Asymmetric Expression of LincGET Biases Cell Fate in Two-Cell Mouse Embryos

Jiaqiang Wang, Leyun Wang, Guihai Feng, Yukai Wang, Yufei Li, Xin Li, Chao Liu, Guanyi Jiao, Cheng Huang, Junchao Shi, Tong Zhou, Qi Chen, Zhonghua Liu, Wei Li, Qi Zhou

Research output: Contribution to journalArticlepeer-review

87 Scopus citations


In early mammalian embryos, it remains unclear how the first cell fate bias is initially triggered and amplified toward cell fate segregation. Here, we report that a long noncoding RNA, LincGET, is transiently and asymmetrically expressed in the nucleus of two- to four-cell mouse embryos. Overexpression of LincGET in one of the two-cell blastomeres biases its progeny predominantly toward the inner cell mass (ICM) fate. Mechanistically, LincGET physically binds to CARM1 and promotes the nuclear localization of CARM1, which can further increase the level of H3 methylation at Arginine 26 (H3R26me), activate ICM-specific gene expression, upregulate transposons, and increase global chromatin accessibility. Simultaneous overexpression of LincGET and depletion of Carm1 no longer biased embryonic fate, indicating that the effect of LincGET in directing ICM lineage depends on CARM1. Thus, our data identify LincGET as one of the earliest known lineage regulators to bias cell fate in mammalian 2-cell embryos. An endogenous retrovirus-associated nuclear long noncoding RNA biases cell fate in mouse two-cell embryos.

Original languageEnglish (US)
Pages (from-to)1887-1901.e18
Issue number7
StatePublished - Dec 13 2018


  • CARM1
  • cell fate determination
  • chromatin accessibility
  • early embryos
  • long noncoding RNA

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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