• Effects of PmDOME and PmSTAT knockdown on white spot syndrome virus infection in Penaeus monodon

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22/09/2023 by   

Metadata

Document Title

Effects of PmDOME and PmSTAT knockdown on white spot syndrome virus infection in Penaeus monodon

Author

Laohawutthichai P., Jatuyosporn T., Supungul P., Tassanakajon A., Krusong K.

Affiliations

Center of Excellence in Structural and Computational Biology, Department of Biochemistry, Faculty of Science, Chulalongkorn University, Bangkok, 10330, Thailand; Center of Excellence for Molecular Biology and Genomics of Shrimp, Department of Biochemistry, Faculty of Science, Chulalongkorn University, Bangkok, 10330, Thailand; National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency (NSTDA), Pathumthani, 12120, Thailand

Type

Article

Source Title

Scientific Reports

ISSN

20452322

Year

2023

Volume

13

Issue

1

Open Access

All Open Access, Gold, Green

Publisher

Nature Research

DOI

10.1038/s41598-023-37085-1

Format

PDF

Abstract

Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway plays an important role in antiviral immunity. This research reports the full-length DOME receptor gene in Penaeus monodon (PmDOME) and examines the effects of PmDOME and PmSTAT silencing on immune-related gene expressions in shrimp hemocytes during white spot syndrome virus (WSSV) infection. PmDOME and PmSTAT were up-regulated in shrimp hemocytes upon WSSV infection. Suppression of PmDOME and PmSTAT showed significant impacts on the expression levels of ProPO2 (melanization), Vago5 (interferon-like protein) and several antimicrobial peptides, including ALFPm3, Penaeidin3, CrustinPm1 and CrustinPm7. Silencing of PmDOME and PmSTAT reduced WSSV copy numbers and delayed the cumulative mortality caused by WSSV. We postulated that suppression of the JAK/STAT signaling pathway may activate the proPO, IFN-like antiviral cytokine and AMP production, resulting in a delay of WSSV-related mortality. ? 2023, The Author(s).

License

CC BY

Rights

Authors

Publication Source

WOS

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