Abstract
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: Lhx4loxP conditional knockout and Lhx4tdT reporter knock-in mice. Lhx4tdT/+, Lhx4loxP/+, and Lhx4loxP/loxP were viable, fertile, and did not display any gross abnormalities. By breeding Lhx4loxP 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 Lhx4tdT mice. Thus, Lhx4tdT and Lhx4loxP mouse lines provide valuable tools for unraveling the tissue-specific role of Lhx4 at postnatal stages in mice.
Original language | English (US) |
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Article number | e23328 |
Journal | Genesis |
Volume | 57 |
Issue number | 10 |
DOIs | |
State | Published - Oct 1 2019 |
Externally published | Yes |
Keywords
- LIM-homeodomain
- homeobox
- pituitary gland
- retina
- spinal cord
ASJC Scopus subject areas
- Genetics
- Endocrinology
- Cell Biology