摘要
In plants, the cytokinin metabolic processes, including cytokinin biosynthesis, interconversion, inactivation, and degradation, play critical roles in the regulation of cytokinin homeostasis and plant development. Purine meta- bolic enzymes have been implied to catalyze the cytokinin interconversion in previous works. In this study, we report that Adenine Phosphoribosyl Transferase 1 （APT1） is the causal gene of the high-dose cytokinin-resistant mutants. APT1 catalyzes the cytokinin conversion from free bases to nucleotides, and is functionally predominant among the five members of the Arabidopsis Adenine Phosphoribosyl Transferase family. Loss of APT1 activity in plants leads to excess accumulation of cytokinin bases, thus evoking myriad cytokinin-regulated responses, such as delayed leaf senescence, anthocyanin accumulation, and downstream gene expression. Thus, our study defines APT1 as a key metabolic enzyme participating in the cytokinin inactivation by phosphoribosylation.
In plants, the cytokinin metabolic processes, including cytokinin biosynthesis, interconversion, inactivation, and degradation, play critical roles in the regulation of cytokinin homeostasis and plant development. Purine meta- bolic enzymes have been implied to catalyze the cytokinin interconversion in previous works. In this study, we report that Adenine Phosphoribosyl Transferase 1 （APT1） is the causal gene of the high-dose cytokinin-resistant mutants. APT1 catalyzes the cytokinin conversion from free bases to nucleotides, and is functionally predominant among the five members of the Arabidopsis Adenine Phosphoribosyl Transferase family. Loss of APT1 activity in plants leads to excess accumulation of cytokinin bases, thus evoking myriad cytokinin-regulated responses, such as delayed leaf senescence, anthocyanin accumulation, and downstream gene expression. Thus, our study defines APT1 as a key metabolic enzyme participating in the cytokinin inactivation by phosphoribosylation.
基金
This work was supported by grants from the Ministry of Science and Technology of China （2009CBl19101）, the Ministry of Agriculture of China （2010ZX08010-002）, and the National Natural Science Foundation of China （91017010） to H.G.We thank Dr Zhigang Jiang and Dr Di Guo for manu- script preparation and critical discussion, and Dr Shuhua Yang （China Agricultural University, China）, Dr Dong Liu （Tsinghua University, China）, and Dr Thomas Schm~lling （Free University of Berlin, Germany） for kindly providing the cytokinin mutants and relevant transgenic plants. We thank Dr Xiangning Jiang （Beijing Forestry University, China） and Dr Meiping Zhao （Peking University, China） for their assis- tance on cytokinin quantification, and Meng Ke （Tsinghua University, China） for guidance on bioinformatics. No conflict of interest declared.
