外界磷素状况调控水稻磷素平衡及株型的分子生理机制研究

Phosphorus is an essential macro nutrition for crop production. Under phosphorus deficient stress, the plant growth, tiller number and leaf angle in rice are significantly reduced, which lead to a dramatic reduction of yield in the field. However, the molecular mechanism of the modulation of shoot architecture by phosphorus availability in rice is still largely unclear. Therefore, the understanding of the mechanism will benefit not only for the molecular breeding of rice cultivars with super architecture for low phosphate tolerance, but also for the phosphate fertilization efficiency in the field. Previously, by characterizing the loss of function mutants for phosphate starvation repressed transcription factor, we have identified OsMYB18. The loss of function mutant for OsMYB18 displays erect-leaf and fewer tillers under normal phosphate condition. Comparing with the wild type, the OsMYB18 overexpressors display increased leaf angle with higher phosphate accumulation. Therefore, transcriptome analysis, DNA binding analysis and plant nutrition physiological analysis will be used to determine the molecular mechanism of OsMYB18 in the regulation of shoot architecture and phosphate homeostasis under the phosphate deficient stress in rice. The potential application of OsMYB18 for breeding low phosphate tolerance rice cultivars will also be determined.

磷素是作物生产所必须的大量营养元素。磷素养分匮乏将影响水稻地上部株型：分蘖减少，叶夹角变小（俗称‘一炷香’），最终导致田间稻米产量下降。但外界磷素状况如何影响水稻株型的营养分子生理机制仍不清楚。因此，解析该机制不仅能够为构建水稻耐低磷优良株型品种的分子育种提供理论基础，也能为保障水稻大田生产过程中的磷素高效利用提供理论依据。利用反向遗传学的方法，本课题组通过对低磷胁迫抑制表达转录因子的功能分析，鉴定了一个OsMYB18基因。OsMYB18功能失活突变体在正常供磷条件下水稻叶片夹角变小，分蘖数减少。而该基因的过量表达能导致叶片的夹角增大，叶片无机磷积累。因此，本研究将围绕OsMYB18参与的磷素代谢与叶片角度调控体系，利用芯片分析系统、蛋白与DNA互作分析、以及养分生理实验，探讨OsMYB18参与水稻低磷胁迫下株型调控及磷素养分平衡的营养分子生理机制及其潜在应用前景。

磷素是作物生产所必须的大量营养元素。磷素养分匮乏将影响水稻地上部株型：分蘖减少，叶夹角变小（俗称‘一炷香’），最终导致田间稻米产量下降。但外界磷素状况如何影响水 稻株型的营养分子生理机制仍不清楚。在本项目中，我们解析了不同土壤磷素供应状况下对水稻地上部株型的细胞学基础，发现土壤磷素养分供应不足将抑制水稻叶枕部位的细胞伸长来调节叶枕大小并调节叶夹角和地上部株型。同时，低磷胁迫能抑制地上部细胞增殖，导致地上部生长受抑。进一步的分子生理机制解析发现，水稻能够感受土壤磷素供应水平，通过诱导磷信号负调控因子OsSPX1的表达，来抑制水稻地上部叶夹角。我们也鉴定到一个与OsSPX1互作的MYB转录因子OsRLI1，OsRLI1是一个正调控水稻叶夹角的转录因子，增强表达该基因能促进水稻叶夹角的增大。OsRLI1能够直接结合油菜素内酯信号的重要转录因子OsBC1和OsBU1来调节下游油菜素内酯信号和基因表达，最终调节水稻叶枕细胞生长，调控水稻株型。我们也发现低磷能抑制OsRLI1的表达，且OsSPX1与OsRLI1互作后能抑制OsRLI1的表达和活力。因此，SPX和RLI1蛋白形成了一对模块能够整合外界磷素供应状况调节水稻叶片夹角。同时，我们也发现水稻在低磷胁迫条件下通过诱导OsCYCP4家族来负调控地上部细胞分裂能力，从而抑制地上部生长。总之，我们的相关研究结果对于培养磷高效作物品种提供了理论支撑。