Involvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.

Infection of non-enveloped polyomaviruses depends on an intact microtubular network. Here we focus on mouse polyomavirus (MPyV). We show that the dynamics of MPyV cytoplasmic transport reflects the characteristics of microtubular motor-driven transport with bi-directional saltatory movements. In cel...

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Autores principales: Vojtech Zila, Francesco Difato, Lucie Klimova, Sandra Huerfano, Jitka Forstova
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Publicado: Public Library of Science (PLoS) 2014
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spelling oai:doaj.org-article:bcbbd0c8638a469b840181288c86c9e32021-11-18T08:20:08ZInvolvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.1932-620310.1371/journal.pone.0096922https://doaj.org/article/bcbbd0c8638a469b840181288c86c9e32014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24810588/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Infection of non-enveloped polyomaviruses depends on an intact microtubular network. Here we focus on mouse polyomavirus (MPyV). We show that the dynamics of MPyV cytoplasmic transport reflects the characteristics of microtubular motor-driven transport with bi-directional saltatory movements. In cells treated with microtubule-disrupting agents, localization of MPyV was significantly perturbed, the virus was retained at the cell periphery, mostly within membrane structures resembling multicaveolar complexes, and at later times post-infection, only a fraction of the virus was found in Rab7-positive endosomes and multivesicular bodies. Inhibition of cytoplasmic dynein-based motility by overexpression of dynamitin affected perinuclear translocation of the virus, delivery of virions to the ER and substantially reduced the numbers of infected cells, while overexpression of dominant-negative form of kinesin-1 or kinesin-2 had no significant impact on virus localization and infectivity. We also found that transport along microtubules was important for MPyV-containing endosome sequential acquisition of Rab5, Rab7 and Rab11 GTPases. However, in contrast to dominant-negative mutant of Rab7 (T22N), overexpression of dominant-negative mutant Rab11 (S25N) did not affect the virus infectivity. Altogether, our study revealed that MPyV cytoplasmic trafficking leading to productive infection bypasses recycling endosomes, does not require the function of kinesin-1 and kinesin-2, but depends on functional dynein-mediated transport along microtubules for translocation of the virions from peripheral, often caveolin-positive compartments to late endosomes and ER - a prerequisite for efficient delivery of the viral genome to the nucleus.Vojtech ZilaFrancesco DifatoLucie KlimovaSandra HuerfanoJitka ForstovaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 5, p e96922 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Vojtech Zila
Francesco Difato
Lucie Klimova
Sandra Huerfano
Jitka Forstova
Involvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.
description Infection of non-enveloped polyomaviruses depends on an intact microtubular network. Here we focus on mouse polyomavirus (MPyV). We show that the dynamics of MPyV cytoplasmic transport reflects the characteristics of microtubular motor-driven transport with bi-directional saltatory movements. In cells treated with microtubule-disrupting agents, localization of MPyV was significantly perturbed, the virus was retained at the cell periphery, mostly within membrane structures resembling multicaveolar complexes, and at later times post-infection, only a fraction of the virus was found in Rab7-positive endosomes and multivesicular bodies. Inhibition of cytoplasmic dynein-based motility by overexpression of dynamitin affected perinuclear translocation of the virus, delivery of virions to the ER and substantially reduced the numbers of infected cells, while overexpression of dominant-negative form of kinesin-1 or kinesin-2 had no significant impact on virus localization and infectivity. We also found that transport along microtubules was important for MPyV-containing endosome sequential acquisition of Rab5, Rab7 and Rab11 GTPases. However, in contrast to dominant-negative mutant of Rab7 (T22N), overexpression of dominant-negative mutant Rab11 (S25N) did not affect the virus infectivity. Altogether, our study revealed that MPyV cytoplasmic trafficking leading to productive infection bypasses recycling endosomes, does not require the function of kinesin-1 and kinesin-2, but depends on functional dynein-mediated transport along microtubules for translocation of the virions from peripheral, often caveolin-positive compartments to late endosomes and ER - a prerequisite for efficient delivery of the viral genome to the nucleus.
format article
author Vojtech Zila
Francesco Difato
Lucie Klimova
Sandra Huerfano
Jitka Forstova
author_facet Vojtech Zila
Francesco Difato
Lucie Klimova
Sandra Huerfano
Jitka Forstova
author_sort Vojtech Zila
title Involvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.
title_short Involvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.
title_full Involvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.
title_fullStr Involvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.
title_full_unstemmed Involvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.
title_sort involvement of microtubular network and its motors in productive endocytic trafficking of mouse polyomavirus.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/bcbbd0c8638a469b840181288c86c9e3
work_keys_str_mv AT vojtechzila involvementofmicrotubularnetworkanditsmotorsinproductiveendocytictraffickingofmousepolyomavirus
AT francescodifato involvementofmicrotubularnetworkanditsmotorsinproductiveendocytictraffickingofmousepolyomavirus
AT lucieklimova involvementofmicrotubularnetworkanditsmotorsinproductiveendocytictraffickingofmousepolyomavirus
AT sandrahuerfano involvementofmicrotubularnetworkanditsmotorsinproductiveendocytictraffickingofmousepolyomavirus
AT jitkaforstova involvementofmicrotubularnetworkanditsmotorsinproductiveendocytictraffickingofmousepolyomavirus
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