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Mre11 assembles linear DNA fragments into DNA damage signaling complexes

Costanzo, Vincenzo ; Paull, Tanya ; Gottesman, Max ; Gautier, Jean James Haber

PLoS biology, 2004-05, Vol.2 (5), p.E110-0600 [Periódico revisado por pares]

United States: Public Library of Science

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Título:
Mre11 assembles linear DNA fragments into DNA damage signaling complexes
Autor: Costanzo, Vincenzo ; Paull, Tanya ; Gottesman, Max ; Gautier, Jean
James Haber
Assuntos: Amino Acid Motifs ; Animals ; Antigens, Nuclear - chemistry ; Biotinylation ; Blotting, Western ; Cancer Biology ; Cell Biology ; Deoxyribonucleic acid ; Dimerization ; DNA ; DNA - chemistry ; DNA Damage ; DNA Fragmentation ; DNA repair ; DNA-Binding Proteins - chemistry ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - physiology ; Enzymes ; Gene Deletion ; Genetics ; Homo (Human) ; Humans ; In Situ Nick-End Labeling ; Kinases ; Ku Autoantigen ; Microscopy, Atomic Force ; Molecular Biology/Structural Biology ; Molecular Weight ; MRE11 Homologue Protein ; Mutation ; Peptides - chemistry ; Phenotype ; Protein Binding ; Protein Structure, Tertiary ; Proteins ; Recombinant Proteins - chemistry ; Replication Protein A - metabolism ; Signal Transduction ; Xenopus ; Zinc - chemistry
É parte de: PLoS biology, 2004-05, Vol.2 (5), p.E110-0600
Notas: ObjectType-Article-2
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Descrição: Mre11/Rad50/Nbs1 complex (MRN) is essential to suppress the generation of double-strand breaks (DSBs) during DNA replication. MRN also plays a role in the response to DSBs created by DNA damage. Hypomorphic mutations in Mre11 (which causes an ataxia-telangiectasia-like disease [ATLD]) and mutations in the ataxia-telangiectasia-mutated (ATM) gene lead to defects in handling damaged DNA and to similar clinical and cellular phenotypes. Using Xenopus egg extracts, we have designed a simple assay to define the biochemistry of Mre11. MRN is required for efficient activation of the DNA damage response induced by DSBs. We isolated a high molecular weight DNA damage signaling complex that includes MRN, damaged DNA molecules, and activated ATM. Complex formation is partially dependent upon Zn(2+) and requires an intact Mre11 C-terminal domain that is deleted in some ATLD patients. The ATLD truncation can still perform the role of Mre11 during replication. Our work demonstrates the role of Mre11 in assembling DNA damage signaling centers that are reminiscent of irradiation-induced foci. It also provides a molecular explanation for the similarities between ataxia-telangiectasia (A-T) and ATLD.
Editor: United States: Public Library of Science
Idioma: Inglês

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Mre11 assembles linear DNA fragments into DNA damage signaling complexes

Costanzo, Vincenzo ; Paull, Tanya ; Gottesman, Max ; Gautier, Jean James Haber

United States: Public Library of Science

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