tailieunhanh - Báo cáo khoa học: The association of viral proteins with host cell dynein components during virus infection

After fusion with the cellular plasma membrane or endosomal membranes, viral particles are generally too large to diffuse freely within the crowded cytoplasm environment. Thus, they will never reach the cell nucleus or the perinuclear areas where replication or reverse transcription usually takes place. | fFEBS Journal MINIREVIEW The association of viral proteins with host cell dynein components during virus infection Javier Merino-Gracia1 Maria F. Garcia-Mayoral2 and Ignacio Rodriguez-Crespo1 1 Departamento de Bioquimica y Biologia Molecular I Universidad Complutense Madrid Spain 2 Departamento de Quimica-Fisica Biologica Instituto de Quimica-Fisica Rocasolano Madrid Spain Keywords dynein DYNLL1 DYNLT1 infection retrograde transport virus Correspondence I. Rodriguez-Crespo Departamento de Bioquimica y Biologia Molecular I Universidad Complutense 28040 Madrid Spain Fax 34 91 394 4159 Tel 34 91 394 4137 E-mail nacho@ Received 8 February 2011 revised 8 July 2011 accepted 13 July 2011 doi After fusion with the cellular plasma membrane or endosomal membranes viral particles are generally too large to diffuse freely within the crowded cytoplasm environment. Thus they will never reach the cell nucleus or the perinuclear areas where replication or reverse transcription usually takes place. It has been proposed that many unrelated viruses are transported along microtubules in a retrograde manner using the cellular dynein machinery or at least some dynein components. A putative employment of the dynein motor in a dynein-mediated transport has been suggested from experiments in which viral capsid proteins were used as bait in yeast two-hybrid screens using libraries composed of cellular proteins and dynein-associated chains were retrieved as virus-interacting proteins. In most cases DYNLL1 DYNLT1 or DYNLRB1 were identified as the dynein chains that interact with viral proteins. The importance of these dynein-virus interactions has been supported in principle by the observation that in some cases the dynein-interacting motifs of viral proteins altered by site-directed mutagenesis result in non-infective virions. Furthermore overexpression of p50 dynamitin which blocks the dynein-dynactin interaction or incubation of infected cells .