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, 38 (10), 829-35

Revisiting Apoplastic Auxin Signaling Mediated by AUXIN BINDING PROTEIN 1


Revisiting Apoplastic Auxin Signaling Mediated by AUXIN BINDING PROTEIN 1

Mingxiao Feng et al. Mol Cells.


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.

Keywords: ABP1; apoplastic signaling; auxin; auxin binding; hormone receptor.


Fig. 1.
Fig. 1.
ABP1 signaling pathway in leaf pavement cells. In leaf pavement cells, auxin in the apoplast is sensed by secreted ABP1, which binds to its PM-localized receptor, TMK, to activate two intertangled downstream pathways: ROP2-RIC4 and ROP6-RIC1. The former contributes to lobe outgrowth through the stabilization of cortical actin microfilaments, which suppresses PIN2 endocytosis; the latter, via KTN1, inhibits indentation outgrowth through the reorganization of cortical TMs, which suppresses the endocytosis of PIN1 and possibly other PINs as well. SPK1 may also contribute to the ROP6-RIC1 pathway as it does in the root. Dotted lines and question marks indicate potential signaling and signaling components, respectively.
Fig. 2.
Fig. 2.
ABP1 signaling pathway in root cells. In the root, SPK1, after perceiving the ABP1-mediated auxin signal from the apoplast, induces the ROP6-RIC1 signaling pathway, stabilizes the cortical F-actin networks instead of MT and further suppresses the endocytosis of PIN1, PIN2 and possibly other PINs. TMK may also contribute to PIN endocytosis, and ROP3, after receiving a signal from unknown upstream components, promotes PIN1 and PIN3 exocytosis. Dotted lines and question marks indicate potential signaling and signaling components, respectively.

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