ERF115 Controls Root Quiescent Center Cell Division and Stem Cell Replenishment
ERF115 Controls Root Quiescent Center Cell Division and Stem Cell Replenishment
复制标题
DOI：
10.1126/science.1240667
复制
发表时间：
2013-11-15
期刊：
影响因子：
56.9
通讯作者：
De Veylder, Lieven
中科院分区：
文献类型：
--
作者：
Heyman, Jefri;Cools, Toon;De Veylder, Lieven
静止中心（QC）在根的发育过程中起着至关重要的作用，通过创造一个微环境，保持其周围细胞的干细胞命运。尽管被高度有丝分裂活跃的细胞包围，QC细胞仍以低增殖率自我更新。在这里，我们确定了ERF 115转录因子作为QC细胞分裂的限速因子，作为植物磺因子PSK 5肽激素的转录激活因子。ERF 115标记QC细胞分裂，但通过APC/C-CCS 52 A2泛素连接酶的蛋白水解而受到抑制，而QC增殖由油菜素类固醇依赖性ERF 115表达驱动。这两种拮抗机制共同界定了ERF 115活性，当周围的干细胞受损时，ERF 115活性被调用，揭示了干细胞生态位寿命的细胞周期调节机制。
The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Despite being surrounded by highly mitotic active cells, QC cells self-renew at a low proliferation rate. Here, we identified the ERF115 transcription factor as a rate-limiting factor of QC cell division, acting as a transcriptional activator of the phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/C-CCS52A2 ubiquitin ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Together, these two antagonistic mechanisms delimit ERF115 activity, which is called upon when surrounding stem cells are damaged, revealing a cell cycle regulatory mechanism accounting for stem cell niche longevity.