Roles of chicken growth hormone receptor antisense transcript in chicken muscle development and myoblast differentiation
文献类型： 外文期刊
作者： Xu, H. D. 1 ; Li, T. 1 ; Wang, Z. 1 ; Adu-Asiamah, P. 1 ; Leng, Q. Y. 1 ; Zheng, J. H. 1 ; Zhao, Z. H. 1 ; An, L. L. 1 ; Zha 1 ;
作者机构： 1.Guangdong Ocean Univ, Agr Coll, Zhanjiang 524088, Peoples R China
2.South China Agr Univ, Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Guangdong, Peoples R China
关键词： chicken; growth hormone receptor; natural antisense transcript; myoblast; differentiation
期刊名称：POULTRY SCIENCE （ 影响因子：3.352； 五年影响因子：3.679 ）
ISSN： 0032-5791
年卷期： 2019 年 98 卷 12 期
页码：
收录情况： SCI
摘要： Muscle is one of the important economic traits in poultry production, and its production depends on the increased number of muscle fibers during the embryonic stage. Chicken GHR gene can transcribe in double directions, possessing not only GHR-S but also GHR-AS. The 2 kinds of transcripts are partially complementation in sequences and interact with each other. Until now, the roles and mechanisms of GHR-AS in myoblast differentiation was still unknown. In this study, we not only analyzed the GHR-AS expression patterns in myoblast differentiation phase but also clarified that GHR-AS promoted myoblast differentiation via GH-GHR-IGF1 signal pathway. Quantitative PCR analysis indicated that GHR-AS was increased during myoblast differentiation. Sub-cellular localization showed that GHR-AS and GHR-S were expressed at a higher level in the nucleus than that in the cytoplasm. The expression of MyoD and MyHC and the myoblast differentiation significantly increased after GHR-AS overexpression, while the distance between wounds decreased, suggesting that GHR-AS repressed myoblast migration and promoted differentiation. Additionally, the expression of GHR-AS, IGF1 and MyHC increased after GH protein treated, and the myoblast differentiation also increased. In conclusion, GHR-AS promoted myoblast differentiation by enhancing fusion and inhibiting migration possibly via GH-GHR-IGF1 signal pathway.
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