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Originally published as Genetics Published Articles Ahead of Print on December 29, 2008.
Genetics, Vol. 181, 945-963, March 2009, Copyright © 2009
doi:10.1534/genetics.108.097675
Isolation and Characterization of cul1-7, a Recessive Allele of CULLIN1 That Disrupts SCF Function at the C Terminus of CUL1 in Arabidopsis thaliana
Jonathan Gilkerson*,
,
Jianhong Hu
,
Jessica Brown*,
Alexander Jones*,1,
Tai-ping Sun and
Judy Callis*,,2
* Department of Molecular and Cellular Biology and Plant Biology Graduate Group, University of California, Davis, California 95616 and Department of Biology, Duke University, Durham, North Carolina 27708-1000
2 Corresponding author: Department of Molecular and Cellular Biology, University of California, One Shields Ave., Davis, CA 95616.
E-mail: jcallis{at}ucdavis.edu
Many aspects of plant biology depend on the ubiquitin proteasome system for degradation of regulatory proteins. Ubiquitin E3 ligases confer substrate specificity in this pathway, and SCF-type ligases comprise a major class of E3s. SCF ligases have four subunits: SKP1, CUL1, RBX1, and an F-box protein for substrate recognition. The Aux/IAAs are a well-characterized family of SCF substrates in plants. Here, we report characterization of a mutant isolated from a genetic screen in Arabidopsis thaliana designed to identify plants defective in degradation of an Aux/IAA fusion protein, Aux/IAA1-luciferase (IAA1-LUC). This mutant exhibited fourfold slower IAA1-LUC degradation compared with the progenitor line, and seedlings displayed altered auxin responses. Experiments identified the mutant as an allele of CUL1, named cul1-7. The cul1-7 mutation affects the C terminus of the protein, results in reduced cul1-7 levels, and interferes with RBX1 interaction. cul1-7 seedlings are defective in degradation of an endogenous SCF substrate, Repressor of ga1-3 (RGA), and have altered responses to gibberellins. cul1-7 seedlings exhibit slower degradation of the light-labile red/far-red photoreceptor phytochrome A and are photomorphogenic in the dark. This mutation represents the first reported allele of CUL1 to directly affect subunit interactions at the CUL1 C terminus.
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