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Acute heat stress induces differential gene expressions in the small yellow follicles of a broiler-type strain of Taiwan country chickens

ABSTRACT: To realize the gene expression in response to acute heat stress in chicken small yellow follicles, we have employed whole genome microarray expression profiling as we have employed whole genome microarray expression profiling as a tool to identify genes response to acute heat stress. Female B strain Taiwan country chickens were subjected to acute heat stress (38℃) for 2 h, and then exposed to 25℃, with small yellow follicles collected 0, 2, and 6 h after the cessation of heat stress, using non heat-stressed hens as a control group (n = 3 hens per group). Based on a chicken 44K oligo microarray, 69, 51, and 76 genes were upregulated and 58, 15, 56 genes were downregulated after heat treatment of H2R0, H2R2, and H2R6, respectively, using a cutoff value of two-fold or higher in the small yellow follicles of the heat-stressed chickens from those of the control chickens. Upregulation of heat shock protein 25, interleukin 6, metallopeptidase 1, and metalloproteinase 13, and downregulation of type II alpha 1 collagen, discoidin domain receptor tyrosine kinase 2, and Kruppel-like factor 2 were confirmed through quantitative real-time polymerase chain reaction (qRT-PCR).

ORGANISM(S): Gallus gallus

PROVIDER: GSE71091 | GEO | 2015/07/21

SECONDARY ACCESSION(S): PRJNA290479

REPOSITORIES: GEO

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Project description:Heat stress (HS) can damage the integrity of the intestinal mucosal barrier, leading to decreased poultry productivity. This study aimed to identify candidate genes related to acute HS in breeder hens and provide insight into the molecular mechanisms underlying acute HS in gut health. Fifty 28-week-old breeder hens were divided into two groups (25 hens each) raised under thermoneutral zone (23 °C) and acute HS (36 °C, 6 hours) conditions. The heart rate and cloacal temperature were measured in all hens, and jejunal mucosa tissues were randomly collected from 12 hens per treatment for RNA-sequencing analysis. The results indicated a significant increase in the heart rate and cloacal temperature in hens exposed to acute HS (P < 0.05). Transcriptome analysis identified 138 differentially expressed genes (DEGs) in heat-stressed breeder hens, including 75 upregulated DEGs containing heat shock protein (HSP), energy homeostasis metabolism-related gene (PDK4), and fat metabolism-related genes (PPARA and CD36), and 63 downregulated DEGs containing the bile acid transporter gene (SLC10A2). Gene ontology analysis revealed significant enrichment in biological processes related to heat response and cholesterol biosynthesis. Kyoto Encyclopedia of Genes and Genomes analysis highlighted several significant pathways, including steroid biosynthesis, steroid hormone biosynthesis, protein processing in endoplasmic reticulum, the peroxisome proliferator-activated receptor (PPAR) signaling pathway, and the adipocytokine signaling pathway. Protein-protein interaction network analysis involving two large networks: one containing several upregulated HSPs and genes related to energy homeostasis and fat metabolism (PDK4, PPARA, and CD36) and glucose transporter (SLC2A5), and the other containing downregulated DEGs related to cholesterol biosynthesis. Overall, acute HS might affect energy metabolism, fat metabolism, and glucose transport in the jejunal mucosa of breeder hens. Heat-stressed hens could restore the nutritional function of the jejunal mucosa by increasing the expression of HSPs. These findings provide a theoretical framework for further investigation into the molecular regulatory mechanisms responsible for HS-induced changes in the gut health of poultry.

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Acute heat stress induces differential gene expressions in the small yellow follicles of a broiler-type strain of Taiwan country chickens

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