Gene co-expression network analysis identifies BEH3 as a stabilizer of secondary vascular development in Arabidopsis
Gene co-expression network analysis identifies BEH3 as a stabilizer of secondary vascular development in Arabidopsis
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DOI：
10.1093/plcell/koab151
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发表时间：
2021-06-01
期刊：
影响因子：
11.6
通讯作者：
Kondo, Yuki
中科院分区：
文献类型：
--
作者：
Furuya, Tomoyuki;Saito, Masato;Kondo, Yuki
在植物中，位于形成层中的维管干细胞在次生生长过程中不断进行自我更新和分化。细胞分选技术的最新进展使得能够获得形成层细胞的转录调控框架。然而，血管干细胞的强大控制机制仍不清楚。在这里，我们确定了一个新的形成层相关的调控模块，通过共表达网络分析，使用多个转录组数据集获得从异位维管细胞转分化系统，拟南芥子叶，维管细胞诱导培养系统，拟南芥叶（VISUAL）。形成层基因列表包括编码转录因子BES 1/BZR 1同源物3（BEH 3）的基因，其同源物BES 1对血管干细胞维持有负面影响。有趣的是，空beh 3突变等位基因显示出其血管大小的较大变化，表明BEH 3作为血管干细胞的稳定剂发挥作用。遗传分析表明，BEH 3和BES 1在视觉系统的背景下，在调节血管干细胞和血管细胞分化方面执行相反的功能。在生化水平上，BEH 3表现出弱的转录抑制活性，并通过竞争与油菜素类固醇反应元件结合而与其他BES/BZR成员拮抗。此外，数学建模表明，BES/BZR同源物之间的竞争关系导致血管干细胞的鲁棒调节。
In plants, vascular stem cells located in the cambium continuously undergo self-renewal and differentiation during secondary growth. Recent advancements in cell sorting techniques have enabled access to the transcriptional regulatory framework of cambial cells. However, mechanisms underlying the robust control of vascular stem cells remain unclear. Here, we identified a new cambium-related regulatory module through co-expression network analysis using multiple transcriptome datasets obtained from an ectopic vascular cell transdifferentiation system using Arabidopsis cotyledons, Vascular cell Induction culture System Using Arabidopsis Leaves (VISUAL). The cambium gene list included a gene encoding the transcription factor BES1/BZR1 Homolog 3 (BEH3), whose homolog BES1 negatively affects vascular stem cell maintenance. Interestingly, null beh3 mutant alleles showed a large variation in their vascular size, indicating that BEH3 functions as a stabilizer of vascular stem cells. Genetic analysis revealed that BEH3 and BES1 perform opposite functions in the regulation of vascular stem cells and the differentiation of vascular cells in the context of the VISUAL system. At the biochemical level, BEH3 showed weak transcriptional repressor activity and functioned antagonistically to other BES/BZR members by competing for binding to the brassinosteroid response element. Furthermore, mathematical modeling suggested that the competitive relationship between BES/BZR homologs leads to the robust regulation of vascular stem cells.