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Transcriptome analysis of fry2 mutants-Transcriptome analysis of fry2 mutants

ABSTRACT: ra08-01_cpl1 - transcriptome analysis of fry2 mutants - Compare the transcriptome of 2 mutants affected in FRY2 (fry2-1 and 14-5sep) to control plants. - The Arabidopsis 14-5sep mutant was isolated as overexpressing a NII::LUC construct fusing a tobacco nitrite reductase gene with the luciferase reporter gene. This mutant overexpressed also the endogenous Arabidopsis nitrite reductase gene. Map-based cloning showed that the 14-5 sep mutant was affected in the FRY2 gene. Transciptome analysis was performed on both the 14-5sep and the fry2-1 mutants and their respective controls (either the C24 ecotype containing the RD29A::LUC transgene for fry2-1 or the Col0 accession containing the NII::LUC transgene for the 14-5sep mutant) to analyze which genes are differentially expressed in the mutants versus control plants. Keywords: gene knock out

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE11174 | GEO | 2009/04/15

SECONDARY ACCESSION(S): PRJNA106867

REPOSITORIES: GEO

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Project description:DNA methylation is a chromatin modification that is associated with gene silencing in eukaryotic organisms. Although pathways controlling the establishment, maintenance and removal of DNA methylation have been identified, relatively little is understood about how DNA methylation influences gene expression. Using complementary genetic and biochemical approaches we identified a protein complex that antagonizes the transcriptional gene silencing of two LUCIFERASE (LUC) reporters in a manner that requires DNA methylation. At its core, this complex contains LOW IN LUCIFERASE EXPRESSION (LIL), an α-crystallin domain protein, and METHYL-CpG-BINDING DOMAIN 7 (MBD7), a protein previously associated with DNA methylation. At the LUC reporters, loss of MBD7 or LIL resulted in decreased LUC expression concomitant with modest, but reproducible increases in DNA methylation that can be phenocopied by DNA demethylase mutants. These findings are consistent with other reports and reveal a genetic connection between MBD7, LIL and DNA demethylation. However, we found that the hyper-methylation and gene expression phenotypes at a LUC reporter can be genetically uncoupled, demonstrating that changes in DNA methylation alone are not sufficient to silence LUC expression, and suggesting a role for the MBD7-LIL complex downstream of DNA methylation. Consistent with this hypothesis, our more extensive analysis of DNA methylation in mbd7 and lil mutants revealed only a small number of hyper-methylated loci genome wide. Furthermore, these loci displayed minimal overlap with demethylase targets, suggesting that, in general, the DNA demethylation machinery does not function in a manner dependent on the MBD7-LIL complex. Taken together, our findings place the MBD7-LIL complex amongst a small number of factors that regulate gene expression without causing significant changes in DNA methylation. This complex, however, is unique in that it functions to suppress, rather than enforce the silencing effects of DNA methylation, enabling gene expression of several transgene reporters despite high levels of promoter methylation.

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Transcriptome analysis of fry2 mutants-Transcriptome analysis of fry2 mutants

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