The eta7/csn3-3 auxin response mutant of Arabidopsis defines a novel function for the CSN3 subunit of the COP9 signalosome.

Loading...
Thumbnail Image

Persistent link to this item

Statistics
View Statistics

Journal Title

Journal ISSN

Volume Title

Title

The eta7/csn3-3 auxin response mutant of Arabidopsis defines a novel function for the CSN3 subunit of the COP9 signalosome.

Published Date

2012-07

Publisher

Type

Thesis or Dissertation

Abstract

The COP9 signalosome (CSN) is an eight subunit protein complex conserved in all higher eukaryotes. In Arabidopsis thaliana, the CSN regulates plant auxin response by removing the ubiquitin-like protein NEDD8/RUB1 from the CUL1 subunit of the SCFTIR1/AFB ubiquitin-ligase (deneddylation). Previously described null mutations in any CSN subunit resulted in the pleiotropic cop/det/fus phenotype and caused seedling lethality, hampering the study of CSN functions in plant development. In a genetic screen to identify enhancers of the auxin response defects conferred by the tir1-1 mutation, we identified a viable csn mutant of subunit 3 (CSN3), designated eta7/csn3-3. In comparison with eta6/csn1-10, which was identified in the same enhancer screen (Zhang et al., 2008), both csn3-3 and csn1-10 enhanced the auxin response defects of tir1-1. Similar to csn1-10, csn3-3 also confers several phenotypes associated with impaired auxin signaling, including auxin resistant root growth and diminished auxin responsive gene expression. Surprisingly however, unlike csn1-10 as well as other previously characterized csn mutants, csn3-3 plants are not defective in either the CSN-mediated deneddylation of CUL1 or in SCFTIR1/AFB mediated degradation of Aux/IAA proteins. These findings suggest that csn3-3 is an atypical csn mutant that defines a novel CSN or CSN3-specific function. Consistent with this possibility, I observed dramatic differences in double mutant interactions between csn3-3 and other auxin signaling mutants compared to csn1-10. Lastly, unlike other csn mutants, assembly of the CSN holocomplex was unaffected in csn3-3 plants. However, I detected a small CSN3-containing protein complex (sCSN3c) that was altered in csn3-3 plants. I hypothesize that in addition to its role in the CSN as a cullin deneddylase, CSN3 functions in a smaller protein complex that is required for proper auxin signaling. Analyses on the purification of sCSN3c suggested that it is not likely a dimer of CSN3, or a CSN subcomplex. My data resulting from sCSN3c purification using various chromatographic steps provide useful information necessary for identifying the components of the complex.

Description

University of Minnesota Ph.D. dissertation. July 2012. Major: Plant Biological Sciences. Advisor: Dr. William M. Gray. 1 computer file (PDF); vii, 167 [183] pages.

Related to

Replaces

License

Collections

Series/Report Number

Funding information

Isbn identifier

Doi identifier

Previously Published Citation

Other identifiers

Suggested citation

Huang, He. (2012). The eta7/csn3-3 auxin response mutant of Arabidopsis defines a novel function for the CSN3 subunit of the COP9 signalosome.. Retrieved from the University Digital Conservancy, https://hdl.handle.net/11299/133418.

Content distributed via the University Digital Conservancy may be subject to additional license and use restrictions applied by the depositor. By using these files, users agree to the Terms of Use. Materials in the UDC may contain content that is disturbing and/or harmful. For more information, please see our statement on harmful content in digital repositories.