Available online at www.sciencedirect.com The ABA receptors – we report you decide Peter McCourt 1 and Robert Creelman 2 The plant hormone abscisic acid (ABA) has been implicated in a variety of physiological responses ranging from seed dormancy to stomatal conductance. Recently, three groups have reported the molecular identification of three disparate ABA receptors. Unlike the identification of other hormone receptors, in these three cases high affinity binding to ABA rather than the isolation of ABA insensitive mutants led to these receptor genes. Interestingly, two of the receptors encode genes involved in floral timing and chlorophyll biosynthesis, which are not considered traditional ABA responses. And the third receptor has been clouded in issues of its molecular identity. To clearly determine the roles of these genes in ABA perception it will require placing of these ABA-binding proteins into the rich ABA physiological context that has built up over the years. Addresses 1 Department of Cell & Systems Biology, University of Toronto, 25 Willcocks Street, Toronto M5S 3B2, Canada 2 Mendel Biotechnology, Inc., 3935 Point Eden Way, Hayward, CA 94545-3720, USA Corresponding author: McCourt, Peter (mccourt@csb.utoronto.ca) Current Opinion in Plant Biology 2008, 11:474–478 This review comes from a themed issue on Cell Signalling and Gene Regulation Edited by Jason Reed and Bonnie Bartel 1369-5266/$ – see front matter # 2008 Elsevier Ltd. All rights reserved. DOI 10.1016/j.pbi.2008.06.014 Introduction The study of plant hormone signaling has always been a tricky business because these small organic molecules at first glance appear to do everything. If we were ever going to demystify these compounds at a mechanistic level, we would need to know how they are perceived and how changes in concentration are transduced into a cellular response. Over the past few years plant biologists have made great inroads into understanding how hormones are perceived with the molecular identification of many of the key hormone receptors [1,2]. In most of these cases, the trick was to identify a mutant in Arabidopsis that did not respond correctly to the hormone of interest and then through map-based cloning identity the gene. In some cases (e.g. ethylene, cytokinins and brassinosteroids), candidate genes showed some homology to receptor-like kinases from other organisms, suggesting these were receptors. However, in the case of auxin and gibberellins the receptor function was less obvious so biochemistry was needed to unequivocally convince researchers that the genetics had succeeded. Unfortunately, the application of forward genetics to identify the abscisic acid (ABA) receptor(s) has not had the same success as other hormone mutant hunts. For ABA mutant screens, inhibition of seed germination by exogenous ABA has been the assay of choice. By looking for seeds that germinate in the presence of ABA, a collection of mutants (designated abi for ABA insensitive) were identified [3,4]. Of these, five ABI genes have been extensively characterized at the molecular level (Figure 1a). The ABI1 and ABI2 genes encoded related type 2C phosphatases, suggesting phosphorylation is an important aspect of ABA signaling [5–7]. Moreover, domi- nant mutations in either of these genes reduce many ABA responses in Arabidopsis including seed dormancy, sto- matal closure, inhibition of root growth and ABA- regulated gene expression, suggesting these proteins function early in the ABA signal transduction pathway. By contrast ABI3, ABI4 and ABI5 appear to be mostly limited to influencing seed related ABA responses [8–10]. These genes encode three disparate transcription factors, which by inference would suggest they are at the end of a seed-specific ABA signaling pathway. So far, epistatic analysis has not yielded a clear relationship of these gene products to each other. Coupled with a lack of bio- chemical studies, these deficiencies have made it unclear what role ABI genes play in ABA signaling. At first glance, there are a number of possibilities as to why the forward genetics approach may not have worked. First, it is possible that mutations in the ABA receptor are lethal to the plant. This would be surprising since aux- otrophic mutations exist that greatly reduce ABA levels and these mutants are still viable [11]. Possibly there is genetic redundancy in ABA perception, hence loss of any one member of the family results in a phenotype that is too subtle and escapes the watchful eye of geneticists. Certainly, all the other characterized hormone receptors are members of larger families so we would expect the ABA receptor should be no different. However, redun- dancy did not stop genetics from identifying receptors in the other hormone pathways so why should it be a problem for ABA? Perhaps screens need to get more sophisticated than simply a generic germination assay so that subtle phenotypes expected from genetically buffered pathways can be observed. The third possibility is the ABA receptor has phenotypes that are unexpected. In this scenario, the loss-of-function mutants in the receptor may have already been identified but the Current Opinion in Plant Biology 2008, 11:474–478 www.sciencedirect.com