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First published online December 8, 2006; 10.1104/pp.106.091439

Plant Physiology 143:684-696 (2007)
© 2007 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

A New CULLIN 1 Mutant Has Altered Responses to Hormones and Light in Arabidopsis1,[C],[OA]

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

Department of Biology, Indiana University, Bloomington, Indiana 47405 (J.M., M.E.); Section of Cell and Developmental Biology, University of California, La Jolla, California 92093–0116 (Y.Z., X.D.); Section of Molecular Cell and Developmental Biology and The Institute for Cellular and Molecular Biology, University of Texas, Austin, Texas 78712 (J.M., E.H.); and Department of Plant Biology, University of Minnesota, St. Paul, Minnesota 55108 (W.Z., W.M.G.)

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.


1 This work was supported by the National Science Foundation (grant nos. MCB–0519970 [to M.E.] and IBN–0418653 [to E.H.]), the National Institutes of Health (grant nos. GM43644 [to M.E.], GM067203 [to W.M.G.], and GM68631 [to Y.Z.]), and the University of Texas (setup fund to E.H.).

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Mark Estelle (maestell{at}indiana.edu).

[C] Some figures in this article are displayed in color online but in black and white in the print edition.

[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.106.091439

* Corresponding author; e-mail maestell{at}indiana.edu; fax 812–855–6082.

Received October 17, 2006; accepted November 25, 2006; published December 8, 2006.




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