背景回顾：High ambient temperature suppresses Arabidopsis (Arabidopsis thaliana) rosette leaf area and elongates the stem and petiole. While the mechanism underlying the temperature-induced elongation response has been extensively studied, the genetic basis of temperature regulation of leaf size is largely unknown. 

主要发现：Here, we show that warm temperature inhibits cell proliferation in Arabidopsis leaves, resulting in fewer cells compared to the control condition. 

结果1-高温下叶片面积减少依赖于PIF4和TCP4：Cellular phenotyping and genetic and biochemical analyses established the key roles of PHYTOCHROME INTERACTING FACTOR4 (PIF4) and TEOSINTE BRANCHED1/CYCLOIDEA/PCF4 (TCP4) transcription factors in the suppression of Arabidopsis leaf area under high temperature by a reduction in cell number. 

结果2-高温下，PIF4+TCP促进细胞周期抑制因子KRP1表达：We show that temperature-mediated suppression of cell proliferation requires PIF4, which interacts with TCP4 and regulates the expression of the cell cycle inhibitor KIP-RELATED PROTEIN1 (KRP1) to control leaf size under high temperature. 

结果3-高温下，TCP4促进PIF4表达：Warm temperature induces binding of both PIF4 and TCP4 to the KRP1 promoter. PIF4 binding to KRP1 under high temperature is TCP4 dependent as TCP4 regulates PIF4 transcript levels under high temperature. 

结果4-工作模型：We propose a model where a warm temperature-mediated accumulation of PIF4 in leaf cells promotes its binding to the KRP1 promoter in a TCP4-dependent way to regulate cell production and leaf size. 

结论：Our finding of high-temperature-mediated transcriptional upregulation of KRP1 integrates a developmental signal with an environmental signal that converges on a basal cell regulatory process.

 摘 要 

高温抑制拟南芥莲座叶的叶面积，并促进茎和叶柄的伸长。有关温度诱导的伸长生长已经研究得比较透彻，但是关于温度介导的叶片大小调控机制还不清楚。本文中，作者发现温暖温度会抑制拟南芥叶片的细胞增殖，导致相比于对照条件下细胞数量变少。细胞表型和遗传、生化证据表明，PIF4和TCP4在高温下能够减少细胞数目，抑制拟南芥的叶面积。作者在本文中发现，温度介导的细胞增殖抑制需要PIF4，该蛋白能够与TCP4互作，调控细胞周期抑制基因KRP1的表达，从而在高温条件下控制叶片的大小。温暖的温度会诱导PIF4和TCP4结合到KRP1基因的启动子区。高温条件下，TCP4能够调控PIF4基因转录水平，因此高温条件下PIF4结合到KRP1启动子区依赖于TCP4。作者提出一个模型，其中温暖温度介导的PIF4在叶片细胞中积累依赖于TCP4，促进了其结合到KRP1启动子的能力，从而调控了叶片细胞数量和叶片大小。本文的研究结果发现了高温介导的KRP1转录上调同时涉及到植物本身的发育信号和植物周边的环境信号，共同作用于一个基础的细胞调控过程。

 Aashish Ranjan