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Moesin is not a receptor for measles virus entry into mouse embryonic stem cells
1Department of Cell Biology, Faculty of Medicine, Kyoto University, Yoshida-Konoe, Japan.
Abstract:
The involvement of moesin in measles virus (MV) entry was investigated with moesin-positive and -negative mouse embryonic stem (ES) cells. MV infection of these cells was very ineffective and was independent of moesin expression. Furthermore, when these cells were transfected to express human CD46, a 100-fold increase in syncytium formation was observed with these cells and was independent of the expression of moesin. The only obvious difference between moesin-positive and -negative ES cells was the shape of the syncytia formed. Moesin-negative ES cells expressing or not expressing human CD46 formed separate pieces of fragmented syncytia which were torn apart during spreading, whereas ES cells expressing moesin exhibited typical syncytia. In addition, moesin was not detected on the surface of any murine cells or cell lines that we have tested by a flow cytometric assay with moesin-specific antibodies. These findings indicate that murine moesin is neither a receptor nor a CD46 coreceptor for MV entry into mouse ES cells. Moesin is involved in actin filament-plasma membrane interactions as a cross-linker, and it affects only the spreading and shape of MV-mediated syncytia.
Insights
Moesin does not play a role in measles virus (MV) entry into mouse cells. However, moesin influences the shape and spreading of MV-induced syncytia, impacting cell-cell fusion dynamics.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Measles virus (MV) entry into host cells is a critical step in infection.
- Moesin is a protein involved in actin-cytoskeleton dynamics and cell membrane interactions.
- The role of moesin in MV entry and cell fusion remains unclear.
Purpose of the Study:
- To investigate the involvement of moesin in measles virus entry into mouse embryonic stem (ES) cells.
- To determine if moesin acts as a receptor or co-receptor for MV entry, potentially in conjunction with CD46.
- To elucidate moesin's function in MV-mediated syncytia formation.
Main Methods:
- Comparison of MV infection and syncytium formation in moesin-positive and moesin-negative mouse ES cells.
- Transfection of ES cells with human CD46 to assess its interaction with moesin during MV infection.
- Flow cytometry analysis using moesin-specific antibodies to detect moesin expression on the cell surface.
Main Results:
- MV infection and syncytium formation were ineffective and independent of moesin expression in mouse ES cells.
- Transfection with human CD46 significantly increased syncytium formation, but this was also independent of moesin.
- Moesin expression affected the morphology of syncytia, with moesin-positive cells forming typical syncytia and moesin-negative cells forming fragmented syncytia.
- Moesin was not detected on the surface of tested murine cells.
Conclusions:
- Murine moesin is not a receptor or co-receptor for measles virus entry into mouse ES cells.
- Moesin's function is not essential for MV entry or CD46-mediated cell fusion.
- Moesin influences the spreading and shape of MV-induced syncytia by affecting actin-plasma membrane interactions.