Variation in sequence and expression of the avian FTO, and association with glucose metabolism, body weight, fatness and body composition in chickens

Jia, Xiaoyun; Nie, Qinghua; Lamont, Susan J.; Zhang, Xiquan

doi:10.1038/ijo.2011.221

Cited by 25 publications

(27 citation statements)

References 46 publications

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“…Expression of FTO in the hypothalamic nuclei involved in energy balance regulation has been shown to respond to nutritional manipulations such as feeding and fasting [34]–[36]. Fasting has been shown to also increase FTO gene expression in the cerebrum, liver, breast muscle and subcutaneous fat.…”

Section: Discussionmentioning

confidence: 99%

Expression of miR-33 from an SREBF2 Intron Targets the FTO Gene in the Chicken

Shao

Wang

et al. 2014

PLoS ONE

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The sterol regulatory element binding transcription factor 2 (SREBF2) gene encodes a transcription factor that activates the expression of many genes involved in the synthesis and uptake of cholesterol, fatty acids, triglycerides, and phospholipids. Through bioinformatics, we found that intron 16 of the chicken SREBF2 gene might encode the chicken miR-33. Using quantitative RT-PCR, we detected the expression of miR-33 in a variety of chicken tissues including skeletal muscle, adipose tissue, and liver. Three hundred and seventy eight genes were predicted to be potential targets of miR-33 in chickens via miRNA target prediction programs “miRanda” and “TargetScan”. Among these targets, the gene FTO (fat mass and obesity associated) encodes a Fe(II)- and 2-oxoglutarate-dependent nucleic acid demethylase that regulates lipid metabolism, and the possibility that its expression is negatively regulated by miR-33 in the chicken liver was therefore further studied. Co-transfection and dual-luciferase reporter assays showed that the expression of luciferase reporter gene linked to the 3′-untranslated region (3′UTR) of the chicken FTO mRNA was down-regulated by overexpression of the chicken miR-33 in the C2C12 cells (P<0.05). Furthermore, this down-regulation was completely abolished when the predicted miR-33 target site in the FTO 3′UTR was mutated. In contrast, the expression of FTO mRNA in the primary chicken hepatocytes was up-regulated after transfection with the miR-33 inhibitor LNA-anti-miR-33. Using quantitative RT-PCR, we also found that the expression of miR-33 was increased in the chicken liver from day 0 to day 49 of age, whereas that of the FTO mRNA was decreased during the same age period. These data together suggest that miR-33 might play an important role in lipid metabolism in the chicken liver by negatively regulating the expression of the FTO gene.

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Section: Discussionmentioning

confidence: 99%

Expression of miR-33 from an SREBF2 Intron Targets the FTO Gene in the Chicken

Shao

Wang

et al. 2014

PLoS ONE

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“…Multiple comparisons were performed to calculate the least square means (LSM) by the Duncan’s Multiple Range test. Details are reported in our previous study34.…”

Section: Methodsmentioning

confidence: 99%

A short insertion mutation disrupts genesis of miR-16 and causes increased body weight in domesticated chicken

Jia

Lin

Nie

et al. 2016

Sci Rep

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Body weight is one of the most important quantitative traits with high heritability in chicken. We previously mapped a quantitative trait locus (QTL) for body weight by genome-wide association study (GWAS) in an F2 chicken resource population. To identify the causal mutations linked to this QTL, expression profiles were determined on livers of high-weight and low-weight chicken lines by microarray. Combining the expression pattern with SNP effects by GWAS, miR-16 was identified as the most likely potential candidate with a 3.8-fold decrease in high-weight lines. Re-sequencing revealed that a 54-bp insertion mutation in the upstream region of miR-15a-16 displayed high allele frequencies in high-weight commercial broiler line. This mutation resulted in lower miR-16 expression by introducing three novel splicing sites instead of the missing 5′ terminal splicing of mature miR-16. Elevating miR-16 significantly inhibited DF-1 chicken embryo cell proliferation, consistent with a role in suppression of cellular growth. The 54-bp insertion was significantly associated with increased body weight, bone size and muscle mass. Also, the insertion mutation tended towards fixation in commercial broilers (Fst > 0.4). Our findings revealed a novel causative mutation for body weight regulation that aids our basic understanding of growth regulation in birds.

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“…Therefore, chicken IMF accumulation is dependent on the transport and uptake of blood lipids as well as lipogenesis subsequently in muscle rather than de novo fatty acids synthesis (Griffin et al, 1987). Previous studies have identified about 20 quantitative trait loci (QTL) related to chicken IMF, which are mainly located on chromosomes 1, 2, 5, 23 (Jennen et al, 2005; D'Andre et al, 2010; Ye et al, 2010; Jia et al, 2012; Liu et al, 2013; Nassar et al, 2013; Sun et al, 2013; Zhang T. et al, 2015). Otherwise, a large number of genes including GPAT1, ACC, CD36, AGPAT1 , and DGAT2 (Jeong et al, 2012), FABP (Ye et al, 2010; Serao et al, 2011), LPL (Zhang X. D. et al, 2015), DGAT1 (Li et al, 2013) were recognized as candidate genes for IMF, but their molecular mechanisms affecting IMF are still unclear.…”

Section: Introductionmentioning

confidence: 99%

Lower Expression of SLC27A1 Enhances Intramuscular Fat Deposition in Chicken via Down-Regulated Fatty Acid Oxidation Mediated by CPT1A

Qiu

Xie

et al. 2017

Front. Physiol.

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Intramuscular fat (IMF) is recognized as the predominant factor affecting meat quality due to its positive correlation with tenderness, juiciness, and flavor. Chicken IMF deposition depends on the balance among lipid synthesis, transport, uptake, and subsequent metabolism, involving a lot of genes and pathways, however, its precise molecular mechanisms remain poorly understood. In the present study, the breast muscle tissue of female Wenchang chickens (WC) (higher IMF content, 1.24 in D120 and 1.62 in D180) and female White Recessive Rock chickens (WRR; lower IMF content, 0.53 in D120 and 0.90 in D180) were subjected to RNA-sequencing (RNA-seq) analysis. Results showed that many genes related to lipid catabolism, such as SLC27A1, LPL, ABCA1, and CPT1A were down-regulated in WC chickens, and these genes were involved in the PPAR signaling pathway and formed an IPA® network related to lipid metabolism. Furthermore, SLC27A1 was more down-regulated in WRR.D180.B than in WRR.D120.B. Decreased cellular triglyceride (TG) and up-regulated CPT1A were observed in the SLC27A1 overexpression QM-7 cells, and increased cellular triglyceride (TG) and down-regulated CPT1A were observed in the SLC27A1 knockdown QM-7 cells. These results suggest that lower lipid catabolism exists in WC chickens but not in WRR chickens, and lower expression of SLC27A1 facilitate IMF deposition in chicken via down-regulated fatty acid oxidation mediated by CPT1A. These findings indicate that reduced lipid catabolism, rather than increased lipid anabolism, contributes to chicken IMF deposition.

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Variation in sequence and expression of the avian FTO, and association with glucose metabolism, body weight, fatness and body composition in chickens

Cited by 25 publications

References 46 publications

Expression of miR-33 from an SREBF2 Intron Targets the FTO Gene in the Chicken

Expression of miR-33 from an SREBF2 Intron Targets the FTO Gene in the Chicken

A short insertion mutation disrupts genesis of miR-16 and causes increased body weight in domesticated chicken

Lower Expression of SLC27A1 Enhances Intramuscular Fat Deposition in Chicken via Down-Regulated Fatty Acid Oxidation Mediated by CPT1A

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