Mutation of Drosophila Lsd1 disrupts H3-K4 methylation, resulting in tissue-specific defects during development.
Curr Biol
; 17(9): 808-12, 2007 May 01.
Article
em En
| MEDLINE
| ID: mdl-17462898
ABSTRACT
Histone-tail modifications play a fundamental role in the processes that establish chromatin structure and determine gene expression. One such modification, histone methylation, was considered irreversible until the recent discovery of histone demethylases. Lsd1 was the first histone demethylase to be identified. Lsd1 is highly conserved in many species, from yeast to humans, but its function has primarily been studied through biochemical approaches. The mammalian ortholog has been shown to demethylate monomethyl- and dimethyl-K4 and -K9 residues of histone H3. Here we describe the effects of Lsd1 mutation in Drosophila. The inactivation of dLsd1 strongly affects the global level of monomethyl- and dimethyl-H3-K4 methylation and results in elevated expression of a subset of genes. dLsd1 is not an essential gene, but animal viability is strongly reduced in mutant animals in a gender-specific manner. Interestingly, dLsd1 mutants are sterile and possess defects in ovary development, indicating that dLsd1 has tissue-specific functions. Mutant alleles of dLsd1 suppress positional-effect variegation, suggesting a disruption of the balance between euchromatin and heterochromatin. Taken together, these results show that dLsd1-mediated H3-K4 demethylation has a significant and specific role in Drosophila development.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Oxirredutases N-Desmetilantes
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Fenótipo
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Histonas
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Regulação da Expressão Gênica no Desenvolvimento
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Metilação de DNA
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Proteínas de Drosophila
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Drosophila
Limite:
Animals
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article