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Plant biology

Abscisic acid in bloom

Naturevolume 439pages277278 (2006) | Download Citation


To survive environmental stresses, plants must respond to the hormone abscisic acid. The receptors for this hormone have remained elusive, but one receptor with unique functions in flowering has now been identified.

When plants experience drought or cold, they cannot get themselves a glass of water or move to a warmer place. Instead, their ability to survive lack of water, extreme temperatures and such stresses as high salt levels relies heavily on a plant hormone called abscisic acid (ABA). Despite their importance, the genes that encode the cellular receptors for this hormone have not been identified. On page 290 of this issue, however, Razem et al.1 describe the characterization of a protein that binds to messenger RNAand that also binds ABA and controls ABA-dependent flowering in the model plant Arabidopsis.

The question of how plants cope with the recurring stresses of drought, cold and salinity not only engages plant scientists, agronomists, ecologists and climatologists. It also increasingly demands the attention of politicians, given that in arid regions across the globe more than 80% of the available fresh water is consumed by agriculture2. Many avenues of research have shown that ABA is a key player in such stress resistance. Responses mediated by this hormone lead to the induction of complex tolerance mechanisms to drought, cold, salinity and wounding, including the control of closure of the stomatal pores in leaves to reduce water loss3.

Genetic screens with various twists have elucidated ABA signal-transduction mechanisms that act downstream of ABA sensing3. But genes that encode ABA-binding receptor proteins have remained unidentified. This might be because plant genomes have large numbers of homologous — closely related — genes that probably have overlapping functions, or because an ABA receptor is essential, such that plants with mutations in the receptor gene would not survive. Research on ABA signalling is also revealing the robustness of an intricate signal-transduction network. This can limit traditional ‘forward’ genetic approaches4, because a mutation in one pathway may be side-stepped to a degree by using another route that transmits the signal.

Razem and colleagues1 have used an alternative, biochemical approach. They isolated a barley protein that has ABA-binding activity, named ABAP1 (ref. 5), and investigated whether a homologue of ABAP1 functions in an ABA response in Arabidopsis. Their work shows that an RNA-binding protein called FCA binds to ABA and is regulated by it, and that FCA is involved in a less well-studied function of ABA — the inhibition of flowering.

The Arabidopsis FCA protein is homologous to the barley ABAP1 protein in its carboxy-terminal half and, like ABAP1, it has a high affinity for active ABA analogues1,5. (Its dissociation constant, Kd, is 19 nM.) The FCA protein is a component of the so-called autonomous flowering pathway, which reduces the activity of the flowering repressor Flowering Locus C, or FLC (Fig. 1, overleaf)6,7. Two structural regions of the FCA protein are of particular relevance: a protein-interaction region known as a WW domain, and an RNA-recognition motif6,7. The WW domain allows FCA to interact with the protein FY, which is an mRNA processing factor6.

Figure 1: Abscisic acid, RNA metabolism and control of flowering in plants.
Figure 1

Binding of two proteins, FCA and FY, to one another results in a decrease in expression levels of Flowering Locus C (FLC), causing a transition from vegetative growth to flowering. The FCA–FY complex also causes synthesis of a truncated, non-functional FCA messenger RNA in a negative feedback loop that results in fewer full-length FCA mRNA transcripts and less FCA protein6,7. Razem et al.1 report that binding of abscisic acid (ABA) to FCA abolishes the interaction of FCA with FY, leading to an increase in full-length FCA transcripts and — through increased FLC activity — a delay in flowering. Red lines depict negative regulation. (Diagram modified from a figure provided by R. Hill.)

The FCA–FY complex negatively regulates expression of the flowering repressor FLC. It also reduces the amount of functional FCA protein through a negative feedback loop by adding a premature polyadenylation tail to a truncated form of the FCA precursor mRNA6,7. In this negative feedback loop, polyadenylation of the truncated FCA precursor mRNA results in a shortened mRNA, and thus in non-functional FCA protein (Fig. 1). Several reports have established a link between RNA-processing proteins and ABA signalling8,9,10,11,12. But we don't yet know whether these mRNA-processing proteins, which affect ABA action, are components of an FCA-like ABA stress-response pathway.

In the new work, Razem et al.1 report that the FCA–FY complex dissociates when ABA binds to FCA, making the complex non-functional (Fig. 1). As a result, premature polyadenylation of the truncated FCA precursor mRNA is abolished. Thus, ABA causes accumulation of full-length FCA mRNA. Razem et al. show that ABA causes a dramatic increase in FLC mRNA, which in turn would delay the transition to flowering. Consistent with this model, the authors report that ABA causes a delay in flowering in Arabidopsis. As Arabidopsis plants can flower early in response to drought, which increases ABA production, the ABA–FCA response may be overridden during this response13. Possible modulation mechanisms during drought stress could be investigated by analysing the newly revealed direct ABA regulation of FCA mRNA (full-length versus truncated) and the strong ABA-induced increase in levels of FLC mRNA.

Interestingly, the RNA-recognition motif in FCA is absent in the barley ABAP1 protein5. Indeed, ABA-binding studies of Arabidopsis FCA in which the protein lacked specific structural regions show that ABA-binding activity lies in the carboxy-terminal half of FCA, which does share homology with ABAP1 (ref. 1).

Razem et al.1 went on to show that in plants with a loss-of-function mutation in FCA, the ABA-induced closing of stomatal pores and inhibition of seed germination — two classical ABA responses — were not impaired. Furthermore, ABA inhibition of flowering was not affected in two dominant ABA-insensitive mutants, abi1-1 and abi2-1, in which most of the stress-related ABA responses are impaired. Thus, other ABA receptors are needed to explain the classical ABA signalling responses to stress. The hunt could be on to characterize homologues to the ABA-binding carboxy terminus of FCA1 and barley ABAP1. A simple search of protein databases reveals only one distant FCA homologue in the Arabidopsis genome. Alternatively, the FCA and ABAP1 proteins provide an opportunity to elucidate the structure of an ABA-binding pocket, which may reveal important sub-domains and structural constraints for ABA binding.

A door to understanding ABA perception has been opened. The binding of ABA to FCA and ABAP1 is apparently a further example of newly emerging mechanisms by which plant growth regulators mediate their responses. Further questions arise with each advance. Plant scientists will need to keep on trekking to illuminate how their immobile lab subjects perceive abscisic acid when faced with drought, cold and salinity.


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  1. the Division of Biological Sciences, Cell and Developmental Biology Section, University of California, 9500 Gilman Drive, San Diego, La Jolla, 92093-0116, California, USA

    • Julian I. Schroeder
    •  & Josef M Kuhn


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