ABSTRACT: 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.
