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：
10.1073/pnas.2115682119
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发表时间：
2022-02-01
影响因子：
11.1
通讯作者：
Halliday KJ
中科院分区：
文献类型：
--
作者：
Hussain E;Romanowski A;Halliday KJ
光敏色素光感受器可以显着改变叶片生长响应远红（FR）丰富的邻居阴影，但我们有一个有限的了解，这是如何实现的。本研究确定ANGUSTIFOLIA 3（AN 3）作为光敏色素促进叶细胞增殖的核心成分，光敏色素相互作用因子7（PIF 7）作为有效的阻遏物。AN 3和PIF 7通过共同的顺式作用启动子元件对一组共有的基因施加相反的调控。响应于FR光，激活的PIF 7通过在靶启动子处驱逐和取代AN 3来阻断AN 3作用。这种分子开关模块提供了一种机制，通过这种机制，外部光质量的变化可以动态地操纵基因表达、细胞分裂和叶片大小。植物是灵活的、可塑的有机体，能够适应不断变化的环境。不耐荫的物种对来自附近植被的远红外（FR）波长作出反应，引起适应性避荫综合征（SAS），其特征为叶柄伸长、叶片弱性和较小的叶片。我们利用结束的一天FR（EODFR）的治疗，询问分子过程的SAS叶响应的基础。遗传分析确定，植物色素相互作用因子7（PIF 7）是EODFR介导的限制叶片细胞分裂所必需的，而EODFR信使RNA测序数据确定ANGUSTIFOLIA 3（AN 3）作为潜在的PIF 7靶标。我们发现PIF 7可以通过直接与AN 3相互作用并隔离AN 3来抑制AN 3的转录。我们还建立了PIF 7和AN 3通过几个细胞周期调节基因中的共同顺式作用启动子基序对基因表达进行拮抗控制。EODFR在G-box/PBE-box启动子区域触发AN 3到PIF 7的分子取代，并将基因表达从促进转换为抑制。
Phytochrome photoreceptors can markedly alter leaf blade growth in response to far-red (FR) rich neighbor shade, yet we have a limited understanding of how this is accomplished. This study identifies ANGUSTIFOLIA3 (AN3) as a central component in phytochrome promotion of leaf cell proliferation and PHYTOCHROME-INTERACTING FACTOR 7 (PIF7) as a potent repressor. AN3 and PIF7 impose opposing regulation on a shared suite of genes through common cis-acting promoter elements. In response to FR light, activated PIF7 blocks AN3 action by evicting and substituting for AN3 at target promoters. This molecular switch module provides a mechanism through which changes in external light quality can dynamically manipulate gene expression, cell division, and leaf size. Plants are agile, plastic organisms able to adapt to everchanging circumstances. Responding to far-red (FR) wavelengths from nearby vegetation, shade-intolerant species elicit the adaptive shade-avoidance syndrome (SAS), characterized by elongated petioles, leaf hyponasty, and smaller leaves. We utilized end-of-day FR (EODFR) treatments to interrogate molecular processes that underlie the SAS leaf response. Genetic analysis established that PHYTOCHROME-INTERACTING FACTOR 7 (PIF7) is required for EODFR-mediated constraint of leaf blade cell division, while EODFR messenger RNA sequencing data identified ANGUSTIFOLIA3 (AN3) as a potential PIF7 target. We show that PIF7 can suppress AN3 transcription by directly interacting with and sequestering AN3. We also establish that 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.
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