Li Hongmei, Hu Bowen, Luo Qingbin, Hu Shuang, Luo Yabiao, Zhao Bojing, Gan Yanmin, Li Ying, Shi Meiqing, Nie Qinghua, Zhang Dexiang, Zhang Xiquan
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, China.
Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Lab of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, China.
Front Genet. 2020 Jan 17;10:1337. doi: 10.3389/fgene.2019.01337. eCollection 2019.
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 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 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.
鸡的矮小综合征(RSS)通常被称为“僵鸡”。该病的特征是体重较低且生长缓慢,在性连锁矮小鸡(SLD)中的发病率普遍为5%-20%。然而,鸡矮小综合征的病因已经困扰研究人员数十年。在本研究中,组织病理学研究表明,患矮小综合征鸡的肝细胞含有许多线粒体,其外膜和内膜受损,并伴有空泡状水样变性。未检测到线粒体DNA突变,但我们的微阵列数据显示,患矮小综合征的鸡表现出基因表达异常,其中许多基因参与氧化磷酸化(OXPHOS)和脂肪酸代谢。特别是,核基因在患矮小综合征鸡的肝细胞中上调。这些基因的异常表达可能会损害氧化磷酸化,导致患矮小综合征鸡的肝细胞中ATP合成减少,进而可能导致雏鸡体重增加不佳、生长迟缓或发育不良。我们的研究结果表明,线粒体功能障碍而非慢性炎症是导致SLD鸡生长减缓及患矮小综合征的原因。已证明,相关基因的突变会损害SLD鸡的线粒体功能。由于患矮小综合征鸡的线粒体损伤更严重,我们认为可能有额外的基因受到影响,从而加剧了该表型。