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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. 

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. 

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.