CpG methylated minichromosomes become inaccessible for V(D)J recombination after undergoing replication.
AUTOR(ES)
Hsieh, C L
RESUMO
The physical parameters controlling the accessibility of antigen receptor loci to the V(D)J recombination activity are unknown. We have used minichromosome substrates to study the role that CpG methylation might play in controlling V(D)J recombination site accessibility. We find that CpG methylation decreases the V(D)J recombination of these substrates more than 100-fold. The decrease correlates with a considerable increase in resistance to endonuclease digestion of the methylated minichromosome DNA. The minichromosomes acquire resistance to both the intracellular V(D)J recombinase and exogenous endonuclease only after DNA replication. Therefore, CpG methylation specifies a chromatin structure that, upon DNA replication, is resistant to eukaryotic site-specific recombination. These findings are important to V(D)J recombination as well as to the chromatin assembly of methylated DNA during replication.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=556452Documentos Relacionados
- Influence of CpG methylation and target spacing on V(D)J recombination in a transgenic substrate.
- Both V(D)J recombination and radioresistance require DNA-PK kinase activity, though minimal levels suffice for V(D)J recombination
- Chromatin remodeling directly activates V(D)J recombination
- Postcleavage Sequence Specificity in V(D)J Recombination
- Structure of Nonhairpin Coding-End DNA Breaks in Cells Undergoing V(D)J Recombination