Affiliation:
1. State Key Laboratory of Rice Biology and Breeding China National Rice Research Institute Hangzhou 310006 China
2. State Key Laboratory of Plant Genomics and National Center for Plant Gene Research (Beijing), Institute of Genetics and Developmental Biology, The Innovative Academy of Seed Design Chinese Academy of Sciences Beijing 100101 China
3. Seed Center and Plant Genetic Resources Bank Ministry of Environment, Water & Agriculture Riyadh 14712 Saudi Arabia
Abstract
Summary
Rice tillering is one of the most important agronomical traits largely determining grain yield. Photosynthesis and nitrogen availability are two important factors affecting rice tiller bud elongation; however, underlying mechanism and their cross‐talk is poorly understood.
Here, we used map‐based cloning, transcriptome profiling, phenotypic analysis, and molecular genetics to understand the roles of the Decreased Tiller Number 1 (DTN1) gene that encodes the fructose‐1,6‐bisphosphate aldolase and involves in photosynthesis required for light‐induced axillary bud elongation in rice.
Deficiency of DTN1 results in the reduced photosynthetic rate and decreased contents of sucrose and other sugars in both leaves and axillary buds, and the reduced tiller number in dtn1 mutant could be partially rescued by exogenous sucrose treatment. Furthermore, we found that the expression of nitrogen‐mediated tiller growth response 5 (NGR5) was remarkably decreased in shoot base of dtn1‐2, which can be activated by sucrose treatment. Overexpression of NGR5 in the dtn1‐2 could partially rescue the reduced tiller number, and the tiller number of dtn1‐2 was insensitive to nitrogen supply.
This work demonstrated that the sugar level regulated by photosynthesis and DTN1 could positively regulate NGR5 expression, which coordinates the cross‐talk between carbon and nitrate to control tiller bud outgrowth in rice.
Funder
Central Public-interest Scientific Institution Basal Research Fund for Chinese Academy of Tropical Agricultural Sciences
National Natural Science Foundation of China
Cited by
1 articles.
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