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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Growth retardation and abnormal maternal behavior in mice lacking testicular orphan nuclear receptor 4
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Growth retardation and abnormal maternal behavior in mice lacking testicular orphan nuclear receptor 4

机译：缺乏睾丸孤儿核受体4的小鼠的生长发育迟缓和异常的母亲行为

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摘要

Testicular orphan nuclear receptor 4 (TR4) is a member of the nuclear receptor superfamily for which a ligand has not yet been found. In vitro data obtained from various cell lines suggest that TR4 functions as a master regulator to modulate many signaling pathways, yet the in vivo physiological roles of TR4 remain unclear. Here, we report the generation of mice lacking TR4 by means of targeted gene disruption (TR4(-/-)). The number of TR4(-/-) pups generated by the mating of TR4(+/-) mice is well under that predicted by the normal Mendelian ratio, and TR4(-/-) mice demonstrate high rates of early postnatal mortality, as well as significant growth retardation. Additionally, TR4(-/-) females show defects in reproduction and maternal behavior, with pups of TR4(-/-) dams dying soon after birth with no indication of milk intake. These results provide in vivo evidence that TR4 plays important roles in growth, embryonic and early postnatal pup survival, female reproductive function, and maternal behavior.
机译：睾丸孤儿核受体4（TR4）是尚未发现配体的核受体超家族的成员。从各种细胞系获得的体外数据表明，TR4充当调节许多信号传导途径的主要调节剂，但是TR4的体内生理作用仍然不清楚。在这里，我们报告了通过靶向基因破坏（TR4（-/-））缺乏TR4的小鼠的一代。 TR4（+/-）小鼠交配所产生的TR4（-/-）幼崽的数量远低于正常孟德尔比率所预测的数量，而TR4（-/-）小鼠表现出较高的出生后早期死亡率，因为以及明显的生长迟缓。此外，TR4（-/-）雌性动物在生殖和母性行为方面表现出缺陷，幼小的TR4（-/-）大坝幼崽在出生后不久就死亡，没有迹象表明可以摄入牛奶。这些结果提供了体内证据，表明TR4在生长，胚胎和早期产后幼崽存活，女性生殖功能以及母亲行为中起重要作用。

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