背景回顾：The phytohormones gibberellins (GAs) play fundamental roles in almost every aspect of plant growth and development. 

提出问题：Although there is good knowledge about GA biosynthetic and signaling pathways, factors contributing to the mechanisms homeostatically controlling GA levels remain largely unclear. 

主要发现：Here, we demonstrate that homeobox transcription factor HB40 of the HD-Zip family in Arabidopsis thaliana regulates GA content at two additive control levels. 

结果1-HB40诱导表达及其功能：We show that HB40expression is induced by GA and in turn reduces the levels of endogenous bioactive GAs by a simultaneous reduction of GA biosynthesis and increased GA deactivation. 

结果2-HB40过表达：Hence, HB40 overexpression leads to typical GA-deficiency traits, such as small rosettes, reduced plant height, delayed flowering, and male sterility. 

结果3-hb40突变体：In contrast, a loss-of-function hb40 mutation enhances GA-controlled growth. 

结果4-HB40-JUB1：Genome-wide RNA-sequencing combined with molecular-genetic analyses revealed that HB40 directly activates transcription ofJUNGBRUNNEN1(JUB1), a key TF repressing growth by suppressing GA biosynthesis and signaling. 

结果5-HB40-GA2ox：HB40 also activates genes encoding GA 2-oxidases (GA2oxs) which are major GA catabolic enzymes. 

结果6-HB40-DELLA：The effect of HB40 is ultimately mediated through induction of nuclear growth-repressing DELLA proteins. 

结论：Our results thus uncover an important role of the HB40/JUB1/GA2ox/DELLA regulatory network in controlling GA homeostasis during plant growth.

 摘 要 

植物激素赤霉素（GA）在植物生长和发育几乎方方面面都扮演着重要的作用。尽管目前对于GA生物合成和信号转导途径的了解比较多，但是作用于GA水平内稳态维持的分子机制还不是很清楚。本文中，作者发现拟南芥HD-Zip家族中的homeobox转录因子HB40作用于GA含量的控制。作者发现HB40基因的表达受到GA的诱导，反过来HB40会通过同时减少GA生物合成和增加GA失活来降低内源的有活性GA的水平。HB40过表达会导致典型的GA缺陷表型，比如说莲座叶变小、植物高度变矮、开花延迟以及雄性不育。相反，hb40功能缺失突变体会增强由GA控制的生长。结合RNA测序分析和分子遗传方法， 作者发现HB40能够直接激活JUB1基因的转录，而JUB1基因编码一个参与植物生长调控的关键转录因子，其通过抑制GA生物合成和信号转导作用于生长抑制。HB40还能激活编码GA2oxs基因的表达，而GA2oxs是主要的GA分解代谢酶。HB40的作用最终是通过诱导核生长抑制的DELLA蛋白所介导。本文的研究结果发现了一个在植物生长过程中控制GA内稳态的重要调控网络HB40/JUB1/GA2ox/DELLA。

 通讯作者 

** Salma Balazadeh **