Location: Aquatic Animal Health ResearchTitle: Pacific white shrimp (Liptopenaeus vannamei) transcriptome analysis after exposure to recombinant Vibrio parahaemolyticus PirA and PirB proteins
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 6/19/2023
Publication Date: 9/11/2023
Citation: Lange, M.D., Abernathy, J.W., Zhang, D., Shoemaker, C.A., Bader, T.J., Beck, B.H. 2023. Pacific white shrimp (Liptopenaeus vannamei) transcriptome analysis after exposure to recombinant Vibrio parahaemolyticus PirA and PirB proteins [abstract]. 21ST International Conference on Diseases of Fish and Shellfish, September 11-14, 2023. Aberdeen, UK.
Technical Abstract: Introduction: Vibrio parahaemolyticus, a Gram-negative bacterium often present in marine and estuarine environments, is endemic among the global shrimp farming industry. V. parahaemolyticus proteins PirA and PirB are known virulence factors that contribute significantly to the development of acute hepatopancreatic necrosis disease. Previous work from our lab has demonstrated the lethality of recombinant PirA and PirB proteins to Pacific white shrimp (Liptopenaeus vannamei). Methodology: To understand the host response to these proteins, recombinant PirA and PirB proteins were administered using a reverse gavage method and individual shrimp (n=5) were then sampled at 30 minutes, 1-, 2-, 4- and 6-hour post exposure. Shrimp hepatopancreas libraries were generated and RNA sequencing was performed on the control and recombinant PirA/B-treated samples. Differentially expressed genes from each pairwise comparison were subjected to enrichment analyses using both Fisher’s Exact Test and Gene Set Enrichment Analyses in OmicsBox. Results: Following the processing of the raw RNA sequencing data and alignment with the L. vannamei genome, we conducted comparisons between the control and the recombinant PirA/B treatment groups to establish gene expression profiles, which included the sequence libraries from the 30 minutes, 1-, 2-, 4- and 6-hour time points. For each of the different time points, differentially expressed genes were identified among the assayed time points according to the following cutoff criteria (FDR <0.05, fold change >2). Differentially expressed genes that were co-expressed at the later time points (2-, 4- and 6-h) were also identified and gene associations were established to predict functional physiological networks. Conclusion: Our analysis reveals that the recombinant PirA and PirB proteins have likely initiated an early host response involving several cell survival signaling and innate immune processes that will be discussed. As these Pir A/B protein products harbored in V. parahaemolyticus plasmids have been identified as the causative agent in acute hepatopancreatic necrosis disease, information contained within will provide insight into specific host-toxin interactions after exposure.