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Human papillomavirus type 16 infection activates the host serine arginine protein kinase 1 (SRPK1) - splicing factor axis.
- Source :
-
The Journal of general virology [J Gen Virol] 2020 May; Vol. 101 (5), pp. 523-532. Date of Electronic Publication: 2020 Mar 13. - Publication Year :
- 2020
-
Abstract
- The infectious life cycle of human papillomaviruses (HPVs) is tightly linked to keratinocyte differentiation. Evidence suggests a sophisticated interplay between host gene regulation and virus replication. Alternative splicing is an essential process for host and viral gene expression, and is generally upregulated by serine arginine-rich splicing factors (SRSFs). SRSF activity can be positively or negatively controlled by cycles of phosphorylation/dephosphorylation. Here we show that HPV16 infection leads to accumulation of the paradigm SRSF protein, SRSF1, in the cytoplasm in a keratinocyte differentiation-specific manner. Moreover, HPV16 infection leads to increased levels of cytoplasmic and nuclear phosphorylated SRSF1. SR protein kinase 1 (SRPK1) phosphorylates SRSF1. Similar to HPV upregulation of SRSF1, we demonstrate HPV upregulation of SRPK1 via the viral E2 protein. SRPK1 depletion or drug inhibition of SRPK1 kinase activity resulted in reduced levels of SRSF1, suggesting that phosphorylation stabilizes the protein in differentiated HPV-infected keratinocytes. Together, these data indicate HPV infection stimulates the SRPK1-SRSF axis in keratinocytes.
- Subjects :
- 3T3 Cells
Animals
HeLa Cells
Humans
Keratinocytes physiology
Mice
Phosphorylation genetics
Serine-Arginine Splicing Factors genetics
Up-Regulation genetics
Viral Proteins genetics
Virus Replication genetics
Alternative Splicing genetics
Human papillomavirus 16 pathogenicity
Papillomavirus Infections genetics
Protein Serine-Threonine Kinases genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1465-2099
- Volume :
- 101
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- The Journal of general virology
- Publication Type :
- Academic Journal
- Accession number :
- 32182205
- Full Text :
- https://doi.org/10.1099/jgv.0.001402