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Research Project: Validate Causative Mutations in Agriculturally-Important Vertebrates

Location: Plant Genetics Research

Title: Research Note: Up-regulation of Melanophilin (MLPH) gene during avian adipogenesis and decreased fat pad weights with adipocyte hypotrophy in MLPH knockout quail

Author
item KIM, DONG-HWAN - The Ohio State University
item LEE, JOONBUM - The Ohio State University
item SUH, YEUNSU - The Ohio State University
item Chen, Paula
item LEE, KICHOON - The Ohio State University

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/20/2024
Publication Date: N/A
Citation: N/A

Interpretive Summary: Accumulation of excessive fat in poultry can greatly affect their health and productivity as well as result in economic losses. Identifying genes associated with fat accumulation is necessary to understand this process and use as markers for genetic selection to improve productivity and meat quality. Previously, quail were generated that had a mutation in a gene known as melanophilin. The gene edited quail had reduced body weight that was shown to be attributed to reduced fat accumulation. This gene was confirmed to be highly expressed during the process of fat accumulation in both chicken and quail cells. Therefore, melanophilin was discovered to be a novel gene involved in fat accumulation in avian species and could be a marker for selection to reduce fat for production purposes.

Technical Abstract: Advanced genetic and nutritional strategies aimed at modulating fat deposition can significantly reduce production costs and enhance profitability in the poultry industry. Melanophilin (MLPH) is recognized as a key gene regulating pigmentation as shown by diluted hair and feather coloration in MLPH mutant animals, including our avian models. However, the effects of MLPH during fat accretion have not been studied yet. The current in vitro studies reveal that MLPH gene expression levels were considerably elevated during adipogenesis in avian cells [101-fold in DF-1, 28.5-fold in chicken embryonic fibroblasts (CEF) and 4-fold in quail embryonic fibroblasts (QEF), compared to the undifferentiated cells of each cell type, p < 0.05]. In addition, fractionated fat cells (FC) showed increased expression levels of MLPH (5.7-fold, p < 0.05) compared to stromal-vascular cells (SVC). Using the MLPH knockout quail, disruption of the MLPH gene resulted in significantly reduced body weight (BW) and subcutaneous fat (S. Fat) pad weights compared to the wild type (WT) (p < 0.05). Further analysis through sectioning and staining of the fat tissues revealed that the mutation in Rab binding domain (RBD) of quail MLPH resulted in decreased fat cell sizes (p < 0.01). Overall, our data clearly demonstrated that MLPH can be a potential adipogenic marker gene, and MLPH may be associated with fat accretion in the gene edited quail model, highlighting the important role of MLPH in adipogenesis.