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Abstract Plants consist of fundamental units of growth called phytomers (leaf or bract, axillary bud, node, and internode), which are repeated and modified throughout shoot development to give plants plasticity for survival and adaptation. One phytomer modification is the suppression or outgrowth of bracts, the leaves subtending the flowers. The floral meristem identity regulator LEAFY (LFY) and the organ boundary genes BLADE-ON-PETIOLE1 (BOP1) and BOP2 have been shown to suppress bract development in Arabidopsis, as mutations in these genes result in bract outgrowth. However, much less is known about the mechanisms that promote bract outgrowth in Arabidopsis mutants such as these. Further understanding of this mechanism may provide a potential tool for modifying leaf development. Here, we showed that the MADS-box genes SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 (SOC1), FRUITFUL (FUL), and AGAMOUS-LIKE24 (AGL24) play more important roles than BOP1/2 and LFY in bract suppression, and that AINTEGUMENTA (ANT) and the partially redundant AINTEGUMENTA-LIKE6 (AIL6) are necessary for bract outgrowth in these mutant backgrounds. We also demonstrated that misexpression of AIL6 alone is sufficient for bract outgrowth. Our data reveal a mechanism for bract suppression and outgrowth and provide insight into phytomer plasticity. 

Summary The juvenile‐to‐adult vegetative phase change in flowering plants is mediated by a decrease in miR156 levels. Downregulation ofMIR156A/MIR156C, the two major sources of miR156, is accompanied by a decrease in acetylation of histone 3 lysine 27 (H3K27ac) and an increase in trimethylation of H3K27 (H3K27me3) atMIR156A/MIR156CinArabidopsis.Here, we show that histone deacetylase 9 (HDA9) is recruited toMIR156A/MIR156Cduring the juvenile phase and associates with the CHD3 chromatin remodeler PICKLE (PKL) to erase H3K27ac atMIR156A/MIR156C.H2Aub and H3K27me3 become enriched atMIR156A/MIR156C, and the recruitment of Polycomb Repressive Complex 2 (PRC2) toMIR156A/MIR156Cis partially dependent on the activities of PKL and HDA9.Our results suggest that PKL associates with histone deacetylases to erase H3K27ac and promote PRC1 and PRC2 activities to mediate vegetative phase change and maintain plants in the adult phase after the phase transition. 

Organ initiation from the shoot apical meristem first gives rise to leaves during vegetative development and then flowers during reproductive development.LEAFY(LFY) is activated after floral induction and together with other factors promotes the floral program. LFY functions redundantly with APETALA1 (AP1) to activate the class B genesAPETALA3(AP3) andPISTILLATA(PI), the class C geneAGAMOUS(AG), and the class E geneSEPALLATA3, which leads to the specification of stamens and carpels, the reproductive organs of flowers. Molecular and genetic networks that control the activation ofAP3,PI,andAGin flowers have been well studied; however, much less is known about how these genes are repressed in leaves and how their repression is lifted in flowers. Here, we showed that two genes encodingArabidopsisC2H2 ZINC FINGER PROTEIN (ZFP) transcription factors, ZP1 and ZFP8, act redundantly to directly repressAP3,PI,andAGin leaves. AfterLFYandAP1are activated in floral meristems, they down-regulateZP1andZFP8directly to lift the repression onAP3,PI,andAG. Our results reveal a mechanism for how floral homeotic genes are repressed and derepressed before and after floral induction. 

