Overexpression of the non-canonical Aux/IAA genes causes auxin-related aberrant phenotypes in Arabidopsis

Overexpression of the non-canonical Aux/IAA genes causes auxin-related aberrant phenotypes in Arabidopsis
复制标题

DOI:
10.1111/j.1399-3054.2008.01055.x
复制
发表时间:
2008-06-01
影响因子:
6.4
通讯作者:
Yamamoto, Kotaro T.
Yamamoto, Kotaro T.
中科院分区:
生物学2区
文献类型:
--
作者:
Sato, Atsuko;Yamamoto, Kotaro T.

文献摘要

被引文献

相似文献

Aux/IAA蛋白的降解被认为是生长素信号转导的主要反应,其降解由含有生长素F-box受体(AFB)的泛素连接酶复合物触发。在生长素的感知,黄曲霉毒素结合结构域II的Aux/IAA蛋白是保守的,在大多数的29个家族成员在拟南芥。然而,IAA 20和IAA 30缺乏结构域II。IAA 31与IAA 20、IAA 30组成Aux/IAA蛋白家族的一个分支,其结构域II部分保守,其中含有一个可能导致Aux/IAA基因显性突变的氨基酸替换。已经表明,这些蛋白质的半衰期比典型的Aux/IAA蛋白质的半衰期长得多。为了更好地了解拟南芥中非典型Aux/IAA蛋白的分子功能,我们利用花椰菜花叶病毒35 S启动子构建了IAA 20、IAA 30和IAA 31的过表达系。这3个基因的OX表现出相似的生长素相关的异常表型,其中IAA 20 OX表现出最严重的缺陷:部分基因表现出半矮化表型;下胚轴和根的向重力性生长方向经常受到影响;子叶的维管系统畸形;由于根尖分生组织塌陷,初生根在萌发后不久就停止生长。IAA 20和IAA 30是早期生长素诱导的,而IAA 31不是。这些结果表明,野生型基因的三个Aux/IAAs异位过表达时,会干扰生长素的生理。
Degradation of Aux/IAA proteins which are triggered by the ubiquitin ligase complex containing the auxin F-box receptors (AFBs), is thought to be the primary reaction of auxin signaling. Upon auxin perception, AFBs bind domain II of Aux/IAA proteins that is conserved in most of the 29 family members in Arabidopsis. However, IAA20 and IAA30 lack domain II. Furthermore, IAA31, which forms a single clade with IAA20 and IAA30 in Aux/IAA protein family, has a partially conserved domain II, which contains an amino acid substitution that would cause a dominant mutation of Aux/IAA genes. It has been shown that the half-lives of these proteins are much longer than those of the canonical Aux/IAA proteins. We generated overexpression lines (OXs) of IAA20, IAA30 and IAA31 by the use of cauliflower mosaic virus 35S promoter to better understand the molecular function of atypical Aux/IAA proteins in Arabidopsis. OXs of the three genes exhibited similar auxin-related aberrant phenotypes, with IAA20 OX showing the most severe defects: Some of them showed a semi-dwarf phenotype; gravitropic growth orientation was often affected in hypocotyl and root; vasculature of cotyledons was malformed; the primary root stopped growing soon after germination because of collapse of root apical meristem. IAA 20 and IAA30 were early auxin inducible, but IAA31 was not. These results showed that the wild-type genes of the three Aux/IAAs could disturb auxin physiology when ectopically overexpressed.