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Journal of Virology, December 2008, p. 12181-12190, Vol. 82, No. 24
0022-538X/08/$08.00+0     doi:10.1128/JVI.01687-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Chlorovirus-Mediated Membrane Depolarization of Chlorella Alters Secondary Active Transport of Solutes{triangledown}

Irina Agarkova,1 David Dunigan,1,2 James Gurnon,1 Timo Greiner,3 Julia Barres,3 Gerhard Thiel,3 and James L. Van Etten1,2*

Department of Plant Pathology, University of Nebraska—Lincoln, Lincoln, Nebraska 68583-0722,1 Nebraska Center for Virology, Lincoln Nebraska 68583-0900,2 Institute of Botany, Darmstadt University of Technology, 64287 Darmstadt, Germany3

Received 7 August 2008/ Accepted 30 September 2008

Paramecium bursaria chlorella virus 1 (PBCV-1) is the prototype of a family of large, double-stranded DNA, plaque-forming viruses that infect certain eukaryotic chlorella-like green algae from the genus Chlorovirus. PBCV-1 infection results in rapid host membrane depolarization and potassium ion release. One interesting feature of certain chloroviruses is that they code for functional potassium ion-selective channel proteins (Kcv) that are considered responsible for the host membrane depolarization and, as a consequence, the efflux of potassium ions. This report examines the relationship between cellular depolarization and solute uptake. Annotation of the virus host Chlorella strain NC64A genome revealed 482 putative transporter-encoding genes; 224 are secondary active transporters. Solute uptake experiments using seven radioactive compounds revealed that virus infection alters the transport of all the solutes. However, the degree of inhibition varied depending on the solute. Experiments with nystatin, a drug known to depolarize cell membranes, produced changes in solute uptake that are similar but not identical to those that occurred during virus infection. Therefore, these studies indicate that chlorovirus infection causes a rapid and sustained depolarization of the host plasma membrane and that this depolarization leads to the inhibition of secondary active transporters that changes solute uptake.

* Corresponding author. Mailing address: Department of Plant Pathology, University of Nebraska—Lincoln, Lincoln, NE 68583-0900. Phone: (402) 472-3168. Fax: (402) 472-3323. E-mail: jvanetten1{at}unl.edu

{triangledown} Published ahead of print on 8 October 2008.

Journal of Virology, December 2008, p. 12181-12190, Vol. 82, No. 24
0022-538X/08/$08.00+0     doi:10.1128/JVI.01687-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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