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

Madhu Sudhan Ravindran (), Martin F. Engelke, Kristen J. Verhey and Billy Tsai ()
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Madhu Sudhan Ravindran: University of Michigan Medical School
Martin F. Engelke: University of Michigan Medical School
Kristen J. Verhey: University of Michigan Medical School
Billy Tsai: University of Michigan Medical School

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract Viruses exploit cellular machineries to penetrate a host membrane and cause infection, a process that remains enigmatic for non-enveloped viruses. Here we probe how the non-enveloped polyomavirus SV40 penetrates the endoplasmic reticulum (ER) membrane to reach the cytosol, a crucial infection step. We find that the microtubule-based motor kinesin-1 is recruited to the ER membrane by binding to the transmembrane J-protein B14. Strikingly, this motor facilitates SV40 ER-to-cytosol transport by constructing a penetration site on the ER membrane called a ‘focus’. Neither kinesin-2, kinesin-3 nor kinesin-5 promotes foci formation or infection. The specific use of kinesin-1 is due to its unique ability to select posttranslationally modified microtubules for cargo transport and thereby spatially restrict focus formation to the perinucleus. These findings support the idea of a ‘tubulin code’ for motor-dependent trafficking and establish a distinct kinesin-1 function in which a motor is exploited to create a viral membrane penetration site.

Date: 2017
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DOI: 10.1038/ncomms15496

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