TY - JOUR
T1 - Cardiac and Skeletal Muscle Transcriptome Response to Heat Stress in Kenyan Chicken Ecotypes Adapted to Low and High Altitudes Reveal Differences in Thermal Tolerance and Stress Response
AU - Srikanth, Krishnamoorthy
AU - Kumar, Himansu
AU - Park, Woncheoul
AU - Byun, Mijeong
AU - Lim, Dajeong
AU - Kemp, Steve
AU - te Pas, Marinus F.W.
AU - Kim, Jun Mo
AU - Park, Jong Eun
N1 - Publisher Copyright:
© Copyright © 2019 Srikanth, Kumar, Park, Byun, Lim, Kemp, te Pas, Kim and Park.
PY - 2019/10/11
Y1 - 2019/10/11
N2 - 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.
AB - 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.
KW - MAPK signaling
KW - PPAR signaling
KW - RNA-Seq
KW - heat stress
KW - hub genes
KW - p53 signaling
UR - http://www.scopus.com/inward/record.url?scp=85074137412&partnerID=8YFLogxK
U2 - 10.3389/fgene.2019.00993
DO - 10.3389/fgene.2019.00993
M3 - Article
AN - SCOPUS:85074137412
SN - 1664-8021
VL - 10
JO - Frontiers in Genetics
JF - Frontiers in Genetics
M1 - 993
ER -