-
Title:
-
Overexpression of the Tuberous sclerosis complex 2 (TSC2) gene inhibits goat myoblasts proliferation and differentiation in understanding the underlying mechanism of muscle development.
-
Authors:
-
Lyu M; Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China.
Shalitana A; Department of Xinjiang Institute for Cancer Research, Xinjiang Cancer Hospital of Xinjiang Medical University, Urumqi 830011, China.
Luo J; Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China.
He H; Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China.
Sun S; Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China.
Wang P; Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address: .
-
Source:
-
Gene [Gene] 2020 Oct 05; Vol. 757, pp. 144943. Date of Electronic Publication: 2020 Jul 09.
-
Publication Type:
-
Journal Article
-
Language:
-
English
-
Imprint Name(s):
-
Original Publication: Amsterdam, Elsevier/North-Holland, 1976-
-
MeSH Terms:
-
Cell Differentiation*
Cell Proliferation*
Muscle Development*
Myoblasts/*metabolism
Tuberous Sclerosis Complex 2 Protein/*genetics
Animals ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cells, Cultured ; Goats ; Myoblasts/cytology ; Myoblasts/physiology ; Ribosomal Protein S6 Kinases, 70-kDa/genetics ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Tuberous Sclerosis Complex 2 Protein/metabolism ; Up-Regulation
-
Contributed Indexing:
-
Keywords: Differentiation; Goat myoblasts; MTOR/p70S6K; Proliferation; TSC2
-
Substance Nomenclature:
-
0 (Cell Cycle Proteins)
0 (Tuberous Sclerosis Complex 2 Protein)
EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa)
EC 2.7.11.1 (TOR Serine-Threonine Kinases)
-
Entry Date(s):
-
Date Created: 20200712 Date Completed: 20200826 Latest Revision: 20211204
-
Update Code:
-
20240105
-
DOI:
-
10.1016/j.gene.2020.144943
-
PMID:
-
32652105
-
The growth of animal skeletal muscle is mainly determined by the synthesis processes of total proteins in skeletal muscle cells, which has a significant impact on the postnatal growth of young animals. An increasing number of studies are focusing on the functions of Tuberous sclerosis complex 2 (TSC2) during the process of cell protein synthesis and growth. However, it is still unclear the effect of whether and how TSC2 on goat myoblasts proliferation and differentiation. Here, we found that TSC2 gene has opposite expression patterns in proliferation and differentiation of myoblasts. An expression vector containing goat TSC2 cDNA sequences linked with pcDNA3.1 plasmid was constructed. Myoblasts proliferation activity was significantly inhibited and cell cycle transition slowed down after the transfection of pcDNA3.1-TSC2 plasmid into goat primary myoblasts by EdU staining, CCK-8 and flow cytometry. Mechanically, we further confirmed that the overexpression TSC2 was able to down-regulate the mRNA and protein expression of mechanistic target of rapamycin (mTOR), p70 ribosomal S6 kinase 1 (p70S6K) and some cell cycle related genes. In addition, the expression of myogenic genes and myotube formation were attenuated. Collectively, all our results of the experiment demonstrate that TSC2 could regulate myoblasts cells proliferation and differentiation via the activation of the mTOR/p70S6K signaling pathway.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2020 Elsevier B.V. All rights reserved.)
