A PIF7-CONSTANS-Centered Molecular Regulatory Network Underlying the Shade-Accelerated Flowering

First author: Renshan Zhang; Affiliations: Fudan University (复旦大学): Shanghai, China

Corresponding author: Lin Li

To compete with their neighbors for light and escape shaded environments, sun-loving plants have developed shade avoidance syndrome (SAS) to alter plant architecture and initiate early flowering and seed set. Previous studies on SAS mainly focused on dissecting the molecular basis of hypocotyl elongation in seedlings under shade light, however, the molecular mechanisms underlying the shade-accelerated flowering in adult plants remain unknown. Here, we found that CONSTANS (CO) and PHYTOCHROME-INTERACTING FACTOR 7 (PIF7) have an additive effect on shade-induced flowering, but LONG HYPOCOTYL IN FAR-RED1 (HFR1) represses early flowering through binding to CO and PIF7 and preventing the binding of CO to the promoter of FLOWERING LOCUS T (FT) and the binding of PIF7 to the promoter of pri-MIR156E/F. Under shade, dephosphorylated PIF7 and accumulated CO, balanced by HFR1, up-regulate the expression of FT, TSF, SOC1 and SPLs and result in accelerated flowering. Moreover, the function of PIF7 in flowering time is independent of phyA. These regulatory interactions establish a crucial link between the light signal and the genetic network that regulates flowering transition under shade.

为了与邻近生物竞争光照以及避免阴影遮挡，喜阳植物演化出了避荫反应SAS来改变植物结构、起始早期开花和坐果。先前对于SAS的研究多注重于解析阴影条件下幼苗下胚轴伸长的分子机制，然而，阴影促进成年植株开花的分子机制还不是很清楚。本文中，作者发现CO和植物色素互作因子PIF7对于阴影诱导的开花具有加性作用，但HFR1能够通过结合CO及PIF7上阻止CO结合FT启动子及PIF7结合pri-MIR156E/F启动子，从而抑制早期开花。在阴影条件下，去磷酸化的PIF7和积累的CO会上调FT、TSF、SOC1以及SPLs基因的表达，从而促进开花。此外，PIF7对于开花时间的调控功能独立于phyA。这些调控互作建立了一个光信号与遗传网络之间的关联，从而调控植物在阴影条件下的成花转变。

doi: https://doi.org/10.1016/j.molp.2019.09.007

Journal: Molecular Plant

Published date: September 26, 2019