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

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