KETCH1 imports HYL1 to nucleus for miRNA biogenesis in Arabidopsis
KETCH1 imports HYL1 to nucleus for miRNA biogenesis in Arabidopsis
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DOI：
10.1073/pnas.1619755114
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发表时间：
2017-04-11
影响因子：
11.1
通讯作者：
Zhang, Xiuren
中科院分区：
文献类型：
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作者：
Zhang, Zhonghui;Guo, Xinwei;Zhang, Xiuren
MicroRNA(MiRNA)是由核内的微处理器从具有发夹结构的初级转录本(pri-miRNAs)中加工而来的。细胞质携带的微处理器组件是如何运输到细胞核中以实现其功能的，目前还知之甚少。在这里，我们报告了KETCH1(使细胞质HYL1能够运输的核粘附素)是低钠叶1蛋白(HYL1)的合作伙伴，HYL1蛋白是拟南芥微处理器的核心成分，也是Dgcr8/Pasha在动物中的功能对等蛋白。Ketch1的零突变是胚胎致死的，而ketch1的敲除突变导致了形态缺陷，这让人想起miRNA途径中的突变。Ketch1基因敲除突变也大大减少了miRNA的积累，但没有改变miRNAs的核质穿梭。相反，突变显著减少了HYL1蛋白的核部分，并相应地损害了细胞核中的pri-miRNA处理。我们认为KETCH1将HYL1从细胞质转运到细胞核，构成了拟南芥的功能微处理器。这项研究为了解miRNA生物发生成分通过真核生物的核质运输过程提供了洞察力。
MicroRNA (miRNA) is processed from primary transcripts with hairpin structures (pri-miRNAs) by microprocessors in the nucleus. How cytoplasmic-borne microprocessor components are transported into the nucleus to fulfill their functions remains poorly understood. Here, we report KETCH1 (karyopherin enabling the transport of the cytoplasmic HYL1) as a partner of hyponastic leaves 1 (HYL1) protein, a core component of microprocessor in Arabidopsis and functional counterpart of DGCR8/Pasha in animals. Null mutation of ketch1 is embryonic-lethal, whereas knockdown mutation of ketch1 caused morphological defects, reminiscent of mutants in the miRNA pathway. ketch1 knockdown mutation also substantially reduced miRNA accumulation, but did not alter nuclear-cytoplasmic shuttling of miRNAs. Rather, the mutation significantly reduced nuclear portion of HYL1 protein and correspondingly compromised the pri-miRNA processing in the nucleus. We propose that KETCH1 transports HYL1 from the cytoplasm to the nucleus to constitute functional microprocessor in Arabidopsis. This study provides insight into the largely unknown nuclear-cytoplasmic trafficking process of miRNA biogenesis components through eukaryotes.