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Phycodnavirus potassium ion channel proteins question the virus molecular piracy hypothesis.

Hamacher K, Greiner T, Ogata H, Van Etten JL, Gebhardt M, Villarreal LP, Cosentino C, Moroni A, Thiel G - PLoS ONE (2012)

Bottom Line: To determine if these viral K(+) channels are the product of molecular piracy from their hosts, we compared the sequences of the K(+) channel pore modules from seven phycodnaviruses to the K(+) channels from Chlorella variabilis and Ectocarpus siliculosus, whose genomes have recently been sequenced.However, the bacterial protein lacks the consensus motif of all K(+) channels and it does not form a functional channel in yeast, suggesting that the viral channels did not come from a proteobacterium.Alternatively the viral proteins could be the origin of K(+) channels in algae and perhaps even all cellular organisms.

View Article: PubMed Central - PubMed

Affiliation: Computational Biology Group, Technische Universität Darmstadt, Darmstadt, Germany.

ABSTRACT
Phycodnaviruses are large dsDNA, algal-infecting viruses that encode many genes with homologs in prokaryotes and eukaryotes. Among the viral gene products are the smallest proteins known to form functional K(+) channels. To determine if these viral K(+) channels are the product of molecular piracy from their hosts, we compared the sequences of the K(+) channel pore modules from seven phycodnaviruses to the K(+) channels from Chlorella variabilis and Ectocarpus siliculosus, whose genomes have recently been sequenced. C. variabilis is the host for two of the viruses PBCV-1 and NY-2A and E. siliculosus is the host for the virus EsV-1. Systematic phylogenetic analyses consistently indicate that the viral K(+) channels are not related to any lineage of the host channel homologs and that they are more closely related to each other than to their host homologs. A consensus sequence of the viral channels resembles a protein of unknown function from a proteobacterium. However, the bacterial protein lacks the consensus motif of all K(+) channels and it does not form a functional channel in yeast, suggesting that the viral channels did not come from a proteobacterium. Collectively, our results indicate that the viruses did not acquire their K(+) channel-encoding genes from their current algal hosts by gene transfer; thus alternative explanations are required. One possibility is that the viral genes arose from ancient organisms, which served as their hosts before the viruses developed their current host specificity. Alternatively the viral proteins could be the origin of K(+) channels in algae and perhaps even all cellular organisms.

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Related in: MedlinePlus

Growth phenotype ΔtrkΔtrk2 mutants transformed with different genes.Yeast cells were transformed with either an empty vector or with genes encoding viral K+ channel Kcv, or the protein LAP from L. alexandrii DFL-11. All yeasts were grown on non-selective medium containing either 100 mM K+ or lesser amounts. Only yeast transformed with KcvPBCV-1 grew on selective medium with low 0.5 mM and 1 mM K+ concentrations.
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pone-0038826-g008: Growth phenotype ΔtrkΔtrk2 mutants transformed with different genes.Yeast cells were transformed with either an empty vector or with genes encoding viral K+ channel Kcv, or the protein LAP from L. alexandrii DFL-11. All yeasts were grown on non-selective medium containing either 100 mM K+ or lesser amounts. Only yeast transformed with KcvPBCV-1 grew on selective medium with low 0.5 mM and 1 mM K+ concentrations.

Mentions: We tested the functionality of LPA as a K+ channel by cloning and expressing its gene in mutants of yeast that are devoid of K+ uptake systems. These mutants only grow in a medium with high K+ (100 mM). Growth on a medium with low K+ can only occur by expressing a heterologous K+ channel [29]. The data in Fig. 8 show that all yeast mutants grow on medium with high K+. Growth on medium with low K+ only occurred when cells are transformed with the functional KcvPBCV-1. This result is consistent with the previous observation that functional viral K+ channels can rescue the yeast mutants under selective conditions [29]. However, LPA from L. alexandrii DFL-11 did not rescue the mutant defect. Although this result does not provide definitive proof that LPA is not a K+ channel protein, it indicates that it probably does not form a functional channel in yeast. Together, these results indicate it is unlikely that the viral channels came from proteobacteria.


