Differential expression of genes related to gain and intake in the liver of beef cattleReport as inadecuate

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BMC Research Notes

, 10:1



BackgroundTo better understand which genes play a role in cattle feed intake and gain, we evaluated differential expression of genes related to gain and intake in the liver of crossbred beef steers. Based on past transcriptomics studies on cattle liver, we hypothesized that genes related to metabolism regulation and the inflammatory response would be differentially expressed. This study used 16 animals with diverse gain and intake phenotypes to compare transcript abundance after a 78 day ad libitum feed study.

ResultsA total of 729 genes were differentially expressed. These genes were analyzed for over-representation among biological and cellular functions, and pathways. Cell transport processes and metabolic processes, as well as functions related to transport, were identified. Pathways related to immune function, such as the proteasome ubiquitination pathway and the chemokine signaling pathway, were also identified.

ConclusionsOur results were consistent with past transcriptomics studies that have found immune and transport processes play a role in feed efficiency. Gain and intake are impacted by complex processes in the liver, which include cellular transport, metabolism regulation, and immune function.

KeywordsFeed efficiency Transcriptome Steers Beef cattle Immune response Metabolism Cellular transport AbbreviationsDEdifferentially expressed

ERendoplasmic reticulum

FDRfalse discovery rate

IPAingenuity pathway analysis

qRT-PCRquantitative real time polymerase chain reaction

PANTHERProtein Analysis through Evolutionary Relationships

PCRpolymerase chain reaction

RFIresidual feed intake

RINRNA integrity number

Electronic supplementary materialThe online version of this article doi:10.1186-s13104-016-2345-3 contains supplementary material, which is available to authorized users.

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Author: C. M. Zarek - A. K. Lindholm-Perry - L. A. Kuehn - H. C. Freetly

Source: https://link.springer.com/

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