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Whole-transcriptome analysis of atrophic ovaries in broody chickens reveals regulatory pathways associated with proliferation and apoptosis

Authors :
Animal and Poultry Sciences
Liu, Lingbin
Xiao, Qihai
Gilbert, Elizabeth R.
Cui, Zhifu
Zhao, Xiaoling
Wang, Yan
Yin, Huadong
Li, Diyan
Zhang, Haihan
Zhu, Qing
Animal and Poultry Sciences
Liu, Lingbin
Xiao, Qihai
Gilbert, Elizabeth R.
Cui, Zhifu
Zhao, Xiaoling
Wang, Yan
Yin, Huadong
Li, Diyan
Zhang, Haihan
Zhu, Qing
Publication Year :
2018

Abstract

Broodiness in laying hens results in atrophy of the ovary and consequently decreases productivity. However, the regulatory mechanisms that drive ovary development remain elusive. Thus, we collected atrophic ovaries (AO) from 380-day-old broody chickens (BC) and normal ovaries (NO) from evenaged egg-laying hens (EH) for RNA sequencing. We identified 3,480 protein-coding transcripts that were differentially expressed (DE), including 1,719 that were down-regulated and 1,761 that were up-regulated in AO. There were 959 lncRNA transcripts that were DE, including 56 that were downregulated and 903 that were up-regulated. Among the116 miRNAs that were DE, 79 were downregulated and 37 were up-regulated in AO. Numerous DE protein-coding transcripts and target genes for miRNAs/lncRNAs were significantly enriched in reproductive processes, cell proliferation, and apoptosis pathways. A miRNA-intersection gene-pathway network was constructed by considering target relationships and correlation of the expression levels between ovary development-related genes and miRNAs. We also constructed a competing endogenous RNA (ceRNA) network by integrating competing relationships between protein-coding genes and lncRNA transcripts, and identified several lncRNA transcripts predicted to regulate the CASP6, CYP1B1, GADD45, MMP2, and SMAS2 genes. In conclusion, we discovered protein-coding genes, miRNAs, and lncRNA transcripts that are candidate regulators of ovary development in broody chickens.

Details

Database :
OAIster
Notes :
English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1357751826
Document Type :
Electronic Resource