Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Yélamos, J. et al.

Yélamos, Monreal, Saenz, Aguado, Schreiber, Mota, Fuente, Minguela, Parrilla, de Murcia, Almarza, Aparicio, Ménissier-de Murcia,

PARP-2 deficiency affects the survival of CD4(+)CD8(+) double-positive thymocytes.

Poly-(ADP-ribose) polymerase-2 ( PARP-2) belongs to a large family of enzymes that synthesize and transfer ADP-ribose polymers to acceptor proteins, modifying their functional properties. PARP-2-deficient ( Parp-2(-/-)) cells, similar to Parp-1(-/-) cells, are sensitive to both ionizing radiation and alkylating agents. Here we show that inactivation of mouse Parp-2, but not Parp-1, produced a two-fold reduction in CD4(+)CD8(+) double-positive (DP) thymocytes associated with decreased DP cell survival. Microarray analyses revealed increased expression of the proapoptotic Bcl-2 family member Noxa in Parp-2(-/-) DP thymocytes compared to littermate controls. In addition, DP thymocytes from Parp-2(-/-) have a reduced expression of T-cell receptor (TCR)alpha and a skewed repertoire of TCRalpha toward the 5' Jalpha segments. Our results show that in the absence of PARP-2, the survival of DP thymocytes undergoing TCRalpha recombination is compromised despite normal amounts of Bcl-x(L). These data suggest a novel role for PARP-2 as an important mediator of T-cell survival during thymopoiesis by preventing the activation of DNA damage-dependent apoptotic response during the multiple rounds of TCRalpha rearrangements preceding a positively selected TCR.[1]

References

PARP-2 deficiency affects the survival of CD4(+)CD8(+) double-positive thymocytes. Yélamos, J., Monreal, Y., Saenz, L., Aguado, E., Schreiber, V., Mota, R., Fuente, T., Minguela, A., Parrilla, P., de Murcia, G., Almarza, E., Aparicio, P., Ménissier-de Murcia, J. EMBO J. (2006) [Pubmed]

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