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Japanese Flounder pol-miR-155 Is Involved in Edwardsiella tarda Infection via ATG3
Zhanwei Zhang1,2, Xiaolu Guan1
1CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao 266071, China.
Abstract:
MicroRNAs (miRNAs) are small RNA molecules that function in the post-transcriptionally regulation of the expression of diverse genes, including those involved in immune defense. Edwardsiella tarda can infect a broad range of hosts and cause severe disease in aquatic species, including Japanese flounder (Paralichthys olivaceus). In this study, we examined the regulation mechanism of a flounder miRNA, pol-miR-155, during the infection of E. tarda. Pol-miR-155 was identified to target flounder ATG3. Overexpression of pol-miR-155 or knockdown of ATG3 expression suppressed autophagy and promoted the intracellular replication of E. tarda in flounder cells. Overexpression of pol-miR-155 activated the NF-κB signaling pathway and further promoted the expression of downstream immune related genes of interleukin (IL)-6 and IL-8. These results unraveled the regulatory effect of pol-miR-155 in autophagy and in E. tarda infection.
Insights
Flounder microRNA (miRNA) pol-miR-155 targets ATG3, suppressing autophagy and promoting Edwardsiella tarda infection. This miRNA also activates immune pathways, highlighting its role in fish immunity.
Area of Science:
- Molecular Biology
- Immunology
- Aquatic Animal Health
Background:
- MicroRNAs (miRNAs) regulate gene expression post-transcriptionally, impacting immune responses.
- Edwardsiella tarda causes significant disease in aquatic species like Japanese flounder (Paralichthys olivaceus).
Purpose of the Study:
- To investigate the regulatory role of flounder microRNA pol-miR-155 during Edwardsiella tarda infection.
- To elucidate the molecular mechanisms underlying pol-miR-155's function in host-pathogen interactions.
Main Methods:
- Identification of target genes for pol-miR-155 in Japanese flounder.
- Experimental manipulation of pol-miR-155 and ATG3 expression in flounder cells.
- Analysis of autophagy levels and E. tarda replication.
- Assessment of NF-κB signaling pathway activation and immune gene expression.
Main Results:
- Pol-miR-155 was identified as a direct target of flounder ATG3.
- Overexpression of pol-miR-155 or ATG3 knockdown inhibited autophagy and enhanced intracellular E. tarda replication.
- Pol-miR-155 activated the NF-κB signaling pathway, upregulating IL-6 and IL-8 expression.
Conclusions:
- Pol-miR-155 plays a crucial role in regulating autophagy during E. tarda infection in Japanese flounder.
- This miRNA influences host immune responses by modulating the NF-κB pathway and promoting bacterial replication.
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