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Published on December 8, 2006; 10.1104/pp.106.091439

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Received October 17, 2006
Accepted November 25, 2006

A New CUL1 Mutant has Altered Responses to Hormones and Light in Arabidopsis

Jennifer Moon , Yunde Zhao , Xinhua Dai , Wenjing Zhang , William M. Gray , Enamul Huq , and Mark Estelle *

Department of Biology, Indiana University, Bloomington, IN 47405; Section of Molecular Cell and Developmental Biology and The Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712
Section of Cell and Developmental Biology, University of California San Diego, La Jolla, CA 92093-0116
Department of Plant Biology, University of Minnesota, St. Paul, MN 55108
Section of Molecular Cell and Developmental Biology and The Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712
Department of Biology, Indiana University, Bloomington, IN 47405

* Corresponding author; email: maestell{at}indiana.edu.

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 multi-subunit SCF is the best-studied class of ubiquitin ligases in Arabidopsis thaliana. However the extent of SCF participation in signaling networks is unclear. SCFs are comprised of four subunits: 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 and development. 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-modification and interaction with the SCF regulatory protein CAND1 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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