LHX4 is a LIM‐homeodomain transcription factor essential for the development of spinal cord and pituitary gland. Mice with homozygous Lhx4‐null mutation suffer early postnatal death from lung defect. In this study, to facilitate the research on Lhx4 function, we designed a targeting construct to generate two novel Lhx4 mouse lines: Lhx4 ^loxP conditional knockout and Lhx4 ^tdT reporter knock‐in mice. Lhx4 ^tdT/+, Lhx4 ^loxP/+, and Lhx4 ^loxP/loxP were viable, fertile, and did not display any gross abnormalities. By breeding Lhx4 ^loxP line with Cre‐expressing mice, the Exon 3 of Lhx4 was efficiently removed, resulting in a shift in the reading frame and the inactivation of Lhx4. The expression of tdTomato knock‐in reporter recapitulated the endogenous LHX4 expression and was detected in the retina, spinal cord, pituitary gland, and hindbrain of Lhx4 ^tdT mice. Thus, Lhx4 ^tdT and Lhx4 ^loxP mouse lines provide valuable tools for unraveling the tissue‐specific role of Lhx4 at postnatal stages in mice.

中文翻译：

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Lhx4tdT报告基因敲入和Lhx4loxP条件敲除小鼠的产生和特征。

LHX4是LIM同源域转录因子，对脊髓和垂体的发育至关重要。具有Lhx4-null纯合突变的小鼠在出生后因肺缺陷而死亡。在这项研究中，为了促进对Lhx4功能的研究，我们设计了一种靶向构建体，以生成两种新型Lhx4小鼠品系：Lhx4 ^loxP条件敲除小鼠和Lhx4 ^tdT报告基因敲入小鼠。Lhx4 ^{tdT / +}，Lhx4 ^{loxP / +}和Lhx4 ^{loxP / loxP}是可行的，可育的，并且没有显示任何严重异常。通过繁殖Lhx4 ^loxP 在表达Cre的小鼠中，Lhx4的第3外显子被有效地去除，导致阅读框发生变化，Lhx4失活。tdTomato敲入报告基因的表达概括了内源性LHX4的表达，并在Lhx4 ^tdT小鼠的视网膜，脊髓，垂体和后脑中检测到。因此，Lhx4 ^tdT和Lhx4 ^loxP小鼠系为揭示小鼠出生后Lhx4的组织特异性作用提供了有价值的工具。