvrPita proteins (Jia et al., 1999).An array of R genes that provide protection against viruses, bacteria, fungi, and oomycetes has been cloned from both monocots and dicots during the past 6 years (Staskawicz et al., 1995; Bent, 1996; Baker et al., 1997; DeWit, 1997). Many contain a nucleotide binding site (NBS). Often located closer to the N terminus of the R protein is either a leucine zipper or a TIR domain, which is sim...