Microtubules in Polyomavirus Infection
Microtubules, part of the cytoskeleton, are indispensable for intracellular movement, cell division, and maintaining cell shape and polarity. In addition, microtubules play an important role in viral infection. In this review, we summarize the role of the microtubules’ network during polyo...
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2020-01-01
|
| Series: | Viruses |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1999-4915/12/1/121 |
| _version_ | 1818033210296107008 |
|---|---|
| author | Lenka Horníková Kateřina Bruštíková Jitka Forstová |
| author_facet | Lenka Horníková Kateřina Bruštíková Jitka Forstová |
| author_sort | Lenka Horníková |
| collection | DOAJ |
| description | Microtubules, part of the cytoskeleton, are indispensable for intracellular movement, cell division, and maintaining cell shape and polarity. In addition, microtubules play an important role in viral infection. In this review, we summarize the role of the microtubules’ network during polyomavirus infection. Polyomaviruses usurp microtubules and their motors to travel via early and late acidic endosomes to the endoplasmic reticulum. As shown for SV40, kinesin-1 and microtubules are engaged in the release of partially disassembled virus from the endoplasmic reticulum to the cytosol, and dynein apparently assists in the further disassembly of virions prior to their translocation to the cell nucleus—the place of their replication. Polyomavirus gene products affect the regulation of microtubule dynamics. Early T antigens destabilize microtubules and cause aberrant mitosis. The role of these activities in tumorigenesis has been documented. However, its importance for productive infection remains elusive. On the other hand, in the late phase of infection, the major capsid protein, VP1, of the mouse polyomavirus, counteracts T-antigen-induced destabilization. It physically binds microtubules and stabilizes them. The interaction results in the G2/M block of the cell cycle and prolonged S phase, which is apparently required for successful completion of the viral replication cycle. |
| first_indexed | 2024-12-10T06:19:39Z |
| format | Article |
| id | doaj.art-75b715aec9ee434695fe907aec48f80e |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-12-10T06:19:39Z |
| publishDate | 2020-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-75b715aec9ee434695fe907aec48f80e2022-12-22T01:59:22ZengMDPI AGViruses1999-49152020-01-0112112110.3390/v12010121v12010121Microtubules in Polyomavirus InfectionLenka Horníková0Kateřina Bruštíková1Jitka Forstová2Department of Genetics and Microbiology, Faculty of Science, Charles University, BIOCEV, 25250 Vestec, Czech RepublicDepartment of Genetics and Microbiology, Faculty of Science, Charles University, BIOCEV, 25250 Vestec, Czech RepublicDepartment of Genetics and Microbiology, Faculty of Science, Charles University, BIOCEV, 25250 Vestec, Czech RepublicMicrotubules, part of the cytoskeleton, are indispensable for intracellular movement, cell division, and maintaining cell shape and polarity. In addition, microtubules play an important role in viral infection. In this review, we summarize the role of the microtubules’ network during polyomavirus infection. Polyomaviruses usurp microtubules and their motors to travel via early and late acidic endosomes to the endoplasmic reticulum. As shown for SV40, kinesin-1 and microtubules are engaged in the release of partially disassembled virus from the endoplasmic reticulum to the cytosol, and dynein apparently assists in the further disassembly of virions prior to their translocation to the cell nucleus—the place of their replication. Polyomavirus gene products affect the regulation of microtubule dynamics. Early T antigens destabilize microtubules and cause aberrant mitosis. The role of these activities in tumorigenesis has been documented. However, its importance for productive infection remains elusive. On the other hand, in the late phase of infection, the major capsid protein, VP1, of the mouse polyomavirus, counteracts T-antigen-induced destabilization. It physically binds microtubules and stabilizes them. The interaction results in the G2/M block of the cell cycle and prolonged S phase, which is apparently required for successful completion of the viral replication cycle.https://www.mdpi.com/1999-4915/12/1/121virusmicrotubulespolyomavirust antigensvp1 capsid proteinmolecular motorsdyneinkinesinvirus traffickingcell cycle block |
| spellingShingle | Lenka Horníková Kateřina Bruštíková Jitka Forstová Microtubules in Polyomavirus Infection Viruses virus microtubules polyomavirus t antigens vp1 capsid protein molecular motors dynein kinesin virus trafficking cell cycle block |
| title | Microtubules in Polyomavirus Infection |
| title_full | Microtubules in Polyomavirus Infection |
| title_fullStr | Microtubules in Polyomavirus Infection |
| title_full_unstemmed | Microtubules in Polyomavirus Infection |
| title_short | Microtubules in Polyomavirus Infection |
| title_sort | microtubules in polyomavirus infection |
| topic | virus microtubules polyomavirus t antigens vp1 capsid protein molecular motors dynein kinesin virus trafficking cell cycle block |
| url | https://www.mdpi.com/1999-4915/12/1/121 |
| work_keys_str_mv | AT lenkahornikova microtubulesinpolyomavirusinfection AT katerinabrustikova microtubulesinpolyomavirusinfection AT jitkaforstova microtubulesinpolyomavirusinfection |