The Arabidopsis transcription factor ABIG1 relays ABA signaled growth inhibition and drought induced senescence.

Tie Liu,Franklin Talavera-Rauh,Adam D Longhurst,Samuel A Hokin,M Kathryn Barton

doi:10.7554/elife.13768

Tie Liu, Franklin Talavera-Rauh + Show 3 more

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https://doi.org/10.7554/elife.13768

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Abstract

Drought inhibits plant growth and can also induce premature senescence. Here we identify a transcription factor, ABA INSENSITIVE GROWTH 1 (ABIG1) required for abscisic acid (ABA) mediated growth inhibition, but not for stomatal closure. ABIG1 mRNA levels are increased both in response to drought and in response to ABA treatment. When treated with ABA, abig1 mutants remain greener and produce more leaves than comparable wild-type plants. When challenged with drought, abig1 mutants have fewer yellow, senesced leaves than wild-type. Induction of ABIG1 transcription mimics ABA treatment and regulates a set of genes implicated in stress responses. We propose a model in which drought acts through ABA to increase ABIG1 transcription which in turn restricts new shoot growth and promotes leaf senescence. The results have implications for plant breeding: the existence of a mutant that is both ABA resistant and drought resistant points to new strategies for isolating drought resistant genetic varieties.

Highlights

One way for plants to withstand drought is to slow, or stop, new growth thereby conserving resources until better times return (Dolferus, 2014)
Since abscisic acid (ABA) signaling genes are prominent among the small set of ORK genes (genes oppositely regulated by the REV and KAN transcription factors (Reinhart et al, 2013; Figure 1A), we reasoned that other genes oppositely regulated by them may play a role in ABA signaling in the plant
We present six lines of evidence that ABA INSENSITIVE GROWTH 1 (ABIG1)/HAT22 plays a part in ABA signaling in the regulation of plant growth: 1/ ABIG1/HAT22 has similar regulation patterns to two other known ABA signaling genes, PYL6 and CIPK12; 2/ Expression of ABIG1/HAT22 increases in response to exogenous ABA and drought; 3/ This response is dependent on ABI1 function; 4/ Induction of the ABIG1/HAT22 transcription factor mimics the application of exogenous ABA; 5/ Loss of function mutations in ABIG1/HAT22 cause resistance to ABA mediated growth inhibition and to drought induced leaf yellowing; 6/ Induction of ABIG1/HAT22 regulates CYP707A3, a gene encoding an enzyme that mediates ABA breakdown

Summary

Introduction

One way for plants to withstand drought is to slow, or stop, new growth thereby conserving resources until better times return (Dolferus, 2014). Levels of the ABA biosynthetic enzyme AtNCED3 in the vascular parenchyma increase in Arabidopsis (Endo et al, 2008) This causes an increase in ABA which causes plants to close stomatal apertures, reducing water loss (Schroeder et al, 2001). ABA acts by binding to PYR-like co-receptors and bringing them together with PP2C family phosphatases (Cutler et al, 2010) This frees downstream SNRK2 kinases from repression by the PP2C phosphatase, allowing the kinase to modify protein targets at the plasma membrane - to alter turgor in guard cells - or to modify a set of transcription factors - to promote maturation and dormancy in the developing seed

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