Phycodnavirus potassium ion channel proteins question the virus molecular piracy hypothesis.

Hamacher K, Greiner T, Ogata H, Van Etten JL, Gebhardt M, Villarreal LP, Cosentino C, Moroni A, Thiel G - PLoS ONE (2012)

Growth phenotype ΔtrkΔtrk2 mutants transformed with different genes.Yeast cells were transformed with either an empty vector or with genes encoding viral K+ channel Kcv, or the protein LAP from L. alexandrii DFL-11. All yeasts were grown on non-selective medium containing either 100 mM K+ or lesser amounts. Only yeast transformed with KcvPBCV-1 grew on selective medium with low 0.5 mM and 1 mM K+ concentrations.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3369850&req=5

pone-0038826-g008: Growth phenotype ΔtrkΔtrk2 mutants transformed with different genes.Yeast cells were transformed with either an empty vector or with genes encoding viral K+ channel Kcv, or the protein LAP from L. alexandrii DFL-11. All yeasts were grown on non-selective medium containing either 100 mM K+ or lesser amounts. Only yeast transformed with KcvPBCV-1 grew on selective medium with low 0.5 mM and 1 mM K+ concentrations.
Mentions: We tested the functionality of LPA as a K+ channel by cloning and expressing its gene in mutants of yeast that are devoid of K+ uptake systems. These mutants only grow in a medium with high K+ (100 mM). Growth on a medium with low K+ can only occur by expressing a heterologous K+ channel [29]. The data in Fig. 8 show that all yeast mutants grow on medium with high K+. Growth on medium with low K+ only occurred when cells are transformed with the functional KcvPBCV-1. This result is consistent with the previous observation that functional viral K+ channels can rescue the yeast mutants under selective conditions [29]. However, LPA from L. alexandrii DFL-11 did not rescue the mutant defect. Although this result does not provide definitive proof that LPA is not a K+ channel protein, it indicates that it probably does not form a functional channel in yeast. Together, these results indicate it is unlikely that the viral channels came from proteobacteria.

Bottom Line: To determine if these viral K(+) channels are the product of molecular piracy from their hosts, we compared the sequences of the K(+) channel pore modules from seven phycodnaviruses to the K(+) channels from Chlorella variabilis and Ectocarpus siliculosus, whose genomes have recently been sequenced.However, the bacterial protein lacks the consensus motif of all K(+) channels and it does not form a functional channel in yeast, suggesting that the viral channels did not come from a proteobacterium.Alternatively the viral proteins could be the origin of K(+) channels in algae and perhaps even all cellular organisms.

View Article: PubMed Central - PubMed

Affiliation: Computational Biology Group, Technische Universität Darmstadt, Darmstadt, Germany.

ABSTRACT
Phycodnaviruses are large dsDNA, algal-infecting viruses that encode many genes with homologs in prokaryotes and eukaryotes. Among the viral gene products are the smallest proteins known to form functional K(+) channels. To determine if these viral K(+) channels are the product of molecular piracy from their hosts, we compared the sequences of the K(+) channel pore modules from seven phycodnaviruses to the K(+) channels from Chlorella variabilis and Ectocarpus siliculosus, whose genomes have recently been sequenced. C. variabilis is the host for two of the viruses PBCV-1 and NY-2A and E. siliculosus is the host for the virus EsV-1. Systematic phylogenetic analyses consistently indicate that the viral K(+) channels are not related to any lineage of the host channel homologs and that they are more closely related to each other than to their host homologs. A consensus sequence of the viral channels resembles a protein of unknown function from a proteobacterium. However, the bacterial protein lacks the consensus motif of all K(+) channels and it does not form a functional channel in yeast, suggesting that the viral channels did not come from a proteobacterium. Collectively, our results indicate that the viruses did not acquire their K(+) channel-encoding genes from their current algal hosts by gene transfer; thus alternative explanations are required. One possibility is that the viral genes arose from ancient organisms, which served as their hosts before the viruses developed their current host specificity. Alternatively the viral proteins could be the origin of K(+) channels in algae and perhaps even all cellular organisms.

Show MeSH
Related in: MedlinePlus