Centrosomal protein FOR20 knockout mice display embryonic lethality and left-right patterning defects

FEBS Letters

article

Zhangqi Xu¹  Min Liu¹  Cheng Gao¹  Wenjun Kuang¹  Xiying Chen¹  Feifei Liu²  Bai Ge³  Xiaoyi Yan¹  Tianhua Zhou¹  Shanshan Xie⁸ 

[1] Department of Cell Biology, Zhejiang University School of Medicine;Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University;Department of Neurobiology, Zhejiang University School of Medicine;Department of Neurology of Second Affiliated Hospital, Zhejiang University School of Medicine;NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University;Cancer Center, Zhejiang University;Department of Molecular Genetics, University of Toronto;The Children's Hospital, Zhejiang University School of Medicine

关键词: angiogenesis;    cilia;    embryonic lethality;    FOR20;    left-right patterning;    mouse embryogenesis;   

DOI  :  10.1002/1873-3468.14071

来源: John Wiley & Sons Ltd.

【 摘 要 】

Centrosomal protein FOR20 has been reported to be crucial for essential cellular processes, including ciliogenesis, cell migration, and cell cycle in vertebrates. However, the function of FOR20 during mammalian embryonic development remains unknown. To investigate the in vivo function of the For20 gene in mammals, we generated For20 homozygous knockout mice by gene targeting. Our data reveal that homozygous knockout of For20 results in significant embryonic growth arrest and lethality during gestation, while the heterozygotes show no obvious defects. The absence of For20 leads to impaired left-right patterning of embryos and reduced cilia in the embryonic node. Deletion of For20 also disrupts angiogenesis in yolk sacs and embryos. These results highlight a critical role of For20 in early mammalian embryogenesis.

【 授权许可】

Unknown