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Journal of Virology, May 2007, p. 4892-4894, Vol. 81, No. 9
0022-538X/07/$08.00+0     doi:10.1128/JVI.02698-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Role for Actin in the Polarized Release of Rotavirus{triangledown}

Agnès Gardet,1 Michelyne Breton,1 Germain Trugnan,1 and Serge Chwetzoff1,2,3*

UMRS 538, Membrane Traffic and Signalization in Epithelial Cells, CHU Saint Antoine, 27 rue de Chaligny, 75012 Paris, France,1 UPMC, Faculté de Médecine Pierre & Marie Curie, CHU Saint Antoine, 27 rue de Chaligny, 75012 Paris, France,2 INRA, Département de Pathologie Animale, France3

Received 7 December 2006/ Accepted 5 February 2007

Rotaviruses are characterized by polarized release from the apical side of infected enterocytes, and the rotavirus VP4 spike protein specifically binds to the actin network at the apical pole of differentiated enterocytic cells. To determine the functional consequences of this VP4-actin interaction, fluorescence recovery after photobleaching experiments were carried out to measure the diffusional mobility of VP4 associated with the microfilaments. Results show that VP4 binds to barbed ends of microfilaments by using actin treadmilling. Actin treadmilling inhibition results in the loss of rotavirus apical preferential release, suggesting a major role for actin in polarized rotavirus release.

* Corresponding author. Mailing address: UMRS 538, Membrane Traffic and Signalization in Epithelial Cells, CHU Saint Antoine, 27 rue de Chaligny, 75012 Paris, France. Phone: 33140011342. Fax: 33140011390. E-mail: chwetzof{at}ccr.jussieu.fr

{triangledown} Published ahead of print on 14 February 2007.

Journal of Virology, May 2007, p. 4892-4894, Vol. 81, No. 9
0022-538X/07/$08.00+0     doi:10.1128/JVI.02698-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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