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  • The EMBO Journal (2003) 22, 5690 - 5699
  • doi:10.1093/emboj/cdg546

High throughput virus-induced gene silencing implicates heat shock protein 90 in plant disease resistance

Rui Lu2, Isabelle Malcuit1, Peter Moffett1, Maria T. Ruiz3, Jack Peart1, Ai-Jiuan Wu1, John P. Rathjen1, Abdelhafid Bendahmane4, Louise Day1 and David C. Baulcombe1

  1. The Sainsbury Laboratory, John Innes Centre, Colney Lane, Norwich NR4 7UH, UK
  2. Present address: Department of Plant Pathology, University of California, Riverside, 900 University Avenue, Riverside, CA 92521, USA
  3. Present address: Instituto de Bioquímica Vegetal y Fotosíntesis, Avenida Americo Vespucio s/n, 41092-Sevilla, Spain
  4. Present address: INRA-URGV, 2 Rue Gaston Cremieux CP 5708, 91057 Evry Cedex, France

Correspondence to:

David C. Baulcombe, E-mail: baulcombe@sainsbury-laboratory.ac.uk

Received 28 May 2003; Accepted 4 September 2003; Revised 2 September 2003

Virus-induced gene silencing was used to assess the function of random Nicotiana benthamiana cDNAs in disease resistance. Out of 4992 cDNAs tested from a normalized library, there were 79 that suppressed a hypersensitive response (HR) associated with Pto-mediated resistance against Pseudomonas syringae. However, only six of these clones blocked the Pto-mediated suppression of P.syringae growth. The three clones giving the strongest loss of Pto resistance had inserts corresponding to HSP90 and also caused loss of Rx-mediated resistance against potato virus X and N-mediated tobacco mosaic virus resistance. The role of HSP90 as a cofactor of disease resistance is associated with stabilization of Rx protein levels and could be accounted for in part by SGT1 and other cofactors of disease resistance acting as co-chaperones. This approach illustrates the potential benefits and limitations of RNA silencing in forward screens of gene function in plants.

  • Keywords:

    • gene silencing,
    • HSP90,
    • plant disease,
    • resistance