The ability to lactate is a process restricted to mammals and is necessary for the survival of nonhuman mammals. Female mice carrying a null mutation in the winged helix transcription factor Foxb1 (previously Mf3/Fkh5/TWH) have lactation defects on inbred genetic backgrounds. To determine the cellular basis of the Foxb1 lactation defect we have inserted a tau-lacZ lineage marker into the locus to follow the fate of Foxb1 expressing cells. This approach has revealed that Foxb1 is expressed in epithelial cells of developing and adult mammary glands as well as previously described regions of the central nervous system. Mammary glands from C57BL/6 Foxb1-/- mice have incomplete lobuloalveolar development. In addition, the tau-lacZ lineage label was used to determine that the mammillothalamic tract was lost in all Foxb1-/- mice. Finally, morphological defects in the inferior colliculi of the midbrain in Foxb1-/- mice correlate with the inability to lactate, suggesting that the midbrain defect, but not the loss of the mammillothalamic tract, may be responsible for the lactation defect.
Copyright 2001 Wiley-Liss, Inc.