Project description:Cryptocaryonosis caused by Cryptocaryon irritans is one of the major diseases of large yellow croaker (Larimichthys crocea), which lead to massive economic losses annually. The pathogenesis for cryptocaryonosis has been researched by a series of transcriptome studies under different infection conditions. However, little is known about the roles of tissue-specifically expressed genes during the infection of C. irritans. In this study, we analyzed the tissue-specific expression of transcripts in the major infection organs including gill and skin of L. crocea after C. irritans infection. we constructed transcriptome expression profiles of L. crocea gill and skin, including 23,172 protein-coding genes and 7,503 long noncoding RNAs (lncRNAs). By comparing transcriptome data from different tissues of L. crocea, we observed tissue specificity of transcripts in gill and skin, including 3,003 protein coding genes and 639 lncRNAs. A total of 212 of the protein coding genes were involved in immune system. Further analysis revealed that the tissue-specific DEGs in gill and skin were mainly involved in HIF-1 signaling pathway and Complement and coagulation cascades, respectively. In addition, 9 non-tissue-specific hub genes, including CCL4, DDIT4, LEP, ect., which are highly associated with C. irritans infection were identified. To our knowledge, this is the first comparative transcriptome analysis of gill and skin after C. irritans infection. Our results are helpful to understand the molecular mechanism of pathogenesis for cryptocaryonosis, espec-tissue specificity of protein-coding genes and lncRNAs involved in immune regulation.
2021-11-28 | GSE174221 | GEO
Project description:Transcriptome Analysis of Amphiprion percula against Cryptocaryon irritans
| PRJNA832516 | ENA
Project description:Transcriptome analysis of Cryptocaryon irritans from South China
Project description:Cryptocaryon irritans causes marine "white spot disease" in various fish hosts, including the golden pompano, a highly sensitive species with significant economic value in the coastal regions of South China. Therefore, exploring the molecular mechanisms that C. irritans infection is important for accelerating molecular breeding programs. In this study, we artificially infected golden pompano with C. irritans. Morphological observations of the gills using tissue sections revealed significant histological changes following infection. RNA-seq was employed to profile gene expression in the gills of golden pompano at different time points post-infection to investigate the molecular mechanisms of the disease. After filtering low-quality sequences, a total of 781,496,198 clean reads were obtained, with Q30 greater than 95%. Differentially expressed genes (DEGs) were identified at 24 hours, 3 days, and 5 days post-infection, with 800, 4208, and 2712 DEGs, respectively. After combining and removing false positives, a total of 2968 DEGs were analyzed for spatiotemporal expression patterns, and these DEGs could be categorized into two down-regulated expression patterns. KEGG enrichment analysis revealed that DEGs were associated with cell-cell junctions, cell-ECM interactions, signal transduction, and immune-related pathways. Further analysis suggested that gill tissue damage during infection led to reduced dissolved oxygen intake, increasing physiological and metabolic stress. This was accompanied by widespread downregulation of collagen genes and deprivation of growth factors, indicating impaired tissue repair. Additionally, as an apoptosis inhibitor, Bcl-2 was found to be downregulated in the infected fish. Therefore, C. irritans infection-induced gill damage leads to hypoxia and subsequently triggers cellular apoptosis.