谷氨酰胺作为长距离信号分子介导低磷胁迫和调节根际酸化的分子机制

Phosphorus (P) is one of the most important plant nutrients that significantly affect growth and metabolism. Although the total amount of P in soil may be high, it is often present in unavailable forms. Low availability of P is a major constraint for crop production in many low-input systems of agriculture worldwide. Higher plants adapt to phosphorus deficiency through a complex of biological processes. Rhizosphere acidification is one of the important adaptive processes to acquire phosphorus efficiently from soil. But the mechanism of rhizosphere acidification induced by low phosphate remains unclear. p444 is a mutant with deficient rhizosphere acidification induced by low phosphate in Arabidopsis. Mapping clone studies indicate that p444 is allelic to GLU1, Which encodes the glutamate synthase (glutamine-oxoglutarate aminotransferase or GOGAT). The deficiency of GLU1 results in more glutamine accumulation in arabidopsis. The results of grafting and adding glutamine to incision of petiole indicate that glutamine can act as a long-distance signal molecular come from leaves and regulate the low phosphate induced rhizosphere acidification. In this project, we will identify the molecular mechanism for the transcription of GLU1 and the accumulation of glutamine regulated by low phosphate signals. We will also analysis the mechanism for glutamine regulate the activity of plasma membrane H+-ATPase and the secretion of organic acid from root.

根际酸化是植物适应低磷胁迫的一种生理反应，根际酸化能够活化根际不溶磷、提高土壤磷营养的利用效率，但低磷诱导根际酸化的分子机制还不清楚。p444是我们筛选得到的低磷诱导根际酸化缺失拟南芥突变体，其突变基因GLU1受低磷胁迫诱导，在叶片中表达；GLU1催化谷氨酰胺转化生成谷氨酸，GLU1功能缺失导致p444突变体的谷氨酰胺积累和根际酸化缺失；培养基中添加谷氨酰胺可抑制野生型拟南芥的根际酸化反应；嫁接和叶注射谷氨酰胺的实验表明，谷氨酰胺可能作为叶源长距离信号分子调控低磷诱导的根际酸化。本项目将进一步分析GLU1基因在响应低磷胁迫、调控根际酸化反应中的特异性，分析GLU1对谷氨酰胺含量的调控、以及谷氨酰胺作为信号分子调控根细胞质膜H+-ATPase活性和有机酸分泌的分子机制；揭示谷氨酰胺作为叶源长距离信号分子介导低磷胁迫和调控根际酸化的信号转导机制，为培育土壤磷高效作物新品种奠定理论基础。

根际酸化是植物适应低磷胁迫的一种生理反应，根际酸化能够活化根际难溶磷、提高土壤磷营养的利用效率。但低磷诱导根际酸化反应（PDRA）的分子机制还不清楚。p444是我们筛选得到的PDRA缺失的拟南芥突变体，其突变基因GLU1编码GS/GOGAT循环的关键酶之一。通过本项目的研究发现，GLU1基因突变导致植株地上部分无机磷含量上升、花青素积累减少、低磷响应基因表达下调，表明突变体对低磷胁迫的响应减弱。GLU1在叶片中特异性表达，其表达受低磷胁迫诱导上调。GLU1功能缺失导致GS-GOGAT循环功能紊乱，叶片中谷氨酰胺和游离铵积累，氨基酸及有机酸代谢谱发生变化。外施实验表明谷氨酰胺和游离铵可能作为长距离信号远程调控PDRA反应。此外，叶片中特异表达的GS-GOGAT循环成员GLN2功能受损也导致PDRA缺失及游离铵积累，推测地上部分GS/GOGAT循环功能的完整性是根系PDRA所必需。GLU1突变导致根系H+-ATPase酶活降低，编码H+-ATPase的AHAs基因家族成员中AHA1、AHA2和AHA7的表达下调。此外，低磷条件下glu1突变体根系分泌物中苹果酸、琥珀酸、丙酮酸和α-酮戊二酸的含量显著降低，然而根系合成的苹果酸与WT相比未见显著减少。突变体中苹果酸分泌通道编码基因ALMT1的表达显著下调，调控ALMT1的转录因子STOP1蛋白积累减少。根据以上结果，推测GLU1基因突变导致GS/GOGAT循环功能受损，游离铵或谷氨酰胺作为长距离信号分子，一方面调控根中AHA1、AHA2和AHA7在低磷下的表达，进一步影响质子泵活性和根系质子的分泌；另一方面，通过调控ALMT1基因的表达，影响根系苹果酸的分泌。通过这两个方面的作用共同调控低磷诱导的根际酸化反应。该项目的研究成果可以为提高土壤磷素的吸收利用及培育磷高效作物新品种奠定理论基础，为绿色农业的发展提供新的思路。

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