Centrosomal protein FOR20 knockout mice display embryonic lethality and left-right patterning defects
Centrosomal protein FOR20 knockout mice display embryonic lethality and left-right patterning defects
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中心体蛋白 FOR20 敲除小鼠表现出胚胎致死性和左右图案缺陷
DOI：
10.1002/1873-3468.14071
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发表时间：
2021-03-23
期刊：
影响因子：
3.5
通讯作者：
Xie, Shanshan
中科院分区：
文献类型：
--
作者：
Xu, Zhangqi;Liu, Min;Xie, Shanshan
中心体蛋白FOR 20在脊椎动物的纤毛发生、细胞迁移和细胞周期等细胞过程中起着重要作用。然而，FOR20在哺乳动物胚胎发育过程中的功能仍然未知。为了研究For20基因在哺乳动物体内的功能，我们通过基因打靶产生了For20纯合敲除小鼠。我们的数据显示，敲除For20基因的纯合子在妊娠期间导致显著的胚胎生长停滞和致死，而杂合子没有表现出明显的缺陷。缺乏For20导致胚胎左右图案受损和胚胎结中纤毛减少。For20的缺失也破坏了卵黄囊和胚胎中的血管生成。这些结果突出了For20在早期哺乳动物胚胎发生中的关键作用。
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.