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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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Maximum likelihood tree of K+ channel acid sequences from phycodnaviruses and host cells C. variabilis and E. siliculosus.Alignment was constructed with the use of MUSCLE [45]. The phylogenetic tree was constructed using PhyML [47] available at Phylogeny.fr [48] using WAG matrix and gamma distribution. Branch labels indicate bootstrap percentages (≥50%) after 100 replicates. The tree is essentially an unrooted tree. Viral K+ channels are indicated in blue, channels from green algae C. variabilis and C. reinhardtii in red. The channels from viruses, which replicate in C. variabilis or E. siliculosus are highlighted by a grey or yellow background respectively.
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pone-0038826-g005: Maximum likelihood tree of K+ channel acid sequences from phycodnaviruses and host cells C. variabilis and E. siliculosus.Alignment was constructed with the use of MUSCLE [45]. The phylogenetic tree was constructed using PhyML [47] available at Phylogeny.fr [48] using WAG matrix and gamma distribution. Branch labels indicate bootstrap percentages (≥50%) after 100 replicates. The tree is essentially an unrooted tree. Viral K+ channels are indicated in blue, channels from green algae C. variabilis and C. reinhardtii in red. The channels from viruses, which replicate in C. variabilis or E. siliculosus are highlighted by a grey or yellow background respectively.

Mentions: First we estimated the phylogenetic relationship of the channels by a maximum likelihood method. It should be noted that this analysis does not provide an in depth phylogenetic analysis of the channels. The goal was to address the question: are the viral channels descendents of host channels or do they form a separate clade? The resulting tree in Fig. 5 shows a clade containing all viral homologs that is separate from the cellular homologs, albeit with relatively low sequence similarities between viral homologs. In the tree, one of the E. siliculosus K+ channels (EsK1) was closely placed with the viral K+ channel Kesv. As mentioned above this result is expected since the entire genome of the lysogenic virus EsV-1 is contained in the genome of the infected host [26]. The paralogs from the two algae and CrK (C. reinhardtii) are more similar to each other than to the viral homologs, even though the last common ancestor between the green alga Chlorella and the brown alga Ectocarpus probably dates back more than 500 million years [27]. Apart from the similarity to EsK1, Kesv is well separated from the putative E. siliculosus channels. Likewise all channels from the chloroviruses form a distinct clade from the algal homologs in the tree; the channels from PBCV-1 and NY-2A, i.e., the C. variabilis viruses, are clearly separated from the C. variabilis channel sequences. The same separation of viral channels from the host channels was also observed in trees produced with a parsimony method and a neighbor-joining algorithm (Figs S1, S2).


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)

Maximum likelihood tree of K+ channel acid sequences from phycodnaviruses and host cells C. variabilis and E. siliculosus.Alignment was constructed with the use of MUSCLE [45]. The phylogenetic tree was constructed using PhyML [47] available at Phylogeny.fr [48] using WAG matrix and gamma distribution. Branch labels indicate bootstrap percentages (≥50%) after 100 replicates. The tree is essentially an unrooted tree. Viral K+ channels are indicated in blue, channels from green algae C. variabilis and C. reinhardtii in red. The channels from viruses, which replicate in C. variabilis or E. siliculosus are highlighted by a grey or yellow background respectively.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0038826-g005: Maximum likelihood tree of K+ channel acid sequences from phycodnaviruses and host cells C. variabilis and E. siliculosus.Alignment was constructed with the use of MUSCLE [45]. The phylogenetic tree was constructed using PhyML [47] available at Phylogeny.fr [48] using WAG matrix and gamma distribution. Branch labels indicate bootstrap percentages (≥50%) after 100 replicates. The tree is essentially an unrooted tree. Viral K+ channels are indicated in blue, channels from green algae C. variabilis and C. reinhardtii in red. The channels from viruses, which replicate in C. variabilis or E. siliculosus are highlighted by a grey or yellow background respectively.
Mentions: First we estimated the phylogenetic relationship of the channels by a maximum likelihood method. It should be noted that this analysis does not provide an in depth phylogenetic analysis of the channels. The goal was to address the question: are the viral channels descendents of host channels or do they form a separate clade? The resulting tree in Fig. 5 shows a clade containing all viral homologs that is separate from the cellular homologs, albeit with relatively low sequence similarities between viral homologs. In the tree, one of the E. siliculosus K+ channels (EsK1) was closely placed with the viral K+ channel Kesv. As mentioned above this result is expected since the entire genome of the lysogenic virus EsV-1 is contained in the genome of the infected host [26]. The paralogs from the two algae and CrK (C. reinhardtii) are more similar to each other than to the viral homologs, even though the last common ancestor between the green alga Chlorella and the brown alga Ectocarpus probably dates back more than 500 million years [27]. Apart from the similarity to EsK1, Kesv is well separated from the putative E. siliculosus channels. Likewise all channels from the chloroviruses form a distinct clade from the algal homologs in the tree; the channels from PBCV-1 and NY-2A, i.e., the C. variabilis viruses, are clearly separated from the C. variabilis channel sequences. The same separation of viral channels from the host channels was also observed in trees produced with a parsimony method and a neighbor-joining algorithm (Figs S1, S2).

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