PIF7 controls leaf cell proliferation through an AN3 substitution-repression mechanism
PIF7 controls leaf cell proliferation through an AN3 substitution-repression mechanism
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DOI：
10.1101/2021.05.31.446395
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发表时间：
2021-05
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影响因子：
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通讯作者：
E. Hussain;A. Romanowski;K. Halliday
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文献类型：
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作者：
E. Hussain;A. Romanowski;K. Halliday
植物是灵活的、可塑的生物，能够适应不断变化的环境。对来自附近植被的远红（FR）波长做出反应，遮荫不耐受的物种会引发适应性遮荫回避综合征（SAS），其特征是叶柄延长，叶片低垂和叶片较小。我们利用日末FR （EODFR）处理来询问SAS叶片反应背后的分子过程。遗传分析表明光光色素相互作用因子7 （PIF7）是EODFR介导的叶片细胞分裂约束所必需的，而EODFR mRNAseq数据鉴定出ANGUSTIFOLIA3 （AN3）是潜在的PIF7靶点。我们发现PIF7可以通过隔离机制抑制AN3的转录，阻止AN3激活其自身的表达。我们还建立了PIF7和AN3通过几个细胞周期调节基因中共同的顺式作用启动子基序对基因表达施加拮抗控制。EODFR触发了G-box/PBE-box启动子区域AN3到PIF7的分子取代，并从促进基因表达转变为抑制基因表达。
Plants are agile, plastic organisms, able to adapt to ever-changing circumstances. Responding to far-red (FR) wavelengths from nearby vegetation, shade-intolerant species elicit the adaptive Shade Avoidance Syndrome (SAS), characterised by elongated petioles, leaf hyponasty and smaller leaves. We utilised end-of-day FR (EODFR) treatments to interrogate molecular processes that underlie the SAS leaf response. Genetic analysis establishes PHYTOCHROME INTERACTING FACTOR 7 (PIF7) is required for EODFR-mediated constraint of leaf blade cell division, while EODFR mRNAseq data identified ANGUSTIFOLIA3 (AN3) as a potential PIF7 target. We show PIF7 can suppress AN3 transcription through a sequestering mechanism that prevents AN3 activation of its own expression. We also establish PIF7 and AN3 impose antagonistic control of gene expression via common cis-acting promoter motifs in several cell cycle regulator genes. EODFR triggers the molecular substitution of AN3 to PIF7 at G-box/PBE-box promoter regions, and a switch from promotion to repression of gene expression.