MAC复合体调控拟南芥铁稳态的分子机制

铁是植物必需的微量元素，缺铁会直接影响植物的生长发育。研究表明MAC复合体通过影响可变剪接(AS)进而调控植物抗逆过程。我们前期研究发现MAC复合体的核心亚基PRL1、CDC5及MAC3缺失会导致植株对缺铁敏感。RNA-seq分析发现在prl1、cdc5、mac3amac3b突变体中缺铁响应基因FIT1及MYB10/72的内含子滞留明显增加，且下游香豆素合成相关基因S8H和YP82C4的表达也显著下调。外源施加香豆素可以互补mac3amac3b、prl1等突变体的缺铁表型。基于这些结果，我们将进一步利用分子生物学、植物生理学和遗传学等方法，明确MAC复合体调控FIT1及MYB10/72可变剪切的生物学效应，阐明MYB72与S8H及CYP82C4间的调控关系，最终解析MAC复合体调控铁稳态的分子机制。

Iron (Fe) is indispensable for plants and Fe deficiency will directly hinder their growth and development. It is known that the MOS4 Associated Complex (MAC) participated in diverse stress responses through affecting stress-related aternative splicing (AS). In our previous study, we found that loss-of-function of the core components of MAC complex, including PRL1, CDC5 and MAC3, rendered the plants more sensitive to Fe deficiency compared with wild type. RNA-seq analysis revealed that the intron retention of Fe-homeostasis associated regulation genes, including FIT1, MYB10 and MYB72, was dramatically increased, and the expression of coumarin biosynthesis genes S8H and CYP82C4 were also greatly down-regulated in prl1, cdc5 and mac3amac3b mutant seedlings. Further analysis demonstrated that exogenous application of fraxetin can rescue the chlorosis phenotype of both mac3a mac3b and prl seedlings under Fe-deficient conditions. Based on these results, we will further determine the biological consequence of the MAC complex regulated aternative splicing of FIT1, MYB10 and MYB72, explore the genetic relationship between MYB72 and S8H or CYP82C4, and finally illustrate the molecular mechanism of iron homeostasis that controlled by MAC complex.