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Quantitative Immunofluorescence Assay to Measure the Variation in Protein Levels at Centrosomes
Published on: December 20, 2014
African swine fever virus infection disrupts centrosome assembly and function
Nolwenn Jouvenet1, Thomas Wileman1
1Department of Immunology and Pathology, Pirbright Laboratories, Institute for Animal Health, Ash Road, Woking, Surrey GU24 0NF, UK.
Abstract:
African swine fever virus (ASFV) is a large, enveloped DNA virus that assembles in perinuclear sites located close to the centrosome. It is reported here that the microtubule network becomes disorganized soon after the onset of viral DNA replication and formation of assembly sites. ASFV infection resulted in loss of gamma-tubulin and pericentrin at the centrosome; this was due to protein relocalization, but not degradation. ASFV infection also inhibited the ability of the centrosome to nucleate microtubules. The reorganization of microtubules seen in ASFV-infected cells may therefore be mediated by gamma-tubulin and pericentrin redistribution, and consequent disruption of centrosome assembly and function.
Insights
African swine fever virus disrupts the cell's microtubule network by affecting the centrosome. This viral interference impairs microtubule organization and cell structure.
Area of Science:
- Virology
- Cell Biology
Background:
- African swine fever virus (ASFV) is a large DNA virus known to assemble near the cell's centrosome.
- Cellular infrastructure, including the microtubule network and centrosome, is crucial for viral replication and cell function.
Purpose of the Study:
- To investigate the impact of ASFV infection on the cellular microtubule network and centrosome.
- To elucidate the mechanisms by which ASFV affects microtubule organization and centrosome function.
Main Methods:
- Observation of microtubule network disorganization post-ASFV infection.
- Analysis of gamma-tubulin and pericentrin localization at the centrosome.
- Assessment of centrosome-mediated microtubule nucleation capacity.
Main Results:
- ASFV infection led to microtubule network disorganization shortly after viral DNA replication.
- Key centrosome proteins, gamma-tubulin and pericentrin, were relocalized, not degraded.
- The centrosome's ability to nucleate microtubules was significantly inhibited.
Conclusions:
- ASFV infection disrupts the microtubule network through the redistribution of gamma-tubulin and pericentrin.
- Viral interference with centrosome assembly and function is a key aspect of ASFV pathogenesis.
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