Publication

Abscisic acid receptors: past, present and future Public

Jianjun Guo, Xiaohan Yang, David J. Weston and Jin-Gui Chen 2011 June 01 Journal of Integrative Plant Biology Volume 53, Issue 6, pages 469-479, June 2011
Download Publication: j.1744-7909.2011.01044.x.pdf

Abstract

Abscisic acid (ABA) is the key plant stress hormone. Consistent with the earlier studies in support of the presence of both membrane- and cytoplasm-localized ABA receptors, recent studies have identified multiple ABA receptors located in various subcellular locations. These include a chloroplast envelope-localized receptor (the H subunit of Chloroplast Mg2+-chelatase/ABA Receptor), two plasma membrane-localized receptors (G-protein Coupled Receptor 2 and GPCR-type G proteins), and one cytosol/nucleus-localized Pyrabactin Resistant (PYR)/PYR-Like (PYL)/Regulatory Component of ABA Receptor 1 (RCAR). Although the downstream molecular events for most of the identified ABA receptors are currently unknown, one of them, PYR/PYL/RCAR was found to directly bind and regulate the activity of a long-known central regulator of ABA signaling, the A-group protein phosphatase 2C (PP2C). Together with the Sucrose Non-fermentation Kinase Subfamily 2 (SnRK2s) protein kinases, a central signaling complex (ABA-PYR-PP2Cs-SnRK2s) that is responsible for ABA signal perception and transduction is supported by abundant genetic, physiological, biochemical and structural evidence. The identification of multiple ABA receptors has advanced our understanding of ABA signal perception and transduction while adding an extra layer of complexity.

Highlights


Under low cellular ABA concentrations: (1) GTG is present as GTP-bound, inactive form; (2) ABAR/ChlH cannot sequester WRKYs, therefore WRKYs bind to the W-box of many key ABA-signaling transcription factors, such as ABI4, ABI5, ABF4, DREB1A, DREB2A, MYB2 and RAB18, and inhibit their expression; and (3) PYR1/PYL/RCAR cannot bind PP2C, hence PP2C binds, de-phosphorylates and deactivates SnRK2s. Under high ABA concentrations (e.g. triggered by environmental stimuli): (1) GDP-bound form of GTG binds ABA and regulates the expression of ABA-responsive genes via an unknown mechanism; (2) ABA-bound ABAR/ChlH sequesters WRKYs to the cytosol, thus allowing the expression of ABA-signaling transcription factors which, through binding to different cis-elements, such as CE1, MYB, DRE and ABRE, activate the expression of ABA-responsive genes; and (3) ABA-bound PYR/PYL/RCARs bind and deactivate the phosphatase activity of PP2C. Consequently, SnRK2 can be activated via autophosphorylation, which in turn phosphorylates AREB1, which recognizes ABRE elements of ABA responsive genes, resulting in the activation of their expression. The transcriptome reprogramming triggered by ABA signaling will eventually cause physiological and developmental readouts, such as stress responses, seed germination and early seedling development. ABA, abscisic acid; GTGs (GPCR type G-proteins); ChlH (Chloroplast Mg2+ chelatase H-subunit)/ABAR (ABA receptor); PYR (pyrabactin resistant)/PYL (pyrabactin resistant-like)/RCARs (regulatory component of ABA receptor); PP2Cs (protein phosphatase 2C proteins); SnRK2s (sucrose non-fermentation kinase 2 proteins); AREB1 (ABRE binding protein 1); ABI4 (ABA insensitive 4); ABI5 (ABA insensitive 5); ABF4 (ABRE binding factor 4); DREB1A (DRE-binding protein 1A); DREB2A (DRE-binding protein 2A); RAB18 (responsive to ABA 18); WRKY (WRKYGQK-containing transcription factor); MYB2 (v-myb myeloblastosis viral oncogene homolog 2); W-box (WRKY-binding cis-elements); MYB (MYB transcription factor-binding cis-elements); DRE (drought responsive cis-element); ABRE (ABA responsive cis-elements); CE1 (coupling element 1, can be bound by ABI4); Pi (phosphate). GCR2 is not included in these modes due to its contradictory role as an ABA receptor.


Under low cellular ABA concentrations: none of the ABA receptors-signaling pathways is activated; the non-phosphorylated SLAC1 channel is closed while the non-phosphorylated KAT1 channel is open, and the stomata stay open. Under high cellular ABA concentrations: (1) both GTG and ABAR/ChlH can mediate ABA signaling and lead to stomatal closure through unknown mechanisms; and (2) sequestration and deactivation of PP2Cs by ABA-bound PYR/PYL/RCAR leads to the activation of SnRK2, which can then phosphorylate/activate SLAC1 and phosphorylate/deactivate KAT1, resulting in a change of ion flux and cellular osmotic pressure leading to stomatal closure. GTGs (GPCR type G-proteins); ChlH (Mg2+ chelatase H-subunit)/ABAR (ABA receptor); PYR (pyrabactin resistant)/PYL (pyrabactin resistant like)/RCARs (regulatory component of ABA receptor); PP2Cs (protein phosphatase 2C proteins); SnRK2s (sucrose non-fermentation kinase 2 proteins); SLAC1 (slow anion channel 1); KAT1 (inward rectifying K+ channel 1); Pi (phosphate). GCR2 is not included in these modes due to its contradictory role as an ABA receptor.

Citation

Guo J, Yang X, Weston DJ, Chen JG. Abscisic acid receptors: past, present and future. J Integr Plant Biol. 2011 Jun;53(6):469-79. doi: 10.1111/j.1744-7909.2011.01044.x. Review. PubMed PMID: 21554537.