How chromatin senses plant hormones

Abstract

Plant hormones activate receptors, initiating intracellular signaling pathways. Eventually, hormone-specific transcription factors become active in the nucleus, facilitating hormone-induced transcriptional regulation. Chromatin plays a fundamental role in the regulation of transcription, the process by which genetic information encoded in DNA is converted into RNA. The structure of chromatin, a complex of DNA and proteins, directly influences the accessibility of genes to the transcriptional machinery. The different signaling pathways and transcription factors involved in the transmission of information from the receptors to the nucleus have been readily explored, but not so much for the specific mechanisms employed by the cell to ultimately instruct the chromatin changes necessary for a fast and robust transcription activation, specifically for plant hormone responses. In this review, we will focus on the advancements in understanding how chromatin receives plant hormones, facilitating the changes necessary for fast, robust, and specific transcriptional regulation.

Figure 1. Model of Chromatin Dynamics in Response to Cytokinin.

Type-B ARRs undergo phosphorylation mediated by AHPs (Cytokinin receptors, the Arabidopsis histidine phosphotransfer proteins), leading to their activation. The phosphorylated Type-B ARRs bind to accessible regions, leading to gained accessibility in most of regions, and activation of transcription. Simultaneously, phosphorylated Type-B ARRs bind to a subset of DNA regions, leading to a reduction of chromatin accessibility, and transcriptional repression.

Figure 2. Model of Chromatin Dynamics in Response to ABA in Guard Cells.

In the presence of ABA, SnRK2 is derepressed, leading to the phosphorylation of ABFs and other ABA-responsive transcription factors (not depicted). Phosphorylated ABFs then bind to accessible chromatin regions, enhancing chromatin accessibility at target loci. Certain regions experience reduced accessibility upon ABA treatment; however, this event is independent of ABFs and involves an unknown molecular mechanism.

Figure 3. Model of How Chromatin Responds to GA based on the study of RGA.

In the absence of GA, RGA interacts with H2A and TF to form a stable protein complex at accessible chromatin regions, effectively inhibiting the function of TFs. Upon exposure to GA, RGAs undergo ubiquitin-mediated protein degradation, leading to the release of H2A and TFs from the complex. This liberation enables TFs to activate transcriptional regulation. Notably, this process does not involve changes in chromatin accessibility.

Figure 4. Model of How Chromatin Changes in Response to Ethylene.

In the presence of ethylene, HAF2-EIN2-ENAP1-EIN3 protein complex targets EIN3 binding loci which are labeled with a higher level of H3K9ac, elevating histone acetylation of H3K14 and H3K23 for transcriptional activation; Concurrently, EIN3-ENAP1 and other unknown factors recruit histone deacetylases SRT1 and SRT2 to loci with lower levels of H3K9ac, facilitating the removal of H3K9ac and subsequent transcriptional repression.