小麦碱胁迫应答基因TaIAA10耐碱机制研究

Soil salinity-alkalinity is mainly due to the accumulation of neutral NaCl and also alkaline salt which cause high pH, and researches have shown that the effects of soil alkalinization on plants may be more destructive than the effects of soil salinization. Plant salinity tolerance mechanisms have been extensively explored and important progress has been made, however, the understanding of plant alkalinity tolerance is lacking. Recently, Arabidopsis protein kinase PKS5 mediated signal pathway was reported to play important roles in alkalinity resistance, and associated with auxin pathway; however, the molecular mechanism of crop alkali resistance has not been reported. We selected an alkalinity-tolerant introgression wheat line SR4, and identified an alkalinity responsive auxin signal pathway gene TaIAA10 in SR4 through transcriptome analysis. The over-expression of TaIAA10 in wheat and Arabidopsis did not change the salt resistance of plants, however, it enhanced the resistance of plants to alkali stress and ABA, and it also changed the expression of ABA signaling pathway genes. Therefore, we speculate that TaIAA10 might play important roles in SR4 to regulate alkali resistance through cross-talk of IAA and ABA signaling pathway. In this proposal, we plan to identify the detail function and molecular mechanism of TaIAA10 in wheat alkali stress resistance, through exploiting the relationship between TaIAA10 and ABA signaling pathway, and also PKS5 signaling pathway.

土壤盐渍化主要由中性盐NaCl和改变其pH的碱性盐导致，研究表明碱胁迫比盐胁迫给植物造成更严重的伤害。目前对植物盐胁迫应答机制的研究较为广泛并已取得重要进展，然而对碱胁迫的研究很少。近期报道拟南芥蛋白激酶PKS5介导的信号途径在碱胁迫抗性中起重要作用且与生长素相关，但是作物耐碱分子机制尚无报道。我们选育了耐碱小麦渐渗系山融4号（SR4），前期从SR4转录组中筛选到应答碱胁迫的生长素信号途径基因TaIAA10,发现该基因过量表达不改变植物在盐胁迫下的表型，却特异提高了植物对碱胁迫和ABA的抗性，并且影响ABA信号途径基因的表达。我们推测该基因在SR4中起重要作用，通过IAA与ABA信号通路的交叉调控耐碱性。本项目拟对TaIAA10在小麦耐碱方面的功能和生理特征进行系统分析，阐明TaIAA10与ABA信号通路及PKS5耐碱信号通路的关系，全面解析TaIAA10基因参与小麦耐碱的作用机制。

已有研究表明碱胁迫比盐胁迫给植物造成更严重的伤害，然而目前对植物应答碱胁迫的分子机制研究很少。我们从耐碱小麦渐渗系山融4号（SR4）中鉴定到应答碱胁迫的生长素信号途径基因TaIAA10, 并对其调控非生物胁迫尤其是碱胁迫的功能及分子机制进行了详细的研究。我们发现TaIAA10过量表达可以提高小麦对碱胁迫和ABA的耐受性，进一步对TaIAA10的互作蛋白筛选发现其可以和TaARF19以及TaIAA34等蛋白互作。我们通过分析发现TaARF19能够激活TaABI5的表达，而TaIAA10能够抑制TaARF19对TaABI5的转录激活作用，从而提高小麦对ABA的耐受性。TaIAA34的功能获得性突变体对碱胁迫敏感，表明其能够负调控小麦耐碱性。TaIAA34能够与TaARF16互作并抑制其对TaSAUR215的转录激活作用，从而调控小麦耐碱性。进一步作用机制解析发现TaSAUR215与钙离子结合蛋白TaCCD1互作并抑制TaPP2C.D1/8的磷酸酶活性，而TaPP2C.D1/8通过去除TaHA2的Thr926位点的磷酸化修饰从而抑制质膜H+-ATPase的活性和根部质子的外排能力，从而调控小麦碱胁迫抗性。