Abstract：
TCP13 belongs to a subgroup of TCP transcription factors implicated in the shade avoidance syndrome (SAS), but its exact role remains unclear. Here, we show that TCP13 promotes the SAS-like response by enhancing hypocotyl elongation and suppressing flavonoid biosynthesis as a part of the incoherent feed-forward loop in light signaling. Shade is known to promote the SAS by activating PHYTOCHROME-INTERACTING FACTOR (PIF)-auxin signaling in plants, but we found no evidence in a transcriptome analysis that TCP13 activates PIF-auxin signaling. Instead, TCP13 mimics shade by activating the expression of a subset of shade-inducible and cell elongation-promoting SAUR genes including SAUR19, by direct targeting of their promoters. We also found that TCP13 and PIF4, a molecular proxy for shade, repress the expression of flavonoid biosynthetic genes by directly targeting both shared and distinct sets of biosynthetic gene promoters. Together, our results indicate that TCP13 promotes the SAS-like response by directly targeting a subset of shade-responsive genes without activating the PIF-auxin signaling pathway.
摘要：
TCP13属于与避荫综合征（SAS）有关的TCP亚群，但其确切作用尚不清楚。这里,我们显示TCP13通过增强下胚轴伸长和抑制类黄酮生物合成促进SAS样反应,作为光信号中不相干前馈环的一部分.众所周知，Shade可以通过激活植物中的PIF-生长素信号来促进SAS，但是我们在转录组分析中没有发现TCP13激活PIF-生长素信号传导的证据。相反，我们发现TCP13通过直接靶向其启动子激活包括SAUR19在内的一组可诱导阴影和促进细胞伸长的SAUR基因的表达来模拟阴影。我们还发现了TCP13和PIF4，这是阴影的分子代表，通过直接靶向共享和不同组的生物合成基因启动子来抑制类黄酮生物合成基因的表达。一起,我们的结果表明,TCP13通过直接靶向一个亚组的阴暗应答基因而不激活PIF-生长素信号通路,从而促进SAS样应答.
