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A comprehensive structure-function analysis of Arabidopsis SNI1 defines essential regions and transcriptional repressor activity.

   
Author Rebecca A Mosher, Wendy E Durrant, Dong Wang, Junqi Song, Xinnian Dong
Citation Information The Plant cell, 18:1750-65 (2006)
Keywords Amino Acid Sequence, Arabidopsis, Arabidopsis Proteins, Cell Nucleus, Chromatin, Gene Expression Profiling, Gene Expression Regulation, Plant, Genes, Reporter, Genome, Plant, Models, Molecular, Molecular Sequence Data, Mutagenesis, Nuclear Proteins, Oligonucleotide Array Sequence Analysis, Promoter Regions, Genetic, Protein Conformation, Repressor Proteins, Sequence Alignment, Sequence Analysis, DNA, Structure-Activity Relationship, Transcription, Genetic
Related Products 07-030
Pub Med ID 16766691
   

Abstract

[Full Text Article]
The expression of systemic acquired resistance (SAR) in plants involves the upregulation of many Pathogenesis-Related (PR) genes, which work in concert to confer resistance to a broad spectrum of pathogens. Because SAR is a costly process, SAR-associated transcription must be tightly regulated. Arabidopsis thaliana SNI1 (for Suppressor of NPR1, Inducible) is a negative regulator of SAR required to dampen the basal expression of PR genes. Whole genome transcriptional profiling showed that in the sni1 mutant, Nonexpresser of PR genes (NPR1)-dependent benzothiadiazole S-methylester-responsive genes were specifically derepressed. Interestingly, SNI1 also repressed transcription when expressed in yeast, suggesting that it functions as an active transcriptional repressor through a highly conserved mechanism. Chromatin immunoprecipitation indicated that histone modification may be involved in SNI1-mediated repression. Sequence comparison with orthologs in other plant species and a saturating NAAIRS-scanning mutagenesis of SNI1 identified regions in SNI1 that are required for its activity. The structural similarity of SNI1 to Armadillo repeat proteins implies that SNI1 may form a scaffold for interaction with proteins that modulate transcription.