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Molecular and Cellular Biology, February 2005, p. 1437-1445, Vol. 25, No. 4
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.4.1437-1445.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Normal Immune System Development in Mice Lacking the Deltex-1 RING Finger Domain

Sébastien Storck,¹ Frédéric Delbos,¹ Nicolas Stadler,² Catherine Thirion-Delalande,³ Florence Bernex,³ Christophe Verthuy,⁴ Pierre Ferrier,⁴ Jean-Claude Weill,^1,* and Claude-Agnès Reynaud^1,*

INSERM U373,¹ Laboratoire d'Expérimentation Animale et de Transgenèse, IFR 94, Faculté de Médecine Necker-Enfants Malades, Paris,² Service d'Anatomie Pathologique et INRA/ENVA UMR955, Ecole Nationale Vétérinaire d'Alfort, Maisons-Alfort,³ Centre d'Immunologie de Marseille-Luminy, INSERM-CNRS, Marseille, France⁴

Received 16 July 2004/ Returned for modification 31 August 2004/ Accepted 10 November 2004

The Notch signaling pathway controls several cell fate decisions during lymphocyte development, from T-cell lineage commitment to the peripheral differentiation of B and T lymphocytes. Deltex-1 is a RING finger ubiquitin ligase which is conserved from Drosophila to humans and has been proposed to be a regulator of Notch signaling. Its pattern of lymphoid expression as well as gain-of-function experiments suggest that Deltex-1 regulates both B-cell lineage and splenic marginal-zone B-cell commitment. Deltex-1 was also found to be highly expressed in germinal-center B cells. To investigate the physiological function of Deltex-1, we generated a mouse strain lacking the Deltex-1 RING finger domain, which is essential for its ubiquitin ligase activity. Deltex-1^/ mice were viable and fertile. A detailed histological analysis did not reveal any defects in major organs. T- and B-cell development was normal, as were humoral responses against T-dependent and T-independent antigens. These data indicate that the Deltex-1 ubiquitin ligase activity is dispensable for mouse development and immune function. Possible compensatory mechanisms, in particular those from a fourth Deltex gene identified during the course of this study, are also discussed.

J.-C.W. and C.-A.R. share senior authorship for this paper.

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