• Molecules and Cells
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• v.38 no.10
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• pp.829-835
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• 2015

It has been suggested that AUXIN BINDING PROTEIN 1 (ABP1) functions as an apoplastic auxin receptor, and is known to be involved in the post-transcriptional process, and largely independent of the already well-known SKP-cullin-F-box-transport inhibitor response (TIR1) /auxin signaling F-box (AFB) ($SCF^{TIR1/AFB}$) pathway. In the past 10 years, several key components downstream of ABP1 have been reported. After perceiving the auxin signal, ABP1 interacts, directly or indirectly, with plasma membrane (PM)-localized transmembrane proteins, transmembrane kinase (TMK) or SPIKE1 (SPK1), or other unidentified proteins, which transfer the signal into the cell to the Rho of plants (ROP). ROPs interact with their effectors, such as the ROP interactive CRIB motif-containing protein (RIC), to regulate the endocytosis/exocytosis of the auxin efflux carrier PIN-FORMED (PIN) proteins to mediate polar auxin transport across the PM. Additionally, ABP1 is a negative regulator of the traditional $SCF^{TIR1/AFB}$ auxin signaling pathway. However, Gao et al. (2015) very recently reported that ABP1 is not a key component in auxin signaling, and the famous abp1-1 and abp1-5 mutant Arabidopsis lines are being called into question because of possible additional mutantion sites, making it necessary to reevaluate ABP1. In this review, we will provide a brief overview of the history of ABP1 research.

• Journal of Plant Biotechnology
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• v.43 no.4
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• pp.405-410
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• 2016

Auxins are essential in plant growth and development. The auxin-stimulated elongation of plant cells has been explained by the "acid-growth theory", which was proposed forty years ago. According to this theory, the auxin activates plasma membrane $H^+-ATPase$ to induce proton extrusion into the apoplast, promoting cell expansion through the activation of cell wall-loosening proteins such as expansins. Even though accepted as the classical theory of auxin-induced cell growth for decades, the major signaling components comprising this model were unknown, until publication of recent reports. The major gap in the acid growth theory is the signaling mechanism by which auxin activates the plasma membrane $H^+-ATPase$. Recent genetic, molecular, and biochemical approaches reveal that several auxin-related molecules, such as TIR1/AFB AUX/IAA coreceptors and SMALL AUXIN UP RNA (SAUR), serve as important components of the acid-growth model, phosphorylating and subsequently activating the plasma membrane $H^+-ATPase$. These researches reestablish the four-decade-old theory by providing us the detailed signaling mechanism of auxininduced cell growth. In this review, we discuss the recent research progress in auxin-induced cell elongation, and a set of possible future works based on the reestablished acid-growth model.