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Runting and Stunting Syndrome Is Associated With Mitochondrial Dysfunction in Sex-Linked Dwarf Chicken

文献类型： 外文期刊

作者： Li, Hongmei 1 ; Hu, Bowen 1 ; Luo, Qingbin 1 ; Hu, Shuang 1 ; Luo, Yabiao 1 ; Zhao, Bojing 1 ; Gan, Yanmin 1 ; Li, Ying 4 ;

作者机构： 1.South China Agr Univ, Coll Anim Sci, Dept Anim Genet Breeding & Reprod, Guangzhou, Peoples R China

2.South China Agr Univ, Coll Anim Sci, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Minist Agr, Guangzhou, Peoples R China

3.South China Agr Univ, Coll Anim Sci, Key Lab Chicken Genet Breeding & Reprod, Minist Agr, Guangzhou, Peoples R China

4.Guangdong Acad Agr Sci, Inst Anim Sci, Guangzhou, Peoples R China

5.Univ Maryland, Virginia Maryland Reg Coll Vet Med, Div Immunol, College Pk, MD 20742 USA

关键词： runting and stunting syndrome; chicken; mitochondrial dysfunction; oxidative phosphorylation; ATP synthesis; vacuoles

期刊名称：FRONTIERS IN GENETICS （ 影响因子：4.599； 五年影响因子：4.888 ）

ISSN：

年卷期： 2020 年 10 卷

页码：

收录情况： SCI

摘要： Runting and stunting syndrome (RSS) in chicken are commonly known as "frozen chicken." The disease is characterized by lower body weight and slow growth and the incidence rate is widely 5%-20% in sex-linked dwarf (SLD) chickens. However, the etiology of RSS in chickens has plagued researchers for several decades. In this study, histopathology studies demonstrated that the hepatocytes of the RSS chickens contain many mitochondria with damaged and outer and inner membrane along with vacuolar hydropic degeneration. No mtDNA mutation was detected, but our microarray data showed that RSS chickens exhibited abnormal expression of genes, many of which are involved in oxidative phosphorylation (OXPHOS) and fatty acid metabolism. In particular, nuclear gene IGF2BP3 was upregulated in RSS chickens' liver cells. The abnormal expression of these genes is likely to impair the OXPHOS, resulting in reduced ATP synthesis in the hepatocytes of the RSS chickens, which may in turn leads to poor weight gain and retarded growth or stunting of chicks. Our findings suggest that mitochondria dysfunction rather than chronic inflammation is responsible for the reduced growth and RSS in SLD chickens. Mutations in GHR have been shown to compromise mitochondrial function in SLD chickens. Since the mitochondrial damage in the RSS chicken is more severe, we suggest that extra genes are likely to be affected to exacerbate the phenotype.

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