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.

Genes
|May 27, 2023
PubMed

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.