Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41598-017-17828-7
Title: Dual repression of endocytic players by ESCC microRNAs and the Polycomb complex regulates mouse embryonic stem cell pluripotency
Authors: Mote, R.D
Mahajan, G
Padmanabhan, A 
Ambati, R
Subramanyam, D
Keywords: microRNA
polycomb group protein
animal
cytology
endocytosis
genetic transcription
genetics
metabolism
mouse
mouse embryonic stem cell
Animals
Endocytosis
Mice
MicroRNAs
Mouse Embryonic Stem Cells
Polycomb-Group Proteins
Transcription, Genetic
Issue Date: 2017
Publisher: Nature Publishing Group
Citation: Mote, R.D, Mahajan, G, Padmanabhan, A, Ambati, R, Subramanyam, D (2017). Dual repression of endocytic players by ESCC microRNAs and the Polycomb complex regulates mouse embryonic stem cell pluripotency. Scientific Reports 7 (1) : 17572. ScholarBank@NUS Repository. https://doi.org/10.1038/s41598-017-17828-7
Rights: Attribution 4.0 International
Abstract: Cell fate determination in the early mammalian embryo is regulated by multiple mechanisms. Recently, genes involved in vesicular trafficking have been shown to play an important role in cell fate choice, although the regulation of their expression remains poorly understood. Here we demonstrate for the first time that multiple endocytosis associated genes (EAGs) are repressed through a novel, dual mechanism in mouse embryonic stem cells (mESCs). This involves the action of the Polycomb Repressive Complex, PRC2, as well as post-transcriptional regulation by the ESC-specific cell cycle-regulating (ESCC) family of microRNAs. This repression is relieved upon differentiation. Forced expression of EAGs in mESCs results in a decrease in pluripotency, highlighting the importance of dual repression in cell fate regulation. We propose that endocytosis is critical for cell fate choice, and dual repression may function to tightly regulate levels of endocytic genes. © 2017 The Author(s).
Source Title: Scientific Reports
URI: https://scholarbank.nus.edu.sg/handle/10635/178551
ISSN: 2045-2322
DOI: 10.1038/s41598-017-17828-7
Rights: Attribution 4.0 International
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