The T cell oncogene Tal2 is necessary for normal development of the mouse brain

Transcription factors are commonly involved in leukemia by activation throu gh chromosomal translocations and normally function in cell type(s) that di ffer from that of the tumor. TAl2 is a member of a basic helix-loop-helix g ene family specifically involved in T cell leukemogenesis. Null mutations o f Tal2 have: been made in mice to determine its function during development . Tal2 null mutant mice show no obvious defects of hematopoiesis. During em bryogenesis, Tal2 expression is restricted to the developing midbrain, dors al diencephalon, and rostroventral diencepharic/telencephalic boundary, par tly along presumptive developing fiber tracts. The null mutant mice are via ble at birth but growth become progressively retarded and they do not survi ve to reproductive age. Tal2-deficient mice show a distinct dysgenesis of t he midbrain tectum. Due to loss of superficial gray and optical layers, the superior colliculus is reduced in size and the inferior colliculus is abno rmally rounded and protruding. Death is most likely due to progressive hydr ocephalus which appears to be caused by obstruction of the foramen of Monro (the connection between the ventricles of the forebrain). Thus, in additio n to its oncogenicity when ectopically expressed, Ta12 normally plays a piv otal role in brain development and without this gene, mice cannot survive t o maturity.