UBC13, an E2 enzyme for Lys63-linked ubiquitination, functions in root development by affecting auxin signaling and Aux/IAA protein stability
UBC13, an E2 enzyme for Lys63-linked ubiquitination, functions in root development by affecting auxin signaling and Aux/IAA protein stability
复制标题
UBC13 是一种用于 Lys63 连接泛素化的 E2 酶，通过影响生长素信号传导和 Aux/IAA 蛋白稳定性在根发育中发挥作用
DOI：
10.1111/tpj.12644
复制
发表时间：
2014-11-01
期刊：
影响因子：
7.2
通讯作者：
Wang, Hong
中科院分区：
文献类型：
--
作者：
Wen, Rui;Wang, Sheng;Wang, Hong
与传统的赖氨酸（K）48连接的多聚泛素化不同，K63连接的多聚泛素化在酵母和动物中发挥信号作用。到目前为止，UBC 13是唯一已知的专门用于K63连接的多聚泛素化的泛素缀合酶（E2）。先前对编码UBC 13及其相互作用伙伴UEV 1的拟南芥基因的鉴定表明，UBC 13介导的泛素化途径在植物中是保守的;然而，对植物中通过K63连接的多聚泛素化介导的功能和信号传导知之甚少。为了解决UBC 13介导的泛素化在植物中的功能，我们创建了拟南芥ubc 13无效突变株系，其中两个UBC 13基因被破坏。与野生型和单突变体植物相比，双突变体显示出改变的根发育，包括较短的主根，较少的侧根和仅少数短根毛，表明UBC 13活性对于根发育的所有主要方面都是至关重要的。双突变体植物对生长素处理不敏感，这表明强大的根表型不仅仅是生长素水平降低的结果。相反，ubc 13突变体具有降低的生长素响应，如生长素响应DR 5启动子-GFP的表达所示。此外，AXR 3/IAA 17-GUS报告基因的酶活性和蛋白水平在ubc 13突变体中大大增加，而许多生长素响应基因的诱导被抑制。总的来说，这些结果表明，Aux/IAA蛋白积累在ubc 13突变体，导致生长素反应减少和有缺陷的根发育。因此，这项研究提供了UBC 13介导的蛋白质泛素化，根发育和生长素信号之间可能的机制联系。
Unlike conventional lysine (K) 48-linked polyubiquitination, K63-linked polyubiquitination plays signaling roles in yeast and animals. Thus far, UBC13 is the only known ubiquitin-conjugating enzyme (E2) specialized in K63-linked polyubiquitination. Previous identification of Arabidopsis genes encoding UBC13 as well as its interacting partner UEV1 indicates that the UBC13-mediated ubiquitination pathway is conserved in plants; however, little is known about functions and signaling mediated through K63-linked polyubiquitination in plants. To address the functions of UBC13-mediated ubiquitination in plants, we created Arabidopsis ubc13 null mutant lines in which the two UBC13 genes were disrupted. The double mutant displayed altered root development, including shorter primary root, fewer lateral roots and only a few short root hairs in comparison with the wild type and single mutant plants, indicating that UBC13 activity is critical for all major aspects of root development. The double mutant plants were insensitive to auxin treatments, suggesting that the strong root phenotypes do not simply result from a reduced level of auxin. Instead, the ubc13 mutant had a reduced auxin response, as indicated by the expression of an auxin-responsive DR5 promoter-GFP. Furthermore, both the enzymatic activity and protein level of an AXR3/IAA17-GUS reporter were greatly increased in the ubc13 mutant, whereas the induction of many auxin-responsive genes was suppressed. Collectively, these results suggest that Aux/IAA proteins accumulate in the ubc13 mutant, resulting in a reduced auxin response and defective root development. Hence, this study provides possible mechanistic links between UBC13-mediated protein ubiquitination, root development and auxin signaling.