科学家发现调控植物分枝形成基因
来源:《The Plant Cell》 时间:2016/01/11

 

 

植物分枝的多少,是植物在形态上适应环境的一种非常重要的方式,还可以影响粮食产量。那么植物的分枝是如何形成的呢?分枝形成的过程又是如何调控的呢?北京大学秦跟基课题组发现了一个重要的调控植物分枝的基因。相关成果日前发布于《植物细胞》

一些名为“腋芽分生组织调控因子”(RAX)的MYB类转录因子对干细胞形成起非常重要的作用。科学家通过正向遗传学方法鉴定了一个促进植物分枝增多的基因,命名为“过多分枝”(EXB1)。在突变体中EXB1基因的表达量升高,植物就长出很多分枝,而且有些叶腋处长出更多个初级分枝和更高级分枝,甚至在子叶的叶腋处也能长出分枝。这说明EXB1基因可促进腋芽干细胞的形成,甚至可以在正常情况下不能形成腋芽干细胞的部位也能形成腋芽干细胞。

研究发现,EXB1基因编码一个植物中特有的转录因子。EXB1通过调控RAX基因的表达来促进分枝,而且体内和体外实验证明EXB1是直接结合到RAX基因的启动子区,从而调控RAX基因的表达。同时,植物激素生长素也在EXB1促进植物分枝形成的过程中起重要作用。(来源:中国科学报 彭科峰)

 

The WRKY Transcription Factor WRKY71/EXB1 Controls Shoot Branching by Transcriptionally Regulating RAX Genes in Arabidopsis

 

Abstract  Plant shoot branching is pivotal for developmental plasticity and crop yield. The formation of branch meristems is regulated by several key transcription factors including REGULATOR OF AXILLARY MERISTEMS1 (RAX1), RAX2, and RAX3. However, the regulatory network of shoot branching is still largely unknown. Here, we report the identification of EXCESSIVE BRANCHES1 (EXB1), which affects axillary meristem (AM) initiation and bud activity. Overexpression of EXB1 in the gain-of-function mutant exb1-D leads to severe bushy and dwarf phenotypes, which result from excessive AM initiation and elevated bud activities. EXB1 encodes the WRKY transcription factor WRKY71, which has demonstrated transactivation activities. Disruption of WRKY71/EXB1 by chimeric repressor silencing technology leads to fewer branches, indicating that EXB1 plays important roles in the control of shoot branching. We demonstrate that EXB1 controls AM initiation by positively regulating the transcription of RAX1, RAX2, and RAX3. Disruption of the RAX genes partially rescues the branching phenotype caused by EXB1 overexpression. We further show that EXB1 also regulates auxin homeostasis in control of shoot branching. Our data demonstrate that EXB1 plays pivotal roles in shoot branching by regulating both transcription of RAX genes and auxin pathways.

 

原文链接:http://www.plantcell.org/content/27/11/3112.full.pdf+html

 

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