Characterization of a nucleus located mollusc mitoferrin and its response to OsHV-1 infection

Lusheng Xin1, Bowen Huang2, Chen Li1

  • 1Qingdao Key Laboratory of Mariculture Epidemiology and Biosecurity, Key Laboratory of Maricultural Organism Disease Control, Ministry of Agriculture, Yellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Qingdao 266071, China; Function Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266071, China.

Insights

Ark clams possess a mitoferrin gene, SbmiFn, crucial for iron metabolism. This gene

Area of Science:

  • Molecular Biology
  • Biochemistry
  • Immunology

Background:

  • Mitoferrins, members of the SLC25 family, regulate cellular iron metabolism.
  • The role of mitoferrin in host defense against pathogens is largely unknown.
  • Iron withholding is a key host defense strategy.

Purpose of the Study:

  • To identify and characterize a novel mollusc mitoferrin gene (SbmiFn) in ark clams.
  • To investigate the function and localization of SbmiFn, particularly its response to viral infection.
  • To explore the role of SbmiFn in the host-pathogen interaction with OsHV-1.

Main Methods:

  • Gene identification and sequence analysis.
  • Iron chelating assay to verify iron binding activity.
  • Immunohistochemistry to determine SbmiFn localization.
  • Analysis of SbmiFn and ferritin expression during OsHV-1 infection.

Main Results:

  • A unique mollusc mitoferrin gene, SbmiFn, was identified with conserved structure and iron binding activity.
  • SbmiFn exhibited both cytoplasmic and nuclear localization, with enhanced nuclear signals upon viral challenge.
  • SbmiFn and ferritin expression decreased coordinately during OsHV-1 infection, correlating with limited viral replication.

Conclusions:

  • SbmiFn plays a role in cellular iron metabolism and host defense in ark clams.
  • Nuclear localization of SbmiFn may be involved in the host's antiviral response.
  • Coordinated regulation of SbmiFn and ferritin suggests a mechanism to manage iron during viral infections, potentially limiting pathogen proliferation.

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