Picó Sara, Ortiz-Marchena M Isabel, Merini Wiam, Calonje Myriam
Institute of Plant Biochemistry and Photosynthesis, Instituto de Bioquímica Vegetal y Fotosíntesis-Consejo Superior de Investigaciones Científicas-University of Seville, Isla de La Cartuja, 41092 Seville, Spain.
Institute of Plant Biochemistry and Photosynthesis, Instituto de Bioquímica Vegetal y Fotosíntesis-Consejo Superior de Investigaciones Científicas-University of Seville, Isla de La Cartuja, 41092 Seville, Spain
Plant Physiol. 2015 Aug;168(4):1286-97. doi: 10.1104/pp.15.00073. Epub 2015 Apr 20.
Polycomb group (PcG) proteins play important roles in regulating developmental phase transitions in plants; however, little is known about the role of the PcG machinery in regulating the transition from juvenile to adult phase. Here, we show that Arabidopsis (Arabidopsis thaliana) B lymphoma Moloney murine leukemia virus insertion region1 homolog (BMI1) POLYCOMB REPRESSIVE COMPLEX1 (PRC1) components participate in the repression of microRNA156 (miR156). Loss of AtBMI1 function leads to the up-regulation of the primary transcript of MIR156A and MIR156C at the time the levels of miR156 should decline, resulting in an extended juvenile phase and delayed flowering. Conversely, the PRC1 component EMBRYONIC FLOWER (EMF1) participates in the regulation of SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE and MIR172 genes. Accordingly, plants impaired in EMF1 function displayed misexpression of these genes early in development, which contributes to a CONSTANS-independent up-regulation of FLOWERING LOCUS T (FT) leading to the earliest flowering phenotype described in Arabidopsis. Our findings show how the different regulatory roles of two functional PRC1 variants coordinate the acquisition of flowering competence and help to reach the threshold of FT necessary to flower. Furthermore, we show how two central regulatory mechanisms, such as PcG and microRNA, assemble to achieve a developmental outcome.
多梳蛋白家族(PcG)蛋白在调控植物发育阶段转变过程中发挥着重要作用;然而,关于PcG机制在调控从幼年期到成年期转变中的作用,我们却知之甚少。在此,我们表明拟南芥B淋巴瘤莫洛尼氏鼠白血病病毒插入区域1同源物(BMI1)多梳抑制复合体1(PRC1)组分参与了对微小RNA156(miR156)的抑制。AtBMI1功能丧失会导致在miR156水平本应下降时,MIR156A和MIR156C初级转录本上调,从而导致幼年期延长和开花延迟。相反,PRC1组分胚胎花(EMF1)参与了对SQUAMOSA启动子结合蛋白样和MIR172基因的调控。相应地,EMF1功能受损的植物在发育早期会出现这些基因的表达异常,这导致了开花位点T(FT)的独立于CONSTANS的上调,进而产生了拟南芥中最早的开花表型。我们的研究结果表明,两种功能性PRC1变体的不同调控作用如何协调开花能力的获得,并有助于达到开花所需的FT阈值。此外,我们还展示了PcG和微小RNA这两种核心调控机制是如何协同作用以实现发育结果的。