Premium
The winged helix gene, Foxb1 , controls development of mammary glands and regions of the CNS that regulate the milk‐ejection reflex
Author(s) -
Kloetzli Jacqueline M.,
FontaineGlover Iris A.,
Brown Erin R.,
Kuo Myrna,
Labosky Patricia A.
Publication year - 2001
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/1526-968x(200102)29:2<60::aid-gene1006>3.0.co;2-l
Subject(s) - biology , lactation , midbrain , central nervous system , mammary gland , medicine , locus (genetics) , endocrinology , transcription factor , gene , microbiology and biotechnology , genetics , pregnancy , cancer , breast cancer
Summary: 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 lobuloavelor 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. genesis 29:60–71, 2001. © 2001 Wiley‐Liss, Inc.