Dataset Information

Transcriptome response to heat stress in a chicken hepatocellular carcinoma cell line.

ABSTRACT: Heat stress triggers an evolutionarily conserved set of responses in cells. The transcriptome responds to hyperthermia by altering expression of genes to adapt the cell or organism to survive the heat challenge. RNA-seq technology allows rapid identification of environmentally responsive genes on a large scale. In this study, we have used RNA-seq to identify heat stress responsive genes in the chicken male white leghorn hepatocellular (LMH) cell line. The transcripts of 812 genes were responsive to heat stress (p < 0.01) with 235 genes upregulated and 577 downregulated following 2.5 h of heat stress. Among the upregulated were genes whose products function as chaperones, along with genes affecting collagen synthesis and deposition, transcription factors, chromatin remodelers, and genes modulating the WNT and TGF-beta pathways. Predominant among the downregulated genes were ones that affect DNA replication and repair along with chromosomal segregation. Many of the genes identified in this study have not been previously implicated in the heat stress response. These data extend our understanding of the transcriptome response to heat stress with many of the identified biological processes and pathways likely to function in adapting cells and organisms to hyperthermic stress. Furthermore, this study should provide important insight to future efforts attempting to improve species abilities to withstand heat stress through genome-wide association studies and breeding.

SUBMITTER: Sun L

PROVIDER: S-EPMC4595433 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature

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Transcriptome response to heat stress in a chicken hepatocellular carcinoma cell line.

Sun Liang L Lamont Susan J SJ Cooksey Amanda M AM McCarthy Fiona F Tudor Catalina O CO Vijay-Shanker K K DeRita Rachael M RM Rothschild Max M Ashwell Chris C Persia Michael E ME Schmidt Carl J CJ

Cell stress & chaperones 20150805 6

Heat stress triggers an evolutionarily conserved set of responses in cells. The transcriptome responds to hyperthermia by altering expression of genes to adapt the cell or organism to survive the heat challenge. RNA-seq technology allows rapid identification of environmentally responsive genes on a large scale. In this study, we have used RNA-seq to identify heat stress responsive genes in the chicken male white leghorn hepatocellular (LMH) cell line. The transcripts of 812 genes were responsive ...[more]

PMID: 26238561

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Project description:Acute heat stress requires immediate adjustment of the stressed individual to sudden changes of ambient temperatures. Chickens are particularly sensitive to heat stress due to development of insufficient physiological mechanisms to mitigate its effects. One of the symptoms of heat stress is endotoxemia that results from release of the lipopolysaccharide (LPS) from the guts. Heat-related cytotoxicity is mitigated by the innate immune system, which is comprised mostly of phagocytic cells such as monocytes and macrophages. The objective of this study was to analyze the molecular responses of the chicken macrophage-like HD11 cell line to combined heat stress and lipopolysaccharide treatment in vitro. The cells were heat-stressed and then allowed a temperature-recovery period, during which the gene expression was investigated. LPS was added to the cells to mimic the heat-stress-related endotoxemia. Semi high-throughput gene expression analysis was used to study a gene panel comprised of heat shock proteins, stress-related genes, signaling molecules and immune response genes. HD11 cell line responded to heat stress with increased mRNA abundance of the HSP25, HSPA2 and HSPH1 chaperones as well as DNAJA4 and DNAJB6 co-chaperones. The anti-apoptotic gene BAG3 was also highly up-regulated, providing evidence that the cells expressed pro-survival processes. The immune response of the HD11 cell line to LPS in the heat stress environment (up-regulation of CCL4, CCL5, IL1B, IL8 and iNOS) was higher than in thermoneutral conditions. However, the peak in the transcriptional regulation of the immune genes was after two hours of temperature-recovery. Therefore, we propose the potential influence of the extracellular heat shock proteins not only in mitigating effects of abiotic stress but also in triggering the higher level of the immune responses. Finally, use of correlation networks for the data analysis aided in discovering subtle differences in the gene expression (i.e. the role of the CASP3 and CASP9 genes).

Project description:Heat stress (HS) negatively affects chicken performance. Agricultural expansion will happen in regions that experience high ambient temperatures, where fast-growing commercial chickens are vulnerable. Indigenous chickens of such regions, due to generations of exposure to environmental challenges, might have higher thermal tolerance. In this study, two indigenous chicken ecotypes, from the hot and humid Mombasa (lowland) and the colder Naivasha (highland) regions, were used to investigate the effects of acute (5?h, 35°C) and chronic (3?days of 35°C for 8?h/day) HS on the cardiac and skeletal muscle, through RNA sequencing. The rectal temperature gain and the number of differentially expressed genes (DEGs) [False Discovery Rate (FDR) < 0.05] were two times higher in the acute stage than in the chronic stage in both ecotypes, suggesting that cyclic exposure to HS can lead to adaptation. A tissue- and stage-specific difference in response to HS was observed, with peroxisome proliferator-activated-receptor (PPAR) signaling and mitogen-activate protein kinase (MAPK) signaling pathways, enriched in heart and skeletal muscle, respectively, and the p53 pathway enriched only in the acute stage in both tissues. The acute and chronic stage DEGs were integrated by a region-specific gene coexpression network (GCN), and genes with the highest number of connections (hub genes) were identified. The hub genes in the lowland network were CCNB2, Crb2, CHST9, SESN1, and NR4A3, while COMMD4, TTC32, H1F0, ACYP1, and RPS28 were the hub genes in the highland network. Pathway analysis of genes in the GCN showed that p53 and PPAR signaling pathways were enriched in both low and highland networks, while MAPK signaling and protein processing in endoplasmic reticulum were enriched only in the gene network of highland chickens. This shows that to dissipate the accumulated heat, to reduce heat induced apoptosis, and to promote DNA damage repair, the ecotypes activated or suppressed different genes, indicating the differences in thermal tolerance and HS response mechanisms between the ecotypes. This study provides information on the HS response of chickens, adapted to two different agro climatic environments, extending our understanding of the mechanisms of HS response and the effect of adaptation in counteracting HS.

Dataset Information

Transcriptome response to heat stress in a chicken hepatocellular carcinoma cell line.

Publications

Transcriptome response to heat stress in a chicken hepatocellular carcinoma cell line.

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