Transcriptome analysis of hepatopancreas of Litopenaeus vannamei after acute exposure to Alexandrium pacificum
TL;DR
Molecular insights are offered into the molecular defense mechanisms of L. vannamei against A. pacificum toxicity as well as enriched pathways including lysosome, C‑type lectin receptor signaling, peroxisome, drug metabolism, and neuroactive ligand‑receptor interactions.
Abstract
Alexandrium pacificum is a toxic species among red tide-forming organisms. Red tide outbreaks can cause seawater hypoxia and discoloration, which impair shrimp feeding and may facilitate toxin accumulation. Exposure to A. pacificum has been linked to oxidative stress and immune disruption in Litopenaeus vannamei, highlighting the need to understand the pathogenic mechanisms involved. To investigate the immune response induced in L. vannamei upon exposure to A. pacificum. Healthy shrimp (2.5 ± 0.5 g) were immersed in A. pacificum lysate (1.0 × 104 cells·mL-1) or natural seawater (control). The hepatopancreas was collected for transcriptome sequencing 72 h post-exposure. Transcriptomic analysis identified 264 differentially expressed genes (DEGs) in the exposure group compared to the control, of which 185 were upregulated and 79 were downregulated. DEGs involved in signal transduction, oxidative phosphorylation, protease inhibitors, and ribosomal protein functions were well prominent. GO enrichment analysis showed that immune system processes, lysosomal-mediated cellular processes, and metabolic functions were significantly enriched. KEGG analysis identified enriched pathways including lysosome, C‑type lectin receptor signaling, peroxisome, drug metabolism, and neuroactive ligand‑receptor interactions. This study offers molecular insights into the molecular defense mechanisms of L. vannamei against A. pacificum toxicity.