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Synthetic lethality between PAXX and XLF in mammalian development.

Gabriel Balmus 1, 2 Ana C. Barros 2, 1 Paul W.G. Wijnhoven 3, 1 Chloé Lescale 4, 5 Hélène Lenden Hasse 5, 4 Katharina Boroviak 2 Carlos Le Sage 1 Brendan Doe 2 Anneliese O. Speak 2 Antonella Galli 2 Matt Jacobsen 6 Ludovic Deriano 5, 4 David J. Adams 2 Andrew N. Blackford 7, 1, 8, * Stephen P. Jackson 1, 2, 3, *
* Corresponding author
1 Wellcome Trust/Cancer Research UK Gurdon Institute
2 The Wellcome Trust Sanger Institute [Cambridge]
3 Department of Biochemistry
4 Département de Génomes et Génétique - Department of Genomes and Genetics
5 Développement Lymphocytaire et Oncogenèse
6 AstraZeneca [Cambridge, UK]
7 University of Oxford [Oxford]
8 The Weatherall Institute of Molecular Medicine
Abstract : PAXX was identified recently as a novel nonhomologous end-joining DNA repair factor in human cells. To characterize its physiological roles, we generated Paxx-deficient mice. Like Xlf −/− mice, Paxx −/− mice are viable, grow normally , and are fertile but show mild radiosensitivity. Strikingly, while Paxx loss is epistatic with Ku80, Lig4, and Atm deficiency, Paxx/Xlf double-knockout mice display embryonic lethality associated with genomic instability , cell death in the central nervous system, and an almost complete block in lymphogenesis, phenotypes that closely resemble those of Xrcc4 −/− and Lig4 −/− mice. Thus, combined loss of Paxx and Xlf is synthetic-lethal in mammals.
Keywords : development synthetic lethality PAXX XLF NHEJ ATM
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Gabriel Balmus, Ana C. Barros, Paul W.G. Wijnhoven, Chloé Lescale, Hélène Lenden Hasse, et al.. Synthetic lethality between PAXX and XLF in mammalian development.. Genes and Development, Cold Spring Harbor Laboratory Press, 2016, 30 (19), pp.2152 - 2157. ⟨10.1101/gad.290510.116⟩. ⟨pasteur-01416628⟩

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