Merkel Cell Polyomavirus DNA Replication Induces Senescence in Human Dermal Fibroblasts in a Kap1/Trim28-Dependent Manner
Identifieur interne : 000113 ( Main/Exploration ); précédent : 000112; suivant : 000114Merkel Cell Polyomavirus DNA Replication Induces Senescence in Human Dermal Fibroblasts in a Kap1/Trim28-Dependent Manner
Auteurs : Svenja Siebels [Allemagne] ; Manja Czech-Sioli [Allemagne] ; Michael Spohn [Allemagne] ; Claudia Schmidt [Allemagne] ; Juliane Theiss [Allemagne] ; Daniela Indenbirken [Allemagne] ; Thomas Günther [Allemagne] ; Adam Grundhoff [Allemagne] ; Nicole Fischer [Allemagne]Source :
- mBio [ 2150-7511 ] ; 2020.
Abstract
We here describe Kap1 as a restriction factor in MCPyV infection. We report a novel, indirect mechanism by which Kap1 affects MCPyV replication. In contrast with from other DNA viruses, Kap1 does not associate with the viral genome in MCPyV infection and has no impact on viral gene expression. In MCPyV-infected nHDF cells, Kap1 phosphorylation (pKap1 S824) accumulates because of genomic stress mainly induced by viral DNA replication. In contrast, ectopic expression of LT or LT MCPyV mutants, previously shown to be important for induction of genotoxic stress, does not result in a similar extent of pKap1 accumulation. We show that cells actively replicating MCPyV accumulate pKap1 (in a manner dependent on the presence of ATM) and display a senescence phenotype reflected by G2 arrest. These results are supported by transcriptome analyses showing that LT antigen, in a manner dependent on the presence of Kap1, induces expression of secreted factors, which is known as the senescence-associated secretory phenotype (SASP).
Url:
DOI: 10.1128/mBio.00142-20
PubMed: 32156811
PubMed Central: 7064754
Affiliations:
Links toward previous steps (curation, corpus...)
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>We here describe Kap1 as a restriction factor in MCPyV infection. We report a novel, indirect mechanism by which Kap1 affects MCPyV replication. In contrast with from other DNA viruses, Kap1 does not associate with the viral genome in MCPyV infection and has no impact on viral gene expression. In MCPyV-infected nHDF cells, Kap1 phosphorylation (pKap1 S824) accumulates because of genomic stress mainly induced by viral DNA replication. In contrast, ectopic expression of LT or LT MCPyV mutants, previously shown to be important for induction of genotoxic stress, does not result in a similar extent of pKap1 accumulation. We show that cells actively replicating MCPyV accumulate pKap1 (in a manner dependent on the presence of ATM) and display a senescence phenotype reflected by G<sub>2</sub>
arrest. These results are supported by transcriptome analyses showing that LT antigen, in a manner dependent on the presence of Kap1, induces expression of secreted factors, which is known as the senescence-associated secretory phenotype (SASP).</p>
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</TEI>
<affiliations><list><country><li>Allemagne</li>
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<region><li>Hambourg</li>
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<settlement><li>Hambourg</li>
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