The ubiquitin pathway is required for innate immunity in Arabidopsis

Authors

  • Sandra Goritschnig,

    1. Michael Smith Laboratories, Room 301, 2185 East Mall, University of British Columbia, Vancouver, BC V6T 1Z4, Canada
    2. Department of Botany, Room 3529, 6270 University Blvd., University of British Columbia, Vancouver, BC V6T 1 Z4, Canada
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  • Yuelin Zhang,

    1. Michael Smith Laboratories, Room 301, 2185 East Mall, University of British Columbia, Vancouver, BC V6T 1Z4, Canada
    2. National Institute of Biological Sciences, Zhongguancun Life Science Park, 7 Science Park Road, Beijing 102206, China
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  • Xin Li

    Corresponding author
    1. Michael Smith Laboratories, Room 301, 2185 East Mall, University of British Columbia, Vancouver, BC V6T 1Z4, Canada
    2. Department of Botany, Room 3529, 6270 University Blvd., University of British Columbia, Vancouver, BC V6T 1 Z4, Canada
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(fax +1 604 822 2144; e-mail xinli@interchange.ubc.ca).

Summary

Plant defences require a multitude of tightly regulated resistance responses. In Arabidopsis, the unique gain-of-function mutant suppressor of npr1-1 constitutive 1 (snc1) carries a point mutation in a Resistance (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 suppresses snc1-mediated constitutive resistance is modifier of snc1 5 (mos5), which carries a 15-bp deletion in UBA1, one of two ubiquitin-activating enzyme genes in Arabidopsis. A mutation in UBA2 does not suppress snc1, suggesting that these two genes are not equally required in Arabidopsis disease resistance. On the other hand, a mos5 uba2 double mutant is lethal, implying partial redundancy of the two homologues. Apart from affecting snc1-mediated resistance, mos5 also exhibits enhanced disease susceptibility to a virulent pathogen and is impaired in response to infection with avirulent bacteria carrying the protease elicitor AvrRpt2. The mos5 mutation 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 the SNC1-related R-genes RPP4 and RPP5, are dispensable in snc1-mediated resistance. Our data reveal the definite requirement for the ubiquitination pathway in the activation and downstream signalling of several R-proteins.

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