Department of Botany and Plant Sciences, Institute of Integrative Genome Biology, University of California, Riverside, CA, USA.
Key Laboratory of Plant Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.
Dev Cell. 2022 Apr 25;57(8):995-1008.e5. doi: 10.1016/j.devcel.2022.03.015. Epub 2022 Apr 15.
Mobile microRNAs (miRNAs) serve as local and long-distance signals in the developmental patterning and stress responses in plants. However, mechanisms governing the non-cell autonomous activities of miRNAs remain elusive. Here, we show that mutations that disrupt microtubule dynamics are specifically defective for the non-cell autonomous actions of mobile miRNAs, including miR165/6 that is produced in the endodermis and moves to the vasculature to pattern xylem cell fates in Arabidopsis roots. We show that KTN1, a subunit of a microtubule-severing enzyme, is required in source cells to inhibit the loading of miR165/6 into ARGONUATE1 (AGO1), which is cell autonomous, to enable the miRNA to exit the cell. Microtubule disruption enhances the association of miR165/6 with AGO1 in the cytoplasm. These findings suggest that although cell-autonomous miRNAs load onto AGO1 in the nucleus, the cytoplasmic AGO1 loading of mobile miRNAs is a key step regulated by microtubules to promote the range of miRNA cell-to-cell movement.
移动 microRNAs (miRNAs) 在植物的发育模式和应激反应中充当局部和远程信号。然而，调控 miRNAs 非细胞自主活性的机制仍不清楚。在这里，我们发现破坏微管动力学的突变对移动 miRNAs 的非细胞自主作用特别有缺陷，包括在内皮层中产生并移动到脉管系统以在拟南芥根中模式木质部细胞命运的 miR165/6。我们表明，微管切割酶的一个亚基 KTN1 在源细胞中是必需的，以抑制 miR165/6 加载到 ARGONUATE1 (AGO1) 中，AGO1 是细胞自主的，以使 miRNA 能够出细胞。微管的破坏增强了细胞质中 miR165/6 与 AGO1 的结合。这些发现表明，尽管细胞自主的 miRNAs 在核内加载到 AGO1 上，但细胞质中移动 miRNAs 的 AGO1 加载是受微管调控以促进 miRNA 细胞间运动范围的关键步骤。
