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Abscisic acid inhibits type 2C protein phosphatases via the PYR/PYL family of START proteins.

Science. 2009 May 22;324(5930):1068-71. Epub 2009 Apr 30
Sang-Youl Park 1 , Pauline Fung , Noriyuki Nishimura , Davin R Jensen , Hiroaki Fujii , Yang Zhao , Shelley Lumba , Julia Santiago , Americo Rodrigues , Tsz-Fung F Chow , Simon E Alfred , Dario Bonetta , Ruth Finkelstein , Nicholas J Provart , Darrell Desveaux , Pedro L Rodriguez , Peter McCourt , Jian-Kang Zhu , Julian I Schroeder , Brian F Volkman , Sean R Cutler
Sang-Youl Park 1 , Pauline Fung , Noriyuki Nishimura , Davin R Jensen , Hiroaki Fujii , Yang Zhao , Shelley Lumba , Julia Santiago , Americo Rodrigues , Tsz-Fung F Chow , Simon E Alfred , Dario Bonetta , Ruth Finkelstein , Nicholas J Provart , Darrell Desveaux , Pedro L Rodriguez , Peter McCourt , Jian-Kang Zhu , Julian I Schroeder , Brian F Volkman , Sean R Cutler
+ et al

[No authors listed]

Author information
  • 1 Department of Botany and Plant Sciences, University of California at Riverside, Riverside, CA 92521, USA.

摘要


Type 2C protein phosphatases (PP2Cs) are vitally involved in abscisic acid (ABA) signaling. Here, we show that a synthetic growth inhibitor called pyrabactin functions as a selective ABA agonist. Pyrabactin acts through PYRABACTIN RESISTANCE 1 (PYR1), the founding member of a family of START proteins called PYR/PYLs, which are necessary for both pyrabactin and ABA signaling in vivo. We show that ABA binds to PYR1, which in turn binds to and inhibits PP2Cs. We conclude that PYR/PYLs are ABA receptors functioning at the apex of a negative regulatory pathway that controls ABA signaling by inhibiting PP2Cs. Our results illustrate the power of the chemical genetic approach for sidestepping genetic redundancy.