N6-甲基腺苷(m6A)mRNA修饰的动力学受到m6A甲基转移酶复合物和去甲基酶的严格控制。这里,我们发现生长素处理改变了对生长素响应基因的m6A修饰。机械上,跨膜激酶4(TMK4),生长素信号通路的一个组成部分,与FKBP12-相互作用蛋白37(FIP37)相互作用并磷酸化,m6A甲基转移酶复合物的核心成分,以生长素依赖的方式。FIP37的磷酸化增强了其与RNA的相互作用,从而增加其靶基因的m6A修饰,例如硝酶1(NIT1),参与吲哚-3-乙酸(IAA)生物合成的基因。1-萘乙酸(NAA)处理以TMK4-和FIP37依赖性方式加速NIT1的mRNA衰减,这导致生长素生物合成的抑制。我们的发现确定了生长素通过磷酸化FIP37调节m6A修饰的调节机制,最终影响植物中的mRNA稳定性和生长素生物合成。
The dynamics of N6-methyladenosine (m6A) mRNA modification are tightly controlled by the m6A methyltransferase complex and demethylases. Here, we find that auxin treatment alters m6A modification on auxin-responsive genes. Mechanically, TRANSMEMBRANE KINASE 4 (TMK4), a component of the auxin signaling pathway, interacts with and phosphorylates FKBP12-INTERACTING PROTEIN 37 (FIP37), a core component of the m6A methyltransferase complex, in an auxin-dependent manner. Phosphorylation of FIP37 enhances its interaction with RNA, thereby increasing m6A modification on its target genes, such as NITRILASE 1 (NIT1), a gene involved in indole-3-acetic acid (IAA) biosynthesis. 1-Naphthalacetic acid (NAA) treatment accelerates the mRNA decay of NIT1, in a TMK4- and FIP37-dependent manner, which leads to inhibition of auxin biosynthesis. Our findings identify a regulatory mechanism by which auxin modulates m6A modification through the phosphorylation of FIP37, ultimately affecting mRNA stability and auxin biosynthesis in plants.