A new CULLIN 1 mutant has altered responses to hormones and light in Arabidopsis

被引:69
作者
Moon, Jennifer
Zhao, Yunde
Dai, Xinhua
Zhang, Wenjing
Gray, William M.
Huq, Enamul
Estelle, Mark [1 ]
机构
[1] Indiana Univ, Dept Biol, Bloomington, IN 47405 USA
[2] Univ Calif, Sect Cell & Dev Biol, La Jolla, CA 92093 USA
[3] Univ Texas, Sect Mol Cell & Dev Biol, Austin, TX 78712 USA
[4] Univ Texas, Inst Cellular & Mol Biol, Austin, TX 78712 USA
[5] Univ Minnesota, Dept Plant Biol, St Paul, MN 55108 USA
关键词
D O I
10.1104/pp.106.091439
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Regulated protein degradation contributes to plant development by mediating signaling events in many hormone, light, and developmental pathways. Ubiquitin ligases recognize and ubiquitinate target proteins for subsequent degradation by the 26S proteasome. The multisubunit SCF is the best-studied class of ubiquitin ligases in Arabidopsis (Arabidopsis thaliana). However, the extent of SCF participation in signaling networks is unclear. SCFs are composed of four subunits: CULLIN 1 (CUL1), ASK, RBX1, and an F-box protein. Null mutations in CUL1 are embryo lethal, limiting insight into the role of CUL1 and SCFs in later stages of development. Here, we describe a viable and fertile weak allele of CUL1, called cul1-6. cul1-6 plants have defects in seedling and adult morphology. In addition to reduced auxin sensitivity, cul1-6 seedlings are hyposensitive to ethylene, red, and blue light conditions. An analysis of protein interactions with the cul1-6 gene product suggests that both RUB (related to ubiquitin) modification and interaction with the SCF regulatory protein CAND1 (cullin associated and neddylation dissociated) are disrupted. These findings suggest that the morphological defects observed in cul1-6 plants are caused by defective SCF complex formation. Characterization of weak cul1 mutants provides insight into the role of SCFs throughout plant growth and development.
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页码:684 / 696
页数:13
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