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© Institut Pasteur
Macrophages et lymphocytes de souris. Image colorisée.
Publication : Cell death and differentiation

PAXX and Xlf interplay revealed by impaired CNS development and immunodeficiency of double KO mice

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cell death and differentiation - 12 Jan 2018

Abramowski V, Etienne O, Elsaid R, Yang J, Berland A, Kermasson L, Roch B, Musilli S, Moussu JP, Lipson-Ruffert K, Revy P, Cumano A, Boussin FD, de Villartay JP

Link to Pubmed [PMID] – 29077092

Cell Death Differ. 2018 Feb;25(2):444-452

The repair of DNA double-stranded breaks (DNAdsb) through non-homologous end joining (NHEJ) is a prerequisite for the proper development of the central nervous system and the adaptive immune system. Yet, mice with Xlf or PAXX loss of function are viable and present with very mild immune phenotypes, although their lymphoid cells are sensitive to ionizing radiation attesting for the role of these factors in NHEJ. In contrast, we show here that mice defective for both Xlf and PAXX are embryonically lethal owing to a massive apoptosis of post-mitotic neurons, a situation reminiscent to XRCC4 or DNA Ligase IV KO conditions. The development of the adaptive immune system in Xlf(-/-)PAXX(-/-) E18.5 embryos is severely affected with the block of B- and T-cell maturation at the stage of IgH and TCRβ gene rearrangements, respectively. This damaging phenotype highlights the functional nexus between Xlf and PAXX, which is critical for the completion of NHEJ-dependent mechanisms during mouse development.Cell Death and Differentiation advance online publication, 27 October 2017; doi:10.1038/cdd.2017.184.

https://www.ncbi.nlm.nih.gov/pubmed/29077092