Abscisic acid‐dependent histone demethylation during postgermination growth arrest in Arabidopsis

Abstract

After germination, seedlings undergo growth arrest in response to unfavourable conditions, a critical adaptation enabling plants to survive harsh environments. The plant hormone abscisic acid (ABA) plays a key role in this arrest. To arrest growth, ABA‐dependent transcription factors change gene expression patterns in a flexible and reversible manner. Although the control of gene expression has important roles in growth arrest, the epigenetic mechanisms in the response to ABA are not fully understood. Here, we show that the histone demethylases JUMONJI‐C domain‐containing protein 30 (JMJ30) and JMJ32 control ABA‐mediated growth arrest in Arabidopsis thaliana. During the postgermination stage (2–3 days after germination), the ABA‐dependent transcription factor ABA‐insensitive3 (ABI3) activates the expression of JMJ30 in response to ABA. JMJ30 then removes a repressive histone mark, H3 lysine 27 trimethylation (H3K27me3), from the SNF1‐related protein kinase 2.8 (SnRK2.8) promoter, and hence activates SnRK2.8 expression. SnRK2.8 encodes a kinase that activates ABI3 and is responsible for JMJ30‐ and JMJ32‐mediated growth arrest. A feed‐forward loop involving the ABI3 transcription factor, JMJ histone demethylases, and the SnRK2.8 kinase fine‐tunes ABA‐dependent growth arrest in the postgermination phase. Our findings highlight the importance of the histone demethylases in mediating adaptation of plants to the environment.

Abscisic acid dynamics, signaling, and functions in plants

“…There may also be multiple other participants in this process. For example, JMJ30, a histone demethylase, is able to block the inhibition mediated by the H3 lysine 27 trimethylation epigenetic mark (H3K27me3) at the promoter of SnRK2.8 and hence release the suppression of ABI3 to promote PGG arrest (Wu et al 2019). Recently, it was reported that RAF22 in Arabidopsis acts as a negative regulator of PGG arrest that is independent of the canonical ABI5‐mediated ABA cascade (Hwang et al 2018).…”

Epigenetic regulation in plant abiotic stress responses

“…BES1 can directly bind to the promoter region of ABI3 and then recruit histone deacetylase HDA19 to deacetylate H3. Additionally, histone modifications are also involved in the fine‐tuning of SnRK2.8 via ABI3 (Wu et al 2019). Abscisic acid treatment induces the expression of ABI3 , and then ABI3 binds to the RY motif in the histone demethylase JMJ30 gene promoter to activate its expression.…”

“…Abscisic acid treatment induces the expression of ABI3 , and then ABI3 binds to the RY motif in the histone demethylase JMJ30 gene promoter to activate its expression. JMJ30 can remove the repressive marker H3K27me3 from the promoter region of SnRK2.8 , and hence activates SnRK2.8 expression; SnRK2.8 kinase, in turn, activates the expression of ABI3 (Wu et al 2019).…”

The Emerging Role of Long Non-Coding RNAs in Plant Defense Against Fungal Stress

“…Indeed, the B3 domain transcription factor ABI3, APETALA2-type transcription factor ABI4, and bZIP transcription factor ABI5 functioned genetically in the downstream of AtNDX. ABA-mediated growth arrest in A. thaliana was controlled by histone demethylases [96]. The expression of ABI3 increased in ndx, but AtNDX could not directly bind to ABI3 [95].…”