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Defective mammopoiesis, but normal hematopoiesis, in mice with a targeted disruption of the prolactin gene
Author(s) -
Horseman Nelson D.,
Zhao Wenzhu,
MontecinoRodriguez Encarnacion,
Tanaka Minoru,
Nakashima Kunio,
Engle Sandra J.,
Smith Frost,
Markoff Edith,
Dorshkind Kenneth
Publication year - 1997
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/16.23.6926
Subject(s) - biology , myelopoiesis , prolactin , endocrinology , medicine , haematopoiesis , gene targeting , mutant , gene , microbiology and biotechnology , genetics , stem cell , hormone
Prolactin (PRL) has been implicated in numerous physiological and developmental processes. The mouse PRL gene was disrupted by homologous recombination. The mutation caused infertility in female mice, but did not prevent female mice from manifesting spontaneous maternal behaviors. PRL‐deficient males were fertile and produced offspring with normal Mendelian gender and genotype ratios when they were mated with heterozygous females. Mammary glands of mutant female mice developed a normal ductal tree, but the ducts failed to develop lobular decorations, which is a characteristic of the normal virgin adult mammary gland. The potential effect of PRL gene disruption on antigen‐independent primary hematopoiesis was assessed. The results of this analysis indicated that myelopoiesis and primary lymphopoiesis were unaltered in the mutant mice. Consistent with these observations in PRL mutant mice, PRL failed to correct the bone marrow B cell deficiency of Snell dwarf mice. These results argue that PRL does not play any indispensable role in primary lymphocyte development and homeostasis, or in myeloid differentiation. The PRL −/− mouse model provides a new research tool with which to resolve a variety of questions regarding the involvement of both endocrine and paracrine sources of PRL in reproduction, lactogenesis, tumorigenesis and immunoregulation.