Abscisic acid-mediated epigenetic processes in plant development and stress responses

Abstract

Abscisic acid (ABA) regulates diverse plant processes, growth and development under non-stress conditions and plays a pivotal role in abiotic stress tolerance. Although ABA-regulated genetic processes are well known, recent discoveries reveal that epigenetic processes are an integral part of ABA-regulated processes. Epigenetic mechanisms, namely, histone modifications and cytosine DNA methylation-induced modification of genome give rise to epigenomes, which add diversity and complexity to the genome of organisms. Histone monoubiquitination appears to regulate ABA levels in developing seeds through histone H2B monoubiquitination. ABA and H2B ubiquitination dependent chromatin remodeling regulate seed dormancy. Transcription factor networks necessary for seed maturation are repressed by histone deacetylases (HDACs)-dependent and PICKLE chromatin remodeling complexes (CRCs), whereas ABA induces the expression of these genes directly or through repression of HDACs. Abiotic stress-induced ABA regulates stomatal response and stress-responsive gene expression through HDACs and HOS15-dependent histone deacetylation, as well as through the ATP-dependent SWITCH/SUCROSE NONFERMENTING CRC. ABA also probably regulates the abiotic stress response through DNA methylation and short interfering RNA pathways. Further studies on ABA-regulated epigenome will be of immense use to understand the plant development, stress adaptation and stress memory.

Figure 1. Abscisic acid (ABA) mediated epigenetic processes regulate seed maturation, dormancy and germination inhibition

HISTONE MONOUBIQUITINATION1 (HUB1) monoubiquitinates H2B, which in turn regulates ABA-levels by inducing NCED and repressing CYP707A2. Enhanced ABA level induces ABI4 expression and H2B monoubiquitination induces the expression of DOG1, ATS2 and PER1. These proteins in turn induce seed dormancy. VP1/ABI3-like (VAL proteins recruits SWI/SNF class chromatin remodeling complex, PIKLE (PKL). PKL and histone deacetylases (HDACs) dependent chromatin remodeling repress the expression of genes involved in seed maturation and stress-induced germination arrest. ABA probably downregulates HDACs (HDA6, HDA19) and also induces the expression of these genes involved in seed maturation and stress-induced germination arrest (ABA2, short chain dehydrogenase; ABI, ABA insensitive; AAO3, abscisic aldehyde oxidase; ATS2, a caleosin-like protein; CYP707A, ABA 8’ hydroxylase; DOG1, DELAY OF GERMINATION1; FUS3, FUSCA3; H2B, histone 2B; LEC1, LEAFY COTYLEDON1; NCED, 9 cis-epoxycarotenoid dioxygenase; PER1, peroxiredoxin family of antioxidants; UQ, ubiquitin; ZEP, zeaxanthin epoxidase).

Figure 2. Abscisic acid (ABA)-mediated chromatin remodeling regulates stress responsive gene expression and stress tolerance

Abiotic stresses induce accumulation of ABA. ABA enhances the expression levels of HOS15, which encodes a protein similar to the human WD-40 repeat protein TBL1 (Transducin Beta-Like protein-1), a component of the chromatin repression complex involved in histone deacetylation. Conversely, ABA can also inhibit histone deacetylation through repression of histone deacetylases (HDACs). ABA and drought induce an ATP-dependent chromatin remodeling complex protein, SNF5. Histone deacetylation dependent and ATP-dependent chromatin remodeling complexes regulate gene expression and stress response (Ac, acetyl group; H4, histone4; HOS15, high expression of osmotically responsive genes 15).