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The development of transgenic technologies in the Cashmere goat ( Capra hircus ) has the potential to improve the quality of the meat and wool. The piggyBac (PB) transposon system is highly efficient and can be used to transpose specific target genes into the genome. Here, we developed a PB transposon system to produce transgenic Cashmere goat fetal fibroblasts (GFFs) with the enhanced green fluorescent protein (EGFP). We then used the genetically modified GFFs as nuclear donors to generate transgenic embryos by somatic cell nuclear transfer (SCNT). The embryos (n = 40) were implanted into female goats (n = 20). One transgenic kid that expressed EGFP throughout the surface features of its body was born. This result demonstrated the usefulness of PB transposon system in generating transgenic Cashmere goats. [ABSTRACT FROM AUTHOR]

Mule ducks accumulate a large amount of fat in their livers when fed high-energy feed, which is predominantly used for producing fatty livers. Nevertheless, there is limited research on the molecular mechanisms underlying the formation of fatty liver in mule ducks. Fatty acid translocase (CD36) is a sensor for fatty acids and lipid metabolism regulator, which may play a crucial role in the accumulation of fat in the liver of mule ducks. In this study, Overexpression and CD36 gene interference for 24 h was followed by induction of liver cells with 400 µmol/L palmitic acid (PA) for 24 h. The results demonstrated that CD36 overexpression increased hepatic triglyceride content, lipid droplet deposition, oxidative stress, and cell apoptosis. However, interference with CD36 had the opposite effect. CD36 overexpression suppressed the expression of AMPK and CPT-1A genes but enhanced the expression of ACC1 and LKB1 genes, with interference yielding contrasting results. Additionally, the expression of CD36 inhibited the AMPK pathway, reduced AMPK phosphorylation, downregulated AMPK protein expression, and upregulated SREBP1 protein expression. This promoted palmitic acid-induced hepatocyte fat accumulation. In summary, CD36 promotes palmitic acid-induced fat accumulation in primary mule duck liver cells through the AMPK signaling pathway. [ABSTRACT FROM AUTHOR]

• The high expression of MSTN and IGF2BP1 inhibited the development of embryonic muscle of white feather Muscovy duck. • FABP2 promotes embryonic muscle development of white feather Muscovy Duck. • The expressions of MSTN, IGF2BP1 and FABP2 mRNA in embryonic white feather Muscovy duck were gender and embryo age specific. To explore the effects of growth-related genes in both sexes and at different growth and development stages, male and female white Muscovy ducks at embryonic day E13, E17, E21, E25 and E29 were assessed in this study. RT-qPCR was used to determine the mRNA transcription levels of selected growth-related genes in the leg muscles of Muscovy ducks of both sexes and at different growth and developmental stages. MSTN , IGF2BP1 and FABP2 mRNAs were expressed in the leg muscles of male and female Muscovy ducks, but with different expression patterns. The MSTN and IGF2BP1 mRNA expression patterns were wavelike. MSTN mRNA expression was elevated at E13, increased at E17, decreased rapidly to the lowest level at E21, increased again at E25, and then decreased. IGF2BP1 mRNA expression was elevated at E13, increased at E17, decreased rapidly at E21, decreased rapidly to the lowest level at E25, and increased at E29. The expression trend of FABP2 mRNA was approximately "⊥" shape; the expression was the lowest at E13, increased slowly from E17 to E25, and increased extremely significantly at E29. In addition, the expression of MSTN in male Muscovy ducks was significantly higher than that in female ducks at E25 (P < 0.05). The expression of IGF2BP1 in male Muscovy ducks was extremely significantly higher than that in female ducks at E17 (P < 0.01). However, the expression of FABP2 in female Muscovy ducks was extremely significantly higher than that in male Muscovy ducks at E21 and E29 (P < 0.01). In conclusion, the mRNA expression of MSTN , IGF2BP1 and FABP2 in white Muscovy ducks is gestational age specific and sex specific. The differential gene expression patterns observed in this study provide a basis for understanding the physiological changes in white Muscovy ducks at different embryonic ages and in both sexes, supplementing the existing research on duck embryo muscle development. In addition, the findings provide a new framework for further discussion of poultry breeding. [ABSTRACT FROM AUTHOR]

Mule ducks tend to accumulate abundant fat in their livers via feeding, which leads to the formation of a fatty liver that is several times larger than a normal liver. However, the mechanism underlying fatty liver formation has not yet been elucidated. Fibroblast growth factor 1 (FGF1), a member of the FGF superfamily, is involved in cellular lipid metabolism and mitosis. This study aims to investigate the regulatory effect of FGF1 on lipid metabolism disorders induced by complex fatty acids in primary mule duck liver cells and elucidate the underlying molecular mechanism. Hepatocytes were induced by adding 1,500:750 µmol/L oleic and palmitic acid concentrations for 36 h, which were stimulated with FGF1 concentrations of 0, 10, 100, and 1000 ng/mL for 12 h. The results showed that FGF1 significantly reduced the hepatic lipid droplet deposition and triglyceride content induced by complex fatty acids; it also reduced oxidative stress; decreased reactive oxygen species fluorescence intensity and malondialdehyde content; upregulated the expression of antioxidant factors nuclear factor erythroid 2 related factor 2 (Nrf2), HO-1, and NQO-1; significantly enhanced liver cell activity; promoted cell cycle progression; inhibited cell apoptosis; upregulated cyclin-dependent kinase 1 (CDK1) and BCL-2 mRNA expression; and downregulated Bax and Caspase-3 expression. In addition, FGF1 promoted AMPK phosphorylation, activated the AMPK pathway, upregulated AMPK gene expression, and downregulated the expression of SREBP1 and ACC1 genes, thereby alleviating excessive fat accumulation in liver cells induced by complex fatty acids. In summary, FGF1 may alleviate lipid metabolism disorders induced by complex fatty acids in primary mule duck liver cells by activating the AMPK signaling pathway. [ABSTRACT FROM AUTHOR]