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

中文翻译：

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高温通过 PIF4 和 TCP4 转录因子的协调来限制细胞分裂和叶片大小。

高环境温度会抑制拟南芥（Arabidopsis thaliana）莲座叶面积并拉长茎和叶柄。虽然温度诱导的伸长响应的机制已被广泛研究，但叶片尺寸温度调节的遗传基础在很大程度上尚不清楚。在这里，我们发现温暖的温度抑制拟南芥叶片的细胞增殖，导致与对照条件相比细胞数量减少。细胞表型分析以及遗传和生化分析确定了 PHYTOCHROME-INTERACTING FACTOR4 (PIF4) 和 TEOSINTE BRANCHED1/CYCLOIDEA/PCF4 (TCP4) 转录因子在高温下通过细胞数量减少来抑制拟南芥叶面积的关键作用。我们发现温度介导的细胞增殖抑制需要 PIF4，PIF4 与 TCP4 相互作用并调节细胞周期抑制剂 KIP 相关蛋白 1 (KRP1) 的表达，以控制高温下叶片的大小。温暖的温度诱导 PIF4 和 TCP4 与 KRP1 启动子结合。高温下 PIF4 与 KRP1 的结合是 TCP4 依赖性的，因为 TCP4 在高温下调节 PIF4 转录水平。我们提出了一个模型，其中温暖的温度介导的 PIF4 在叶细胞中的积累促进其以 TCP4 依赖性方式与 KRP1 启动子结合，从而调节细胞生产和叶片大小。我们发现高温介导的 KRP1 转录上调将发育信号与环境信号整合在一起，汇聚到基底细胞调节过程中。