Abstract The juvenile-to-adult phase transition during vegetative development is a critical decision point in a plant’s life cycle. This transition is mediated by a decline in levels of miR156/157 and an increase in the activities of its direct targets, SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) proteins. In Arabidopsis, the juvenile-to-adult transition is characterized by an increase in the length to width ratio of the leaf blade (a change in the distal region of a leaf), but what mediates this change in lamina shape is not known. Here, we show that ectopic expression of SPL9 and SPL13 produces enlarged and elongated leaves, resembling leaves from the blade-on-petiole1 (bop1) bop2 double mutant. The expression of BOP1/BOP2 is down-regulated in successive leaves, correlating with the amount of miR156 and antagonistic to the expression of SPL9 and SPL13 in leaves. SPL9 and SPL13 bind to the promoters of BOP1/BOP2 directly to repress their expression, resulting in delayed establishment of proliferative regions in leaves, which promotes more blade outgrowth (the distal region of a leaf) and suppresses petiole development (the proximal region of a leaf). Our results reveal a mechanism for leaf development along the proximal–distal axis, a heteroblastic character between juvenile leaves and adult leaves. 

Forage yield is largely dependent on leaf development, during which the number of leaves, leaflets, leaf size, and shape are determined. In this mini-review, we briefly summarize recent studies of leaf development in Medicago truncatula, a model plant for legumes, with a focus on factors that could affect biomass of leaves. These include: floral development and related genes, lateral organ boundary genes, auxin biosynthesis, transportation and signaling genes, and WOX related genes. 

Correct timing of developmental phase transitions is critical for the survival and fitness of plants. Developmental phase transitions in plants are partially promoted by controlling relevant genes into active or repressive status. Polycomb Repressive Complex1 (PRC1) and PRC2, originally identified in Drosophila, are essential in initiating and/or maintaining genes in repressive status to mediate developmental phase transitions. Our review summarizes mechanisms in which the embryo-to-seedling transition, the juvenile-to-adult transition, and vegetative-to-reproductive transition in plants are mediated by PRC1 and PRC2, and suggests that PRC1 could act either before or after PRC2, or that they could function independently of each other. Details of the exact components of PRC1 and PRC2 in each developmental phase transitions and how they are recruited or removed will need to be addressed in the future. 

Abstract Plants that develop under low light (LL) intensity often display a phenotype known as the “shade tolerance syndrome (STS)”. This syndrome is similar to the phenotype of plants in the juvenile phase of shoot development, but the basis for this similarity is unknown. We tested the hypothesis that the STS is regulated by the same mechanism that regulates the juvenile vegetative phase by examining the effect of LL on rosette development in Arabidopsis (Arabidopsis thaliana). We found that LL prolonged the juvenile vegetative phase and that this was associated with an increase in the expression of the master regulators of vegetative phase change, miR156 and miR157, and a decrease in the expression of their SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE (SPL) targets. Exogenous sucrose partially corrected the effect of LL on seedling development and miR156 expression. Our results suggest that the response of Arabidopsis to LL is mediated by an increase in miR156/miR157 expression and by factors that repress SPL gene expression independently of miR156/miR157, and is caused in part by a decrease in carbohydrate production. The effect of LL on vegetative phase change does not require the photoreceptors and transcription factors responsible for the shade avoidance syndrome, implying that light intensity and light quality regulate rosette development through different pathways. 

Vegetative leaves in Arabidopsis are classified as either juvenile leaves or adult leaves based on their specific traits, such as leaf shape and the presence of abaxial trichomes. The timing of the juvenile-to-adult phase transition during vegetative development, called the vegetative phase change, is a critical decision for plants, as this transition is associated with crop yield, stress responses, and immune responses. Juvenile leaves are characterized by high levels of miR156/157, and adult leaves are characterized by high levels of miR156/157 targets, SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) transcription factors. The discovery of this miR156/157-SPL module provided a critical tool for elucidating the complex regulation of the juvenile-to-adult phase transition in plants. In this review, we discuss how the traits of juvenile leaves and adult leaves are determined by the miR156/157-SPL module and how different factors, including embryonic regulators, sugar, meristem regulators, hormones, and epigenetic proteins are involved in controlling the juvenile-to-adult phase transition, focusing on recent insights into vegetative phase change. We also highlight outstanding questions in the field that need further investigation. Understanding how vegetative phase change is regulated would provide a basis for manipulating agricultural traits under various conditions.