Defective mammopoiesis, but normal hematopoiesis, in mice with a targeted disruption of the prolactin gene
Defective mammopoiesis, but normal hematopoiesis, in mice with a targeted disruption of the prolactin gene
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DOI：
10.1093/emboj/16.23.6926
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发表时间：
1997-12-01
期刊：
影响因子：
11.4
通讯作者：
Dorshkind, K
中科院分区：
文献类型：
--
作者：
Horseman, ND;Zhao, WZ;Dorshkind, K
催乳素（PRL）参与了许多生理和发育过程，小鼠PRL基因被同源重组破坏。该突变导致雌性小鼠不育，但并未阻止雌性小鼠表现出自发的母性行为，prl缺陷的雄性小鼠具有可育性，与杂合雌性交配时产生的后代具有正常的孟德尔性别和基因型比例，突变雌性小鼠的乳腺发育正常的导管树，但导管不能发育小叶装饰，这是正常的处女成年乳腺的特征。PRL基因破坏对抗原不依赖性原发性造血的潜在影响被评估，分析结果表明，突变小鼠的骨髓生成和原发性淋巴生成未发生改变，与PRL突变小鼠的观察结果一致，PRL未能纠正Snell矮子小鼠骨髓B细胞缺乏，这些结果表明PRL在原发性淋巴细胞发育和稳态中没有任何不可或缺的作用。或者骨髓分化。PRL-/-小鼠模型提供了一种新的研究工具，用于解决有关PRL在生殖、乳发生、肿瘤发生和免疫调节中的内分泌和旁分泌来源的各种问题。
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.