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Exploiting the kinesin-1 molecular motor to generate a virus membrane penetration site

Madhu Sudhan Ravindran1, Martin F Engelke1, Kristen J Verhey1

  • 1Department of Cell and Developmental Biology, University of Michigan Medical School, 109 Zina Pitcher Place, 3043 BSRB, Ann Arbor, Michigan 48109, USA.

Nature Communications
|May 25, 2017
PubMed

Insights

The kinesin-1 motor protein helps the simian virus 40 (SV40) enter host cells by creating a specific membrane pore. This discovery reveals a new role for kinesin-1 in viral infection mechanisms.

Area of Science:

  • Cellular biology
  • Virology
  • Molecular motors

Background:

  • Non-enveloped viruses utilize host cell machinery for infection.
  • The mechanism of endoplasmic reticulum (ER) membrane penetration by viruses is poorly understood.

Purpose of the Study:

  • To investigate how the non-enveloped simian virus 40 (SV40) penetrates the ER membrane.
  • To identify the cellular factors involved in SV40 ER-to-cytosol transport.

Main Methods:

  • Co-immunoprecipitation to identify interacting proteins.
  • Live-cell imaging to visualize viral transport and focus formation.
  • Genetic manipulation to assess the role of specific kinesin motors.

Main Results:

  • Kinesin-1 binds to the J-protein B14 on the ER membrane.
  • Kinesin-1 facilitates SV40 entry by forming a membrane penetration site, termed a 'focus'.
  • Only kinesin-1, not other kinesins, supports focus formation and infection, due to its selective interaction with modified microtubules.

Conclusions:

  • Kinesin-1 plays a critical role in SV40 ER membrane penetration, acting as a viral entry facilitator.
  • The findings highlight a novel function for kinesin-1 in creating viral membrane pores.
  • This study supports the 'tubulin code' hypothesis, where specific microtubule modifications dictate motor-dependent trafficking and viral entry points.

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