Article
- The EMBO Journal (2000) 19, 5772 - 5781
- doi:10.1093/emboj/19.21.5772
Lactation defect in mice lacking the helix–loop–helix inhibitor Id2
Seiichi Mori2, Shin-Ichi Nishikawa1 and Yoshifumi Yokota2
- Department of Molecular Genetics, Kyoto University Graduate School of Medicine, Shogoin Kawahara-cho 53, Sakyo-ku, Kyoto 606-8507, Japan
- Present address: Department of Biochemistry, Fukui Medical University, Shimoaizuki 23-3, Matsuoka, Fukui, 910-1193, Japan
Correspondence to:
Yoshifumi Yokota, E-mail: yyokota@fmsrsa.fukui-med.ac.jp
Received 11 January 2000; Accepted 15 September 2000; Revised 2 August 2000
Abstract
Id proteins are thought to be negative regulators of cell differentiation and positive regulators of cell proliferation. Mammary glands of Id2-/- female mice reveal severely impaired lobulo-alveolar development during pregnancy. Id2-/- mammary epithelia show no precocious maturation, but instead exhibit intrinsic defects in both cell proliferation and cell survival, implying that the role of Id2 in pregnant mammary epithelia is mainly stimulation of cell proliferation and support of cell viability. Expression studies of genes required for mammary gland development suggest Id2 to be a downstream or parallel factor of these genes. A decrease in the DNA binding activity of Stat5 was also observed in Id2-/- mammary glands at 7 days post-coitus. Our results indicate an indispensable role of Id2 in pregnant mammary glands.
Keywords:
- apoptosis,
- cell proliferation,
- HLH inhibitor,
- Id2,
- mammary gland
