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Updated: Jun 1, 2026

Methodology for the Efficient Generation of Fluorescently Tagged Vaccinia Virus Proteins
Published on: January 17, 2014
Vaccinia virus lacking A17 induces complex membrane structures composed of open membrane sheets
Petr Chlanda1, Maria Alejandra Carbajal, Androniki Kolovou
1European Molecular Biology Laboratory, Heidelberg, Meyerhofstraße 1, 69117 Heidelberg, Germany. chlanda@embl.de
Vaccinia virus (VACV) membrane rupture forming crescents occurs independently of the A17 protein. Instead, tubular and vesicular membranes accumulate when A17 is absent, indicating A17 is not essential for initial membrane rupture.
Area of Science:
- Virology
- Cell Biology
- Membrane Biology
Background:
- The vaccinia virus (VACV) crescent is a precursor membrane formed by cellular compartment rupture.
- The viral membrane protein A17 is hypothesized to play a role in this membrane rupture process.
Purpose of the Study:
- To investigate the role of the viral membrane protein A17 in vaccinia virus crescent formation and membrane rupture.
- To determine if A17 is essential for the formation of open membrane sheets during VACV precursor membrane assembly.
Main Methods:
- Utilized electron tomography (ET) to analyze the ultrastructure of viral membranes.
- Examined VACV membranes formed in the absence of A17 protein synthesis.
Main Results:
- Absence of A17 synthesis prevented crescent formation.
- Accumulation of tubular, vesicular, and novel onion-shaped membranes was observed in the absence of A17.
- These aberrant membrane structures, like crescents, consisted of open membrane sheets.
Conclusions:
- Membrane rupture, a key step in VACV precursor membrane formation, occurs independently of the A17 protein.
- A17 protein is not required for the formation of open membrane sheets, suggesting its role is downstream of or separate from the initial rupture event.
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