Trifurcate Feed-Forward Regulation of Age-Dependent Cell Death Involving miR164 in Arabidopsis
Trifurcate Feed-Forward Regulation of Age-Dependent Cell Death Involving miR164 in Arabidopsis
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DOI：
10.1126/science.1166386
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发表时间：
2009-02-20
期刊：
影响因子：
56.9
通讯作者：
Nam, Hong Gil
中科院分区：
文献类型：
--
作者：
Kim, Jin Hee;Woo, Hye Ryun;Nam, Hong Gil
衰老诱导高等生物（包括一年生植物）中逐渐但大量的细胞死亡。即便如此，尽管人们对这一话题的兴趣由来已久，但其背后的监管机制却鲜为人知。在这里，我们证明了ORE 1，这是一个NAC（NAM，ATAF，和CUC）转录因子，正调控拟南芥叶片衰老诱导的细胞死亡。ORE 1的表达在叶衰老的同时被EIN 2上调，但被miR164负调节。miR164的表达通过EIN 2的负调节而随着衰老逐渐降低，这导致ORE 1表达的精细上调。然而，在不存在ORE 1的情况下，EIN 2仍然有助于衰老诱导的细胞死亡。涉及ORE1、miR164和EIN 2的三叉前馈途径提供了高度稳健的调节以确保衰老诱导拟南芥叶中的细胞死亡。
Aging induces gradual yet massive cell death in higher organisms, including annual plants. Even so, the underlying regulatory mechanisms are barely known, despite the long- standing interest in this topic. Here, we demonstrate that ORE1, which is a NAC ( NAM, ATAF, and CUC) transcription factor, positively regulates aging- induced cell death in Arabidopsis leaves. ORE1 expression is up- regulated concurrently with leaf aging by EIN2 but is negatively regulated by miR164. miR164 expression gradually decreases with aging through negative regulation by EIN2, which leads to the elaborate up- regulation of ORE1 expression. However, EIN2 still contributes to aging- induced cell death in the absence of ORE1. The trifurcate feed- forward pathway involving ORE1, miR164, and EIN2 provides a highly robust regulation to ensure that aging induces cell death in Arabidopsis leaves.