Nitric oxide influences auxin signaling through S-nitrosylation of the Arabidopsis TRANSPORT INHIBITOR RESPONSE 1 auxin receptor

MARÍA C, TERRILE; RAMIRO, PARÍS; LUZ IA, CALDERON-VILLALOBOS; MARÍA J, IGLESIAS; LORENZO, LAMATTINA; MARK, ESTELLE; CLAUDIA A, CASALONGUÉ

PLANT JOURNAL

WILEY-BLACKWELL PUBLISHING, INC

Año: 2012 vol. 70 p. 492 - 500

0960-7412

Previous studies have demonstrated that auxin (indole-3-acetic acid) and nitric oxide (NO) are plant growthregulators that coordinate several plant physiological responses determining root architecture. Nonetheless,the way in which these factors interact to affect these growth and developmental processes is not wellunderstood. The Arabidopsis thaliana F-box proteins TRANSPORT INHIBITOR RESPONSE 1/AUXIN SIGNAL-ING F-BOX (TIR1/AFB) are auxin receptors that mediate degradation of AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA) repressors to induce auxin-regulated responses. A broad spectrum of NO-mediated protein modificationsare known in eukaryotic cells. Here, we provide evidence that NO donors increase auxin-dependent geneexpression while NO depletion blocks Aux/IAA protein degradation. NO also enhances TIR1-Aux/IAAinteraction as evidenced by pull-down and two-hybrid assays. In addition, we provide evidence forNO-mediated modulation of auxin signaling through S-nitrosylation of the TIR1 auxin receptor. S-nitrosylationof cysteine is a redox-based post-translational modification that contributes to the complexity of the cellularproteome. We show that TIR1 C140 is a critical residue for TIR1?Aux/IAA interaction and TIR1 function. Theseresults suggest that TIR1 S-nitrosylation enhances TIR1?Aux/IAA interaction, facilitating Aux/IAA degradationand subsequently promoting activation