Sox‐4 facilitates thymocyte differentiation

Abstract

1he mouse Sry‐like transcription factor Sox‐4 is expressed in thymus, bone marrow, and gonads of adult mice. Sox‐4‐deficient mice die at embryonic day E14 due to cardiac malformation. In transfer experiments to irradiated recipients, B cell development was shown to be severely impaired in Sox‐4‐deficient progenitor cells. However, no drastic effects on T lymphocyte development were noted, despite the high level expression of the Sox‐4 gene in the thymus of normal mice. Here, we report a detailed analysis of T cell development from Sox‐4‐deficient progenitors. Explanted fetal thymic organ cultures (FTOC) of Sox‐4‐deficient thymi yielded 10–50‐fold fewer CD4 CD8 double‐positive and single‐positive cells than FTOC of littermates. This effect was T cell‐autonomous, since similar observations were made when FTOC were performed by culturing of Sox‐4‐deficient progenitors in wild‐type thymus lobes. When Sox‐4‐deficient fetal liver cells were injected together with normal cells intrathymically, they did not compete efficiently for reconstitution. It is concluded that Sox‐4 facilitates thymocyte development.