Jiajie Zhu

Visceral white-nodules disease (VWND), caused by Pseudomonas plecoglossicida, poses a severe threat to the large yellow croaker (Larimichthys crocea) aquaculture industry. Although breeding resistant strains is a promising strategy, the molecular basis of disease resistance in this host remains poorly understood. Here, 1500 fish were artificially infected, and extreme phenotypes (30 resistant, RL; 30 susceptible, SL) were selected based on survival time and liver pathogen load. Liver histopathology revealed that RL fish maintained intact architecture with only mild vacuolation, whereas SL fish exhibited widespread necrosis, inflammation, and hemosiderin deposition. Consistently, RL fish showed lower MDA levels and higher GSH-Px activity and TAC. Transcriptomic analysis identified 172 differentially expressed genes (DEGs): RL fish were characterized by upregulation of anti-inflammatory and tissue-protective genes (Epo, CAV3) and downregulation of pro-coagulant factors (PAI1, K1kb1). Proteomic analysis identified 111 differentially expressed proteins, with significantly enriched pathways including the peroxisome, pentose phosphate, and phagosome pathways. Integrated cross-omics analysis revealed eight co-enriched KEGG pathways; among them, arginine/proline metabolism, phagosome, oxidative phosphorylation, and focal adhesion were consistently upregulated in the RL group. These findings suggest that effective resistance to VWND in L. crocea may involve a coordinated, multi-layered defense program encompassing redox balance, regulated immune responses, metabolic reprogramming, and cellular homeostasis. Cross-omics-supported candidate factors (e.g., P4ha1, COX6B, RAB5A, CAV3) represent promising targets for functional validation via DNA-level experiments in independent sample sets, and the prominent enrichment of arginine-proline metabolism indicates a potential target for dietary intervention that merits further investigation.

Disease outbreaks in aquaculture have recently intensified. In particular, visceral white-nodules disease, caused by Pseudomonas plecoglossicida, has severely hindered the small yellow croaker (Larimichthys polyactis) aquaculture industry. However, research on this disease is limited. To address this gap, the present study employed a 100K SNP chip to genotype individuals from an F1 full-sib family, identify single nucleotide polymorphisms (SNPs), and construct a genetic linkage map for this species. A high-density genetic linkage map spanning a total length of 1395.72 cM with an average interval of 0.08 cM distributed across 24 linkage groups was obtained. Employing post-infection survival time as an indicator of disease resistance, 13 disease resistance-related quantitative trait loci (QTLs) were detected, and these regions included 169 genes. Functional enrichment analyses pinpointed 11 candidate disease resistance-related genes. RT-qPCR analysis revealed that the genes of chmp1a and arg1 are significantly differentially expressed in response to P. plecoglossicida infection in spleen and liver tissues, indicating their pivotal functions in disease resistance. In summary, in addition to successfully constructing a high-density genetic linkage map, this study reports the first QTL mapping for visceral white-nodules disease resistance. These results provide insight into the intricate molecular mechanisms underlying disease resistance in the small yellow croaker.