METTL3-dependent m6A modification of GHR mRNA regulates mitochondrial function through mitochondrial biogenesis during myoblast differentiation
文献类型： 外文期刊
作者： Zhao, Changbin 1 ; Hu, Bowen 1 ; Wang, Zhijun 1 ; Zhang, Ze 1 ; Luo, Wen 1 ; Li, Hongmei 1 ; Zhang, Xiquan 1 ;
作者机构： 1.South China Agr Univ, Coll Anim Sci, State Key Lab Conservat & Utilizat Subtrop Agrobio, Lingnan Guangdong Lab Agr, Guangzhou 510642, Peoples R China
2.Minist Agr, Guangdong Prov Key Lab Agroanim Genom & Mol Breedi, Natl Local Joint Engn Res Ctr Livestock Breeding, Guangzhou 510642, Peoples R China
3.Minist Agr, Key Lab Chicken Genet, Breeding & Reprod, Guangzhou 510642, Peoples R China
关键词： GHR; METTL3; m6A; Mitochondrial biogenesis; Mitochondrial function
期刊名称：POULTRY SCIENCE （ 影响因子：4.2； 五年影响因子：4.5 ）
ISSN： 0032-5791
年卷期： 2025 年 104 卷 7 期
页码：
收录情况： SCI
摘要： N6-methyl-adenosine (m6A) methylation has recently been shown to play a critical role in muscle development. We recently revealed that local GHR knockdown impairs mitochondrial function by inhibiting mitochondrial biogenesis, thereby repressing myoblast differentiation. And we identified m6A modification peaks in the GHR mRNA of chicken muscle tissue. However, whether m6A modification may regulate GHR mRNA expression to impinge on mitochondrial function through mitochondrial biogenesis during myoblast differentiation is lagging. We first predicted three potential m6A modification sites (GHR-139, GHR-203, GHR-385) on GHR mRNA through SRAMP online prediction website. We then confirmed that GHR-139 is the METTL3-dependent m6A modification site. Further, METTL3-dependent m6A modification down-regulated the GHR mRNA and protein expression, and blunted the GHR mediated GH-GHR-IGFs axis signal transduction during myoblast differentiation. We next revealed that METTL3-dependent m6A modification down-regulated GHR mRNA to inhibit mitochondrial biogenesis and impair mitochondrial function during myoblast differentiation. On the other hand, over-expression of METTL3 alone also proved to inhibit the expression of GHR gene, while suppressing mitochondrial biogenesis and mitochondrial function. In terms of the m6A reader protein, we uncovered that m6A modification might regulate the GHR mRNA expression through three m6A reader proteins hnRNPR, hnRNPA3 and hnRNPM. In conclusion, our data corroborate that METTL3-dependent m6A modification down-regulates GHR mRNA expression to impair mitochondrial function by inhibiting mitochondrial biogenesis during myoblast differentiation.
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