This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kelkar, S.
Right arrow Articles by Leopold, P. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kelkar, S.
Right arrow Articles by Leopold, P. L.

 Previous Article  |  Next Article 

Journal of Virology, August 2006, p. 7781-7785, Vol. 80, No. 15
0022-538X/06/$08.00+0     doi:10.1128/JVI.00481-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

A Common Mechanism for Cytoplasmic Dynein-Dependent Microtubule Binding Shared among Adeno-Associated Virus and Adenovirus Serotypes

Samir Kelkar,1,2 Bishnu P. De,1 Guangping Gao,3 James M. Wilson,3 Ronald G. Crystal,1 and Philip L. Leopold1*

Department of Genetic Medicine, Weill Medical College of Cornell University, New York, New York,1 Graduate Program in Physiology and Biophysics and Systems Biology, Weill Medical College of Cornell University, New York, New York,2 Division of Medical Genetics, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania3

Received 7 March 2006/ Accepted 15 April 2006

During infection, adenovirus-associated virus (AAV) undergoes microtubule-dependent retrograde transport as part of a program of vectorial transport of viral genome to the nucleus. A microtubule binding assay was used to evaluate the hypothesis that cytoplasmic dynein mediates AAV interaction with microtubules. Binding of AAV serotype 2 (AAV2) was enhanced in a nucleotide-dependent manner by the presence of total cellular microtubule-associated proteins (MAPs) but not cytoplasmic dynein-depleted MAPs. Excess AAV2 capsid protein prevented microtubule binding by AAV serotypes 2, 5, and rh.10, as well as adenovirus serotype 5, indicating that similar binding sites are used by these viruses.


* Corresponding author. Mailing address: Weill Medical College of Cornell University, Department of Genetic Medicine, 515 E. 71st Street, S-1000, New York, NY 10021. Phone: (212) 746-2258. Fax: (212) 746-8383. E-mail: geneticmedicine{at}med.cornell.edu.


Journal of Virology, August 2006, p. 7781-7785, Vol. 80, No. 15
0022-538X/06/$08.00+0     doi:10.1128/JVI.00481-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Li, X., Dong, C., Shi, S., Wang, G., Li, Y., Wang, X., Shi, Q., Tian, C., Zhou, R., Gao, C., Dong, X. (2009). The octarepeat region of hamster PrP (PrP51-91) enhances the formation of microtubule and antagonize Cu2+-induced microtubule-disrupting activity. Acta Biochim Biophys Sin 41: 929-937 [Abstract] [Full Text]  
  • Cearley, C. N., Wolfe, J. H. (2007). A Single Injection of an Adeno-Associated Virus Vector into Nuclei with Divergent Connections Results in Widespread Vector Distribution in the Brain and Global Correction of a Neurogenetic Disease. J. Neurosci. 27: 9928-9940 [Abstract] [Full Text]