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Transcriptome analysis in Takifugu rubripes and Dicentrarchus labrax gills during Cryptocaryon irritans infection
Takifugu rubripes and Dicentrarchus labrax are important commercial fish in China that are under serious threat from Cryptocaryon irritans. C. irritans is a ciliated obligate parasite that causes marine white spot disease and leads to heavy economic losses. We analysed the transcriptome in the gills...
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Published in: | Journal of fish diseases 2021-03, Vol.44 (3), p.249-262 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Takifugu rubripes and Dicentrarchus labrax are important commercial fish in China that are under serious threat from Cryptocaryon irritans. C. irritans is a ciliated obligate parasite that causes marine white spot disease and leads to heavy economic losses. We analysed the transcriptome in the gills of T. rubripes and D. labrax to compare differentially expressed genes (DEGs) and pathways during infection with C. irritans. In total, we identified 6,901 and 35,736 DEGs from T. rubripes and D. labrax, respectively. All DEGs were annotated into GO terms; 6,901 DEGs from T. rubripes were assigned into 991 sub‐categories, and 35,736 DEGs from D. labrax were assigned into 8,517 sub‐categories. We mapped DEGs to the KEGG database and obtained 153 and 350 KEGG signalling pathways from T. rubripes and D. labrax, respectively. Immune‐related categories included Toll‐like receptors, MAPK, lysosome, C‐type lectin receptor and NOD‐like receptor signalling pathways were significantly enriched pathways. In immune‐related signalling pathways, we found that AP‐1, P38, IL‐1β, HSP90 and PLA were significantly up‐regulated DEGs in T. rubripes, but P38 and PLA were significantly down‐regulated in D. labrax. In this study, transcriptome was used to analyse the difference between scaly and non‐scaly fish infection by C. irritans, which not only provided a theoretical basis for the infection mechanism of C. irritans, but also laid a foundation for effectively inhibiting the occurrence of this disease. Our work provides further insight into the immune response of host resistance to C. irritans. |
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ISSN: | 0140-7775 1365-2761 |
DOI: | 10.1111/jfd.13318 |