4.6 Article

3'UTR-Seq analysis of chicken abdominal adipose tissue reveals widespread intron retention in 3'UTR and provides insight into molecular basis of feed efficiency

Journal

PLOS ONE
Volume 17, Issue 7, Pages -

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PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0269534

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In this study, gene expression profiles in abdominal fat of broiler chickens with different feed efficiency levels were analyzed. The results indicated that efficient muscle growth and fat deposition may be associated with gene expression regulation, extracellular matrix remodeling, and peroxisome and lipid metabolism.
Feed efficiency (FE) is an important trait in the broiler industry due to its direct correlation to efficient muscle growth instead of fat deposition. The present study characterized and compared gene expression profiles in abdominal fat from broiler chickens of different FE levels to enhance the understanding of FE biology. Specifically, traditional whole-transcript RNA-sequencing (RNA-seq) and 3' UTR-sequencing (3' UTR-seq) were applied to 22 and 61 samples, respectively. Overall, these two sequencing techniques shared a high correlation (0.76) between normalized counts, although 3' UTR-seq showed a higher variance in sequencing and mapping performance statistics across samples and a lower rate of uniquely mapped reads. A higher percentage of 3' UTR-seq reads mapped to introns suggested the frequent presence of cleavage sites in introns, thus warranting future research to study its regulatory function. Differential expression analysis identified 1198 differentially expressed genes (DEGs) between high FE (HFE) and intermediate FE (IFE) chickens with False Discovery Rate < 0.05 and fold change > 1.2. The processes that were significantly enriched by the DEGs included extracellular matrix remodeling and mechanisms impacting gene expression at the transcriptional and translational levels. Gene ontology enrichment analysis suggested that the divergence in fat deposition and FE in broiler chickens could be associated with peroxisome and lipid metabolism possibly regulated by G0/G1 switch gene 2 (G0S2).

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