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Statements

Subject Item
n2:RIV%2F00216208%3A11310%2F14%3A10287933%21RIV15-MSM-11310___
rdf:type
n5:Vysledek skos:Concept
rdfs:seeAlso
http://dx.doi.org/10.1371/journal.pone.0096922
dcterms: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. 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.
dcterms:title
Involvement of Microtubular Network and Its Motors in Productive Endocytic Trafficking of Mouse Polyomavirus Involvement of Microtubular Network and Its Motors in Productive Endocytic Trafficking of Mouse Polyomavirus
skos:prefLabel
Involvement of Microtubular Network and Its Motors in Productive Endocytic Trafficking of Mouse Polyomavirus Involvement of Microtubular Network and Its Motors in Productive Endocytic Trafficking of Mouse Polyomavirus
skos:notation
RIV/00216208:11310/14:10287933!RIV15-MSM-11310___
n3:aktivita
n20:S n20:P n20:I
n3:aktivity
I, P(ED1.1.00/02.0109), P(GA13-26115S), S
n3:cisloPeriodika
5
n3:dodaniDat
n10:2015
n3:domaciTvurceVysledku
n11:2474174 n11:3219488 n11:9232907
n3:druhVysledku
n17:J
n3:duvernostUdaju
n8:S
n3:entitaPredkladatele
n9:predkladatel
n3:idSjednocenehoVysledku
22811
n3:idVysledku
RIV/00216208:11310/14:10287933
n3:jazykVysledku
n13:eng
n3:klicovaSlova
movement; pathway; caveolae; infection; bk-virus; living cells; early endosomes; membrane domains; cytoplasmic dynein; vesicular-transport
n3:klicoveSlovo
n4:cytoplasmic%20dynein n4:bk-virus n4:membrane%20domains n4:vesicular-transport n4:pathway n4:living%20cells n4:movement n4:caveolae n4:early%20endosomes n4:infection
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[78CB772D1090]
n3:nazevZdroje
PLoS ONE
n3:obor
n19:EE
n3:pocetDomacichTvurcuVysledku
3
n3:pocetTvurcuVysledku
5
n3:projekt
n15:GA13-26115S n15:ED1.1.00%2F02.0109
n3:rokUplatneniVysledku
n10:2014
n3:svazekPeriodika
9
n3:tvurceVysledku
Žíla, Vojtěch Klimova, Lucie Huerfano- Meneses, Sandra Difato, Francesco Forstová, Jitka
n3:wos
000338213300092
s:issn
1932-6203
s:numberOfPages
15
n16:doi
10.1371/journal.pone.0096922
n14:organizacniJednotka
11310