Transcriptome Analysis Reveals Impaired Fertility and Immunity Under Salinity Exposure in Juvenile Grass Carp
文献类型: 外文期刊
作者: Zhang, Jingjing 1 ; Wu, Zhi 1 ; He, Yujie 1 ; Li, Xinhui 1 ; Li, Jie 1 ;
作者机构: 1.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, Guangzhou, Peoples R China
2.Guangzhou Sci Observing & Expt Stn Natl Fisheries, Guangzhou, Peoples R China
3.Minist Agr & Rural Affairs, Sci Observing & Expt Stn Fishery Resources & Envi, Guangzhou, Peoples R China
4.Key Lab Aquat Anim Immune Technol Guangdong Prov, Guangzhou, Peoples R China
关键词: larval grass carp; RNA-seq; fertility; immunity; seawater intrusion
期刊名称:FRONTIERS IN MARINE SCIENCE ( 影响因子:4.912; 五年影响因子:5.125 )
ISSN:
年卷期: 2021 年 8 卷
页码:
收录情况: SCI
摘要: Grass carp (Ctenopharyngodon idellus) is one of the most economically important aquaculture species and is widely cultured in China. However, its wild populations in many rivers are increasingly declining, and seawater intrusion is one of the most important threats to their survival. However, the mechanisms underlying the decline due to salinity pressure are still unknown. Here, we performed a comparative transcriptome analysis of C. idellus larvae in response to salinity exposures; a total of 481 differentially expressed genes (DEGs) were identified. These DEGs were significantly enriched in eight Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, among which steroid biosynthesis was the most important one, with the highest enrichment score. The pathway plays an important role in the development of the testes and ovary. Interestingly, all DEGs in steroid biosynthesis showed a down regulation, indicating that salinity exposure may pose damage to the fertility of C. idellus. Furthermore, three immunity-associated pathways (cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway, and NOD-like receptor signaling pathway) were also significantly enriched, suggesting impaired immunity and a high risk of disease infection under salinity exposure. Overall, damage to both fertility and immunity would decrease the number of offspring and increase the risk of death due to disease infection. Our results provide a potential molecular mechanism underlying the decline of wild C. idellus populations in the Pearl River.
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