BMB Reports 2018; 51(7): 350-355  https://doi.org/10.5483/BMBRep.2018.51.7.043
The multifunctional RNA-binding protein hnRNPK is critical for the proliferation and differentiation of myoblasts
Yongjie Xu, Rui Li, Kaili Zhang, Wei Wu, Suying Wang, Pengpeng Zhang* & Haixia Xu*
College of Life Science, Xinyang Normal University, Xinyang 464000, China
Correspondence to:

Haixia Xu, Tel: +8618937612780; Fax: +863766391380; E-mail: hxxu214@126.com; Pengpeng Zhang, Tel: +8617739576132; Fax: +863766391380; E-mail: ppzhang15@163.com

Received: February 22, 2018; Revised: March 19, 2018; Accepted: May 29, 2018; Published online: July 31, 2018.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
HnRNPK is a multifunctional protein that participates in chromatin remodeling, transcription, RNA splicing, mRNA stability and translation. Here, we uncovered the function of hnRNPK in regulating the proliferation and differentiation of myoblasts. hnRNPK was mutated in the C2C12 myoblast cell line using the CRISPR/Cas9 system. A decreased proliferation rate was observed in hnRNPK-mutated cells, suggesting an impaired proliferation phenotype. Furthermore, increased G2/M phase, decreased S phase and increased sub-G1 phase cells were detected in the hnRNPK-mutated cell lines. The expression analysis of key cell cycle regulators indicated mRNA of Cyclin A2 was significantly increased in the mutant myoblasts compared to the control cells, while Cyclin B1, Cdc25b and Cdc25c were decreased sharply. In addition to the myoblast proliferation defect, the mutant cells exhibited defect in myotube formation. The myotube formation marker, myosin heavy chain (MHC), was decreased sharply in hnRNPK-mutated cells compared to control myoblasts during differentiation. The deficiency in hnRNPK also resulted in the repression of Myog expression, a key myogenic regulator during differentiation. Together, our data demonstrate that hnRNPK is required for myoblast proliferation and differentiation and may be an essential regulator of myoblast function.
Keywords: C2C12 myoblasts, CRISPR/Cas9, Differentiation, hnRNPK, Proliferation


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Funding Information
  • National Natural Science Foundation of China(NSFC)
      10.13039/501100001809
      U1204326, 31601167
  • Hainan Provincial Department of Science and Technology(Department of Science and Technology of Hainan Province)
      10.13039/501100008111
      182102310211, 182300410027

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