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Suppression of histone H1 genes in Arabidopsis results in heritable developmental defects and stochastic changes in DNA methylation.
- Source :
-
Genetics [Genetics] 2005 Feb; Vol. 169 (2), pp. 997-1008. Date of Electronic Publication: 2004 Oct 16. - Publication Year :
- 2005
-
Abstract
- Histone H1 is an abundant component of eukaryotic chromatin that is thought to stabilize higher-order chromatin structures. However, the complete knock-out of H1 genes in several lower eukaryotes has no discernible effect on their appearance or viability. In higher eukaryotes, the presence of many mutually compensating isoforms of this protein has made assessment of the global function of H1 more difficult. We have used double-stranded RNA (dsRNA) silencing to suppress all the H1 genes of Arabidopsis thaliana. Plants with a >90% reduction in H1 expression exhibited a spectrum of aberrant developmental phenotypes, some of them resembling those observed in DNA hypomethylation mutants. In subsequent generations these defects segregated independently of the anti-H1 dsRNA construct. Downregulation of H1 genes did not cause substantial genome-wide DNA hypo- or hypermethylation. However, it was correlated with minor but statistically significant changes in the methylation patterns of repetitive and single-copy sequences, occurring in a stochastic manner. These findings reveal an important and previously unrecognized link between linker histones and specific patterns of DNA methylation.
- Subjects :
- Arabidopsis metabolism
Chromosome Mapping
DNA, Plant metabolism
Gene Expression Regulation, Developmental
Gene Expression Regulation, Plant
Gene Silencing
Histones chemistry
Histones deficiency
Mutation
Phylogeny
Plants, Genetically Modified
Promoter Regions, Genetic
Protein Structure, Tertiary
Reverse Transcriptase Polymerase Chain Reaction
Transformation, Genetic
Arabidopsis genetics
Arabidopsis growth & development
DNA Methylation
Genes, Plant
Histones genetics
Histones metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0016-6731
- Volume :
- 169
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Genetics
- Publication Type :
- Academic Journal
- Accession number :
- 15489532
- Full Text :
- https://doi.org/10.1534/genetics.104.031997