Plants progress from a juvenile vegetative phase of development to an adult vegetative phase of development before they enter the reproductive phase. miR156 has been shown to be the master regulator of the juvenile-to-adult transition in plants. However, the mechanism of how miR156 is transcriptionally regulated still remains elusive. In a forward genetic screen, we identified that a mutation in the SWI2/SNF2 chromatin remodeling ATPase BRAHMA (BRM) exhibited an accelerated vegetative phase change phenotype by reducing the expression of miR156, which in turn caused a corresponding increase in the levels of SQUAMOSA PROMOTER BINDING PROTEIN LIKE genes. BRM regulates miR156 expression by directly binding to the MIR156A promoter. Mutations in BRM not only increased occupancy of the −2 and +1 nucleosomes proximal to the transcription start site at the MIR156A locus but also the levels of trimethylated histone H3 at Lys 27. The precocious phenotype of brm mutant was partially suppressed by a second mutation in SWINGER (SWN), but not by a mutation in CURLEY LEAF, both of which are key components of the Polycomb Group Repressive Complex 2 in plants. Our results indicate that BRM and SWN act antagonistically at the nucleosome level to fine-tune the temporal expression of miR156 to regulate vegetative phase change in Arabidopsis.

Epigenetic regulation is referred to as changes in gene function that do not involve changes in the DNA sequence, it is usually accomplished by DNA methylation, histone modifications (repressive marks such as H3K9me, H3K27me, H2Aub, or active marks such as H3K4me, H3K36me, H3Ac), and chromatin remodeling (nucleosome composition, occupancy, and location). In plants, the shoot apex produces different lateral organs during development to give rise to distinguishable phases of a juvenile, an adult and a reproductive phase after embryogenesis. The juvenile-to-adult transition is a key developmental event in plant life cycle, and it is regulated by a decrease in the expression of a conserved microRNA-miR156/157, and a corresponding increase in the expression of its target genes encoding a set of plant specific SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) proteins. Recent work has revealed that the miR156/157-SPL pathway is the master regulator of juvenile-to-adult transition in plants, and genes in this pathway are subjected to epigenetic regulation, such as DNA methylation, histone modifications, and chromatin remodeling. In this review, we summarized the recent progress in understanding the epigenetic regulation of the miR156/157-SPL pathway during juvenile-to-adult transition and bring forward some perspectives of future research in this field.

Summary: Higher plants progress through a juvenile and an adult phase of development before they enter the reproductive phase. The transition from the juvenile to the adult phase is referred to as vegetative phase change, and this is signified by the production of trichomes on the abaxial side of leaf blades in Arabidopsis; however, the molecular mechanism underlying this process is poorly understood. We identified a dominant mutation (gl1‐D) in a forward genetic screen that accelerates abaxial trichome production during shoot development. This phenotype is the result of a G‐to‐A substitution in the 3′ noncoding region in the GLABRA1(GL1) gene. We show that TOE1, an AP2‐like transcription factor that acts downstream of the miR156‐SPL pathway, represses GL1 expression by directly binding to this site, and that gl1‐D prevents TOE1 binding. Our work reveals a molecular link between vegetative phase change and abaxial trichome production in Arabidopsis, and answers a long‐standing question of how the vegetative phase change pathway regulates vegetative traits.

Cadmium (Cd) pollution is one of the major threats in agricultural production, and can cause oxidative damage and growth limitation in plants. MicroRNA398 (miR398) is involved in plant resistance to different stresses, and the post-transcriptional regulation of miR398 on CSDs plays a key role. Here, we report that miR398 was down-regulated in tomato in response to Cd stress. Simultaneously, CSD1 and SOD were up-regulated, with CSD2 unchanged, suggesting CSD1 is involved in miR398-induced regulation under Cd stress. In addition, the role of miR398 in Cd tolerance in tomato was evaluated using a transgenic line overexpressing MIR398 (miR398#OE) in which the down-expression of miR398 was disrupted. The results showed that Cd stress induced more significant growth inhibition, oxidative damage, and antioxidant enzymes disorder in miR398#OE than that in wild type (WT). Moreover, higher Cd concentration in the shoot and xylem sap, and net Cd influx rate, were observed in miR398#OE, which could be due to the increased Cd uptake genes (IRT1, IRT2, and NRAMP2) and decreased Cd compartmentalization gene HMA3. Overall, our results indicate that down-regulated miR398 plays a protective role in tomato against Cd stress by modulating the activity of antioxidant enzymes and Cd uptake and translocation.

MicroRNAs (miRNAs) have been shown to be critical components in plant immunity. MicroRNA398 (miR398) is a highly conserved miRNA in all land plants and plays crucial roles in diverse biotic stress responses. However, the role of miR398 has not yet been characterized in tomato resistance against Botrytis cinerea. In this report, the transcript levels of sly-miR398b were strongly decreased in B. cinerea-infected leaves and the overexpression of sly-miR398b resulted in enhanced susceptibility. The attenuated expression of cytosol Cu/Zn-SOD (CSD1), chloroplast Cu/Zn-SOD (CSD2), and guaiacol peroxidase (GPOD), as well as the decreased activities of superoxide dismutase (SOD) and GPOD, collectively led to increased hydrogen peroxide (H₂O₂) accumulation in sly-miR398b overexpressing plants. Furthermore, sly-miR398b was induced by methyl jasmonate (MeJA) treatment. The overexpression of sly-miR398b suppressed the expression of TomLoxD, LapA, and PR-STH2 in response to B. cinerea and MeJA treatment. Our data demonstrate that sly-miR398b overexpression negatively regulates the resistance to B. cinerea in tomato by inducing the accumulation of reactive oxygen species (ROS) and downregulating the expression of MeJA-responsive defense genes.