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First published online February 18, 2005; 10.1105/tpc.104.029728

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The Plant Cell 17:987-999 (2005)
© 2005 American Society of Plant Biologists

Dissecting the ß-Aminobutyric Acid–Induced Priming Phenomenon in Arabidopsis{boxw}

Jurriaan Tona,b,1, Gabor Jakaba,c,1, Valérie Toquinc, Victor Florsa,d, Annalisa Iavicolic, Muriel N. Maederc, Jean-Pierre Métrauxc and Brigitte Mauch-Mania,2

a Department of Science, Laboratory of Biochemistry, University of Neuchâtel, 2007 Neuchâtel, Switzerland
b Section of Phytopathology, Faculty of Biology, Utrecht University, 3584 CA Utrecht, The Netherlands
c Department of Biology, Plant Biology, University of Fribourg, 1700 Fribourg, Switzerland
d Department of Experimental Sciences, Plant Physiology Section, University of Jaume, Borriol s/n, 12071 Castellón, Spain

2 To whom correspondence should be addressed. E-mail brigitte.mauch{at}unine.ch; fax 41-32-7182201.

Plants treated with the nonprotein amino acid ß-aminobutyric acid (BABA) develop an enhanced capacity to resist biotic and abiotic stresses. This BABA-induced resistance (BABA-IR) is associated with an augmented capacity to express basal defense responses, a phenomenon known as priming. Based on the observation that high amounts of BABA induce sterility in Arabidopsis thaliana, a mutagenesis screen was performed to select mutants impaired in BABA-induced sterility (ibs). Here, we report the isolation and subsequent characterization of three T-DNA–tagged ibs mutants. Mutant ibs1 is affected in a cyclin-dependent kinase–like protein, and ibs2 is defective in AtSAC1b encoding a polyphosphoinositide phosphatase. Mutant ibs3 is affected in the regulation of the ABA1 gene encoding the abscisic acid (ABA) biosynthetic enzyme zeaxanthin epoxidase. To elucidate the function of the three IBS genes in plant resistance, the mutants were tested for BABA-IR against the bacterium Pseudomonas syringae pv tomato, the oomycete Hyaloperonospora parasitica, and BABA-induced tolerance to salt. All three ibs mutants were compromised in BABA-IR against H. parasitica, although to a different extent. Whereas ibs1 was reduced in priming for salicylate (SA)-dependent trailing necrosis, mutants ibs2 and ibs3 were affected in the priming for callose deposition. Only ibs1 failed to express BABA-IR against P. syringae, which coincided with a defect in priming for SA-inducible PR-1 gene expression. By contrast, ibs2 and ibs3 showed reduced BABA-induced tolerance to salt, which correlated with an affected priming for ABA-inducible gene expression. For all three ibs alleles, the defects in BABA-induced sterility and BABA-induced protection against P. syringae, H. parasitica, and salt could be confirmed in independent mutants. The data presented here introduce three novel regulatory genes involved in priming for different defense responses.




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