PIF4-mediated activation of YUCCA8 expression integrates temperature into the auxin pathway in regulating arabidopsis hypocotyl growth.
PIF4-mediated activation of YUCCA8 expression integrates temperature into the auxin pathway in regulating arabidopsis hypocotyl growth.
复制标题
PIF4 介导的 YUCCA8 表达激活将温度整合到生长素途径中，调节拟南芥下胚轴生长。
DOI：
10.1371/journal.pgen.1002594
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发表时间：
2012
期刊：
影响因子：
4.5
通讯作者：
Li C
中科院分区：
文献类型：
--
作者：
Sun J;Qi L;Li Y;Chu J;Li C
高等植物通过植物构型的巨大变化来适应高温。研究表明，转录调控因子光敏色素相互作用因子4（PIF4）和植物激素生长素参与了拟南芥高温诱导下胚轴伸长的调控。在这里，我们报告，PIF4调节高温诱导下胚轴伸长通过直接激活生长素生物合成基因YUCCA8（YUC8）。我们发现高温共上调PIF4和YUC 8的转录丰度。高温介导的YUC 8表达诱导以及生长素生物合成的PIF4依赖性，以及PIF4的过表达导致植物中YUC 8表达增加和游离IAA水平升高的发现，表明PIF4直接激活YUC 8表达的可能性。事实上，凝胶位移和染色质免疫沉淀实验表明，PIF 4与YUC 8的含G盒启动子区域相关。本氏烟草叶片中的瞬时表达测定支持PIF4在体内直接激活YUC 8表达。值得注意的是，我们表明yuc8突变可以在很大程度上抑制PIF4过表达植物的长下胚轴表型，也可以减少高温诱导的下胚轴伸长。遗传分析表明，shy2 - 2突变，其中窝藏IAA3蛋白的稳定的突变形式，因此在高温诱导的下胚轴伸长是有缺陷的，在很大程度上抑制了长下胚轴表型的PIF4过表达植物。综上所述，我们的研究结果阐明了一个分子框架，PIF4转录调节因子通过激活特定生长素生物合成基因的表达将其作用整合到生长素途径中。这些研究促进了我们对高温诱导植物构型适应的分子机制的理解。拟南芥暴露于高温（29 ° C）导致下胚轴显著伸长。碱性螺旋-环-螺旋转录因子PIF4和植物激素生长素在高温诱导拟南芥下胚轴伸长过程中起重要作用。然而，PIF4和生长素途径在调节高温诱导的适应性生长中的可能的分子联系仍然未知。在这里，我们报告高温诱导的升高YUCCA8（YUC8）成绩单和内源性游离IAA水平是依赖于PIF4的功能。特别是，我们提供了证据表明PIF 4直接激活YUC 8的表达，以上调生长素的生物合成，从而实现高温诱导的下胚轴伸长。此外，我们发现SHY2/IAA3是PIF4-生长素途径中调节高温诱导下胚轴伸长的重要组成部分。总的来说，我们的研究结果建立了PIF4转录因子和生长素途径在调节高温诱导的适应性生长之间的直接联系。
Higher plants adapt their growth to high temperature by a dramatic change in plant architecture. It has been shown that the transcriptional regulator phytochrome-interacting factor 4 (PIF4) and the phytohormone auxin are involved in the regulation of high temperature–induced hypocotyl elongation in Arabidopsis. Here we report that PIF4 regulates high temperature–induced hypocotyl elongation through direct activation of the auxin biosynthetic gene YUCCA8 (YUC8). We show that high temperature co-upregulates the transcript abundance of PIF4 and YUC8. PIF4–dependency of high temperature–mediated induction of YUC8 expression as well as auxin biosynthesis, together with the finding that overexpression of PIF4 leads to increased expression of YUC8 and elevated free IAA levels in planta, suggests a possibility that PIF4 directly activates YUC8 expression. Indeed, gel shift and chromatin immunoprecipitation experiments demonstrate that PIF4 associates with the G-box–containing promoter region of YUC8. Transient expression assay in Nicotiana benthamiana leaves support that PIF4 directly activates YUC8 expression in vivo. Significantly, we show that the yuc8 mutation can largely suppress the long-hypocotyl phenotype of PIF4–overexpression plants and also can reduce high temperature–induced hypocotyl elongation. Genetic analyses reveal that the shy2-2 mutation, which harbors a stabilized mutant form of the IAA3 protein and therefore is defective in high temperature–induced hypocotyl elongation, largely suppresses the long-hypocotyl phenotype of PIF4–overexpression plants. Taken together, our results illuminate a molecular framework by which the PIF4 transcriptional regulator integrates its action into the auxin pathway through activating the expression of specific auxin biosynthetic gene. These studies advance our understanding on the molecular mechanism underlying high temperature–induced adaptation in plant architecture. Exposure of Arabidopsis to high temperature (29°C) results in a dramatic hypocotyl elongation. The basic helix-loop-helix transcription factor PIF4 and the phytohormone auxin play essential roles in high temperature–mediated induction of Arabidopsis hypocotyl elongation. However, the possible molecular linkage between PIF4 and the auxin pathway in regulating high temperature–induced adaptative growth remains unknown. Here, we report that high temperature–induced elevation of YUCCA8 (YUC8) transcripts and endogenous free IAA levels is dependent on the function of PIF4. In particular, we provide evidence that PIF4 directly activates the expression of YUC8 to upregulate auxin biosynthesis, as a consequence, achieves high temperature–induced hypocotyl elongation. In addition, we found that SHY2/IAA3 is an important component of the PIF4–auxin pathway in regulating high temperature–induced hypocotyl elongation. Overall, our results establish a direct connection between the PIF4 transcription factor and the auxin pathway in regulating high temperature–induced adaptation growth.
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