Apr 25, 2020

Klf4 methylated by Prmt1 is required for lineage segregation of epiblast and primitive endoderm

BioRxiv : the Preprint Server for Biology
Z.-y. ZuoYe Zhang

Abstract

The second cell fate decision in the early stage of mammalian embryonic development is pivotal; however, the underlying molecular mechanism is largely unexplored. Here, we report that Prmt1 acts as an important regulator in primitive endoderm (PrE) formation. First, an embryonic chimeric assay showed that Prmt1 inhibition induces the integration of mouse embryonic stem cells (ESCs) into the PrE. Second, Prmt1 inhibition promotes Gata6 expression in both mouse blastocysts and ESCs. Single-cell RNA sequencing and flow cytometry assays demonstrated that Prmt1 depletion in ESCs contributes to an emerging cluster, where PrE genes are upregulated significantly. Furthermore, the efficiency of extraembryonic endoderm stem cell induction increased in Prmt1-depleted ESCs. Finally, we showed that the pluripotency factor Klf4 methylated at Arg396 by Prmt1 is required for recruitment of the repressive mSin3a/HDAC complex to silence PrE genes. Therefore, we reveal a regulatory mechanism for cell fate decisions centered on Prmt1-mediated Klf4 methylation.

  • References
  • Citations

References

  • We're still populating references for this paper, please check back later.
  • References
  • Citations

Citations

  • This paper may not have been cited yet.

Mentioned in this Paper

Research
Neoplasms
Clone
Massively-Parallel Sequencing
Resistance Process
Response to Treatment
Subclone
Biological Evolution

Related Feeds

BioRxiv & MedRxiv Preprints

BioRxiv and MedRxiv are the preprint servers for biology and health sciences respectively, operated by Cold Spring Harbor Laboratory. Here are the latest preprint articles (which are not peer-reviewed) from BioRxiv and MedRxiv.

Related Papers

Dental Clinics of North America
R M Christopher
Neurologic Clinics
Joseph M Furman, Susan L Whitney
© 2020 Meta ULC. All rights reserved