Characterization of mice carrying a conditional TEAD1 allele. Issue 12 (18th December 2017)

• Record Type: Journal Article
• Authors: Wen, Tong; Yin, Qin; Yu, Luyi; Hu, Guoqing; Liu, Jinhua; Zhang, Wei; Huang, Liang; Su, Huabo; Wang, Menghong; Zhou, Jiliang
• Is Part Of: Genesis. Volume 55:Issue 12(2017)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2017-12-18
• Subjects: conditional knockout -- Cre -- embryonic lethality -- floxed allele mouse -- gene targeting -- Hippo‐YAP pathway -- TEAD1 -- transcription factor; Developmental genetics -- Periodicals; Genetics -- Periodicals; Developmental biology -- Periodicals; Embryology -- Periodicals; Genetic regulation -- Periodicals; 576.5
• DOI: 10.1002/dvg.23085
• Languages: English
• ISSNs: 1526-954X

Abstract

Summary: The Hippo‐ yes‐associated protein (YAP) pathway is essential for controlling organ size and tumorigenesis. Previous studies have demonstrated that the primary outcome of YAP signaling in the nucleus is achieved by interaction with the transcription factor TEA domain transcription factor (TEAD1). The YAP/TEAD1 complex binds to DNA element and regulates the expression of genes involved in cell growth. However, constitutive knockout of TEAD1 leads to early embryonic lethality in mice. Thus, generation of a floxed TEAD1 mouse becomes crucial for further understanding mid‐ to late‐gestation and post‐natal role of TEAD1. Herein, we created and characterized a mouse model that allows for conditional disruption of TEAD1. Embryonic fibroblasts derived from the floxed TEAD1 mice enabled the Cre‐mediated deletion of TEAD1 in vitro using virally delivered Cre recombinase. Furthermore, crossing the floxed TEAD1 mouse with a ubiquitously expressing Cre mouse resulted in efficient ablation of the floxed allele in vivo, and the animals recapitulated early embryonic lethality defects. In conclusion, our data demonstrate an important role of TEAD1 in early development in mice, and the floxed TEAD1 mouse model will be a valuable genetic tool to determine the temporal and tissue‐specific functions of TEAD1.