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The rotavirus enterotoxin (NSP4) promotes re-modeling of the intracellular microtubule network
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Yang, Weiming and McCrae, Malcolm A. (2012) The rotavirus enterotoxin (NSP4) promotes re-modeling of the intracellular microtubule network. Virus Research, Vol.163 (No.1). pp. 269-274. doi:10.1016/j.virusres.2011.10.011 ISSN 0168-1702.
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Official URL: http://dx.doi.org/10.1016/j.virusres.2011.10.011
Abstract
Expression of the rotavirus enterotoxin (NSP4) in transfected monkey kidney cells was found to result in a dramatic re-modeling of the microtubule (MT) network. This important centrosome organized cytoskeletal element was dissolved by expression of NSP4 and re-formed in a ring array at the periphery of the cell, similar to that seen following normal virus infection. Site directed mutagenesis of the N-linked glycosylation sites in NSP4 was employed to show that glycosylation of NSP4 was not required for it to promote changes in the MT network. This result together with experiments using conventional inhibitors indicated that NSP4's ability to cause elevation of intracellular calcium levels was also not necessary to effect the changes in the MT network. Use of the centrosome function inhibitor nocodazole demonstrated that NSP4 based remodeling of the MT network was dominant over the normal organizational role of the centrosome. Finally the remodeling of the MT network was shown not to be linked to cellular apoptosis or necrosis. The potential importance of this newly recognised role for NSP4 in the overall process of intracellular pathogenesis by rotaviruses is discussed.
Item Type: | Journal Article | ||||
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Divisions: | Faculty of Science, Engineering and Medicine > Science > Life Sciences (2010- ) | ||||
Journal or Publication Title: | Virus Research | ||||
Publisher: | Elsevier BV | ||||
ISSN: | 0168-1702 | ||||
Official Date: | January 2012 | ||||
Dates: |
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Volume: | Vol.163 | ||||
Number: | No.1 | ||||
Page Range: | pp. 269-274 | ||||
DOI: | 10.1016/j.virusres.2011.10.011 | ||||
Status: | Peer Reviewed | ||||
Publication Status: | Published | ||||
Access rights to Published version: | Restricted or Subscription Access |
Data sourced from Thomson Reuters' Web of Knowledge
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