FERONIA receptor kinase pathway suppresses abscisic acid signaling in <i>Arabidopsis</i> by activating ABI2 phosphatase

Feng Yu(Hunan Normal University), Lichao Qian(Hunan Normal University), Cândida Nibau(University of Massachusetts Amherst), Qiaohong Duan(University of Massachusetts Amherst), Daniel Kita(University of Massachusetts Amherst), Kathryn Levasseur(University of Massachusetts Amherst), Xiaoqian Li(Hunan Normal University), Changqing Lu(Hunan Normal University), Hui Li(Hunan Normal University), Congcong Hou(Capital Normal University), Legong Li(Capital Normal University), Bob B. Buchanan(University of California, Berkeley), Liangbi Chen(Hunan Normal University), Alice Y. Cheung(University of Massachusetts Amherst), Dong-Ping Li(Hunan Normal University), Sheng Luan(Hunan Normal University)
Proceedings of the National Academy of Sciences
August 20, 2012
Cited by 284Open Access
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Abstract

Plant growth and development are controlled by a delicate balance of hormonal cues. Growth-promoting hormones and growth-inhibiting counterparts often antagonize each other in their action, but the molecular mechanisms underlying these events remain largely unknown. Here, we report a cross-talk mechanism that enables a receptor-like kinase, FERONIA (FER), a positive regulator of auxin-promoted growth, to suppress the abscisic acid (ABA) response through activation of ABI2, a negative regulator of ABA signaling. The FER pathway consists of a FER kinase interacting with guanine exchange factors GEF1, GEF4, and GEF10 that, in turn, activate GTPase ROP11/ARAC10. Arabidopsis mutants disrupted in any step of the FER pathway, including fer, gef1gef4gef10, or rop11/arac10, all displayed an ABA-hypersensitive response, implicating the FER pathway in the suppression mechanism. In search of the target for the FER pathway, we found that the ROP11/ARAC10 protein physically interacted with the ABI2 phosphatase and enhanced its activity, thereby linking the FER pathway with the inhibition of ABA signaling.


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