ABA通过ABI4介导生长素及细胞周期途径进而调控主根生长

根系对于植物抗逆、营养吸收等方面意义重大。生长素在调控根生长、尤其是维持根尖干细胞活性方面具有重要的生理功能；高浓度脱落酸(ABA)抑制拟南芥主根生长，但在此过程中它与生长素互作调控的分子机制尚未明晰。我们前期研究发现，转录因子ABI4在介导ABA抑制主根生长过程中具有重要功能；ABA处理后，abi4突变体根中CDKB2;2等细胞周期正调控基因表达量、以及根尖DR5pro-GFP荧光水平均明显高于野生型，由此推测ABA可能通过ABI4介导生长素及细胞周期途径进而抑制主根生长，但具体分子机制有待深入研究。本项目将利用ABI4现有的相关遗传材料，检测ABI4对根尖生长素、细胞周期途径及根形态建成关键基因表达的影响，测定根尖生长素浓度，并通过染色质免疫共沉淀、凝胶阻滞、酵母单杂交等方法筛选受ABI4直接调控的靶标基因，最终揭示ABA通过ABI4介导生长素及细胞周期途径进而调控主根生长的分子机理。

Root system is of great significance to plant stress resistance and nutrient absorption. Auxin possesses the important physiological function in the regulation of root growth, especially for maintaining root stem cell niche. High level of abscisic acid (ABA) inhibits Arabidopsis primary root growth, but in this process, the molecular mechanisms underlying the crosstalk between ABA and auxin are elusive so far. Our previous studies showed that the transcription factor ABI4 plays the key roles in ABA-mediated inhibition of primary root growth. After treated by ABA, in abi4 mutant root, the transcription level of a positive regulator in cell cycle pathway, CDKB2;2, was remarkable increased compared to in WT (wild type). Further, the DR5-GFP fluorescence level in abi4 root tip is also significantly higher that in WT. Consequently, these evidences indicated that ABA inhibits primary root growth through ABI4-mediated auxin and cell cycle pathways, but the detailed molecular mechanisms need further investigation. This project will use the available genetic materials, and investigate the effects of ABI4 on the expression of key genes involved in auxin and cell cycle pathways and root morphogenesis related, and quantify the auxin concentration in the primary root tip. Subsequently, we will further employ the assays including chromatin immunoprecipitation-qPCR (ChIP-qPCR), electrophoretic mobility shift assay (EMSA) and yeast one hybrid to identify the direct target genes of transcription factor ABI4. Finally, this project will reveal the detailed molecular mechanism that ABA inhibits primary root growth through ABI4-mediated auxin and cell cycle pathways.