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PLANTS INTERACTING WITH OTHER ORGANISMS

The Role of Salicylic Acid in the Induction of Cell Death in Arabidopsis acd11¹

Institute of Molecular Biology, Copenhagen University, DK–1353 Copenhagen, Denmark (P.B., F.G.M., K.H., J.M.); and Institute of Plant Biology, Royal Veterinary and Agricultural University, DK–1871 Frederiksberg, Denmark (M.-A.N.)

Salicylic acid (SA) is implicated in the induction of programmed cell death (PCD) associated with pathogen defense responses because SA levels increase in response to PCD-inducing infections, and PCD development can be inhibited by expression of salicylate hydroxylase encoded by the bacterial nahG gene. The acd11 mutant of Arabidopsis (Arabidopsis thaliana L. Heynh.) activates PCD and defense responses that are fully suppressed by nahG. To further study the role of SA in PCD induction, we compared phenotypes of acd11/nahG with those of acd11/eds5-1 and acd11/sid2-2 mutants deficient in a putative transporter and isochorismate synthase required for SA biosynthesis. We show that sid2-2 fully suppresses SA accumulation and cell death in acd11, although growth inhibition and premature leaf chlorosis still occur. In addition, application of exogenous SA to acd11/sid2-2 is insufficient to restore cell death. This indicates that isochorismate-derived compounds other than SA are required for induction of PCD in acd11 and that some acd11 phenotypes require NahG-degradable compounds not synthesized via isochorismate.

² These authors contributed equally to the paper.

³ Present address: Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, 12 rue du Général Zimmer, 67084 Strasbourg cedex, France.

⁴ Present address: Laboratoire de Biologie Cellulaire, Institut National de la Recherche Agronomique, 78026 Versailles cedex, France.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.105.059303.

^* Corresponding author; e-mail mundy{at}my.molbio.ku.dk; fax 45–35322128.

Received January 10, 2005; returned for revision March 30, 2005; accepted April 4, 2005.

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