Abstract
Abscisic acid (ABA) interacts antagonistically with brassinosteroids (BRs) to control plant growth and development in response to stress. The response to environmental cues includes hormonal control via epigenetic regulation of gene expression. However, the details of the ABA–BR crosstalk remain largely unknown. Here, we show that JUMONJI-C domain containing histone demethylases (JMJs) coordinate the antagonistic interaction between ABA and BR signaling pathways during the post-germination stage in Arabidopsis. BR blocks ABA-mediated seedling arrest through repression of JMJ30. JMJs remove the repressive histone marks from the BRASSINAZOLE RESISTANT1 (BZR1) locus for its activation to balance ABA and BR signaling pathways. JMJs and BZR1 co-regulate genes encoding three membrane proteins, a regulator of vacuole morphology, and two lipid-transfer proteins, each of which play a different role in transport. BZR1 also regulates stimuli-related target genes in a JMJ-independent pathway. Our findings suggest that the histone demethylases integrate ABA and BR signals, leading to changes in growth program after germination.
Highlights
Plants have the ability to respond to various environmental stimuli over the course of their development (Blatt et al, 2017; Bechtold and Field, 2018)
JMJ30 was under developmental control; its expression levels increased with plant growth (mock 0 h vs. mock 3 h: p = 1.2 × 10−6; mock 3 h vs. mock 5 h: p = 7.0 × 10−3 by two-tailed Student’s t-test (Figure 1A; Wu et al, 2019a)
We found that histone demethylases JMJ30 and JMJ32 integrate inputs from abscisic acid (ABA) and BR during post-germination stage (Figure 7)
Summary
Plants have the ability to respond to various environmental stimuli over the course of their development (Blatt et al, 2017; Bechtold and Field, 2018) These responses are characterized by extensive phenotypic plasticity, and entail a balance between stress response and growth (Foyer et al, 2007; Sanchez-Bel et al, 2018). ABA binds to JMJs and ABA-BR Crosstalk receptors such as PYRABACTIN RESISTANCE1 (PYR1), PYR1LIKE (PYL), and REGULATORY COMPONENTS OF ABA RECEPTOR (RCAR) This triggers conformational changes that enable protein-protein interaction between PYRs and PP2Cs, such as ABSCISIC ACID INSENSITIVE 1 (ABI1), ABI2, and HYPERSENSITIVE TO ABA1 (HAB1; Park et al, 2009; Cutler et al, 2010). These transcription factors regulate the expression of ABA-responsive genes including stress response and growth-inhibition targets (Suzuki et al, 2003; Nakabayashi et al, 2005)
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