Role of Nbs1 in the activation of the Atm kinase revealed in humanized mouse models View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2005-07

AUTHORS

Simone Difilippantonio, Arkady Celeste, Oscar Fernandez-Capetillo, Hua-Tang Chen, Bernardo Reina San Martin, Francois Van Laethem, Yong-Ping Yang, Galina V. Petukhova, Michael Eckhaus, Lionel Feigenbaum, Katia Manova, Michael Kruhlak, R. Daniel Camerini-Otero, Shyam Sharan, Michel Nussenzweig, André Nussenzweig

ABSTRACT

Nijmegen breakage syndrome (NBS) is a chromosomal fragility disorder that shares clinical and cellular features with ataxia telangiectasia. Here we demonstrate that Nbs1-null B cells are defective in the activation of ataxia-telangiectasia-mutated (Atm) in response to ionizing radiation, whereas ataxia-telangiectasia- and Rad3-related (Atr)-dependent signalling and Atm activation in response to ultraviolet light, inhibitors of DNA replication, or hypotonic stress are intact. Expression of the main human NBS allele rescues the lethality of Nbs1-/- mice, but leads to immunodeficiency, cancer predisposition, a defect in meiotic progression in females and cell-cycle checkpoint defects that are associated with a partial reduction in Atm activity. The Mre11 interaction domain of Nbs1 is essential for viability, whereas the Forkhead-associated (FHA) domain is required for T-cell and oocyte development and efficient DNA damage signalling. Reconstitution of Nbs1 knockout mice with various mutant isoforms demonstrates the biological impact of impaired Nbs1 function at the cellular and organismal level. More... »

PAGES

675-685

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncb1270

DOI

http://dx.doi.org/10.1038/ncb1270

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1025699748

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15965469


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