Bmced6 enhances BmNPV infection in BmN cells by modulating autophagy and mitochondrial homeostasis

Yuanyuan Xu1, Jing Zhang1, Yan Huang1

  • 1Jiangsu Key Laboratory of Sericultural Biology and Biotechnology, School of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, China; Key Laboratory of Silkworm and Mulberry Genetic Improvement, Ministry of Agriculture and Rural Affairs, Sericultural Scientific Research Center, Chinese Academy of Agricultural Sciences, Zhenjiang 212100, China.

PubMed

Insights

The protein Bmced6 aids silkworm viruses like BmNPV to replicate by boosting autophagy and disrupting mitochondria. Inhibiting Bmced6 reduces viral infection and spread, revealing its role in host-pathogen interactions.

Area of Science:

  • Cellular Biology
  • Virology
  • Insect Pathology

Background:

  • Autophagy is a cellular process involved in both host defense and viral replication.
  • Understanding host-pathogen interactions is crucial for controlling viral diseases in agriculture.

Purpose of the Study:

  • To investigate the role and mechanism of Bmced6 in Bombyx mori during BmNPV infection.
  • To elucidate how Bmced6 influences viral proliferation and host cellular processes.

Main Methods:

  • Immunofluorescence microscopy to determine Bmced6 localization.
  • Overexpression and siRNA-mediated knockdown to assess Bmced6 function.
  • Analysis of viral protein expression (VP39) and viral load (BmNPV-GFP).
  • Assessment of autophagy markers (ATG8 lipidation, autophagosome formation) and autophagy-related gene expression.
  • Evaluation of mitochondrial homeostasis, including mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) production.

Main Results:

  • Bmced6 is primarily localized in the cytoplasm.
  • Overexpression of Bmced6 enhances BmNPV proliferation, while its knockdown inhibits viral infection.
  • Bmced6 facilitates viral infection by promoting virus-induced autophagy and up-regulating autophagy-related genes.
  • Aberrant Bmced6 expression disrupts mitochondrial homeostasis, causing damage, reduced MMP, and altered ROS levels.

Conclusions:

  • Bmced6 acts as a facilitator of BmNPV infection in silkworms.
  • The mechanism involves the interplay between autophagy activation and mitochondrial dysfunction.
  • This study provides novel insights into the molecular mechanisms of insect viral infections.

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