An XRCC4 mutant mouse, a model for human X4 syndrome, reveals interplays with Xlf, PAXX, and ATM in lymphoid development.

doi:10.7554/eLife.69353

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Article

An XRCC4 mutant mouse, a model for human X4 syndrome, reveals interplays with Xlf, PAXX, and ATM in lymphoid development.

eLife - 14 Sept 2021

Roch Benoit, Abramowski Vincent, Etienne Olivier, Musilli Stefania, David Pierre, Charbonnier Jean-Baptiste, Callebaut Isabelle, Boussin François D, de Villartay Jean-Pierre

Abstract excerpt

We developed an Xrcc4M61R separation of function mouse line to overcome the embryonic lethality of Xrcc4-deficient mice. XRCC4M61R protein does not interact with Xlf, thus obliterating XRCC4-Xlf filament formation while preserving the ability to stabilize DNA ligase IV. X4M61R mice, which are DNA repair deficient, phenocopy the Nhej1-/- (known as Xlf -/-) setting with a minor impact on the development of the...

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Share to Ataxia Telangiectasia Mutated Proteins
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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PMID: 34519267
DOI: 10.7554/eLife.69353
PMCID: PMC8516412

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