Plant defences require a multitude of tightly regulated resistance responses. In Arabidopsis, the unique gain-of-function mutantsuppressor of npr1–1 constitutive 1(snc1) carries a point mutation in aResistance(R)-gene, resulting in constitutive activation of defence responses without interaction with pathogens. This has allowed us to identify various downstream signalling components essential in multiple defence pathways. One mutant that suppressessnc1-mediated constitutive resistance ismodifier of snc1 5(mos5), which carries a 15-bp deletion inUBA1, one of two ubiquitin-activating enzyme genes in Arabidopsis. A mutation inUBA2does not suppresssnc1, suggesting that these two genes are not equally required in Arabidopsis disease resistance. On the other hand, amos5 uba2double mutant is lethal, implying partial redundancy of the two homologues. Apart from affectingsnc1-mediated resistance,mos5also exhibits enhanced disease susceptibility to a virulent pathogen and is impaired in response to infection with avirulent bacteria carrying the protease elicitor AvrRpt2. Themos5mutation in the C-terminus of UBA1 might affect binding affinity of the downstream ubiquitin-conjugating enzymes, thus perturbing ubiquitination of target proteins. Furthermore, SGT1b and RAR1, which are necessary for resistance conferred by theSNC1-relatedR-genesRPP4andRPP5, are dispensable insnc1-mediated resistance. Our data reveal the definite requirement for the ubiquitination pathway in the activation and downstream signalling of several R-proteins.