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Beclin-1 is a crucial autophagy regulator that also affects innate immunity, including apoptosis. At the present day, nothing is known about Beclin-1 in crustaceans, especially Penaeid shrimp. This work examined the function of Beclin-1 from the Pacific white shrimp, Penaeus vannamei (PvBECN1), under both normal and white spot syndrome virus (WSSV) challenge circumstances. The phylogenetic tree analysis placed PvBECN1 in the same group as other Beclin-1 from penaeid shrimp. PvBECN1 was composed of BH3 domain, coiled-coil domain, and autophagy-specific (BARA) domain. PvBECN1 transcription was highest in the intestine and gill. Following WSSV infection, PvBECN1 expression increased in gills and hemocytes, though further investigation specifically focused on the hemocytes as a key immunological tissue. PvBECN1 silencing was conducted to obtain insight into the function of PvBECN1 during the virus infection. We discovered that suppressing PvBECN1 increaesd the survival rate of WSSV-infected shrimp by reducing the viral load. In term of immunity, PvBECN1 silencing, in both normal and WSSV infected conditions, led to a decrease in the percentage of autophagic activity. Concurrently, there was a significant increase in late apoptotic hemocyte cells and caspase 3/7 activity, demonstrating the involvement of PvBECN1 in innate immunity. Furthermore, following PvBECN1 knockdown, there was an altered expression of immune-related genes, including antimicrobial peptides and interferon-like genes. Interestingly, during WSSV infection, PvBECN1-silenced shrimp only exhibit overexpression of crustin and vago5. Ultimately, the virus enhances its replication and evades antiviral defense via triggering the PvBECN1 transcript.
Jaree et al. (Wed,) studied this question.