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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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Multiple sequence alignment of K+ channel proteins from different phycodnaviruses.The genes that code for these proteins, originate from viruses with different host specificities. KcvPBCV-1 and KcvNY-2A are from viruses that replicate in C. variabilis, KcvMT325 and KcvCVM-1 from viruses that replicate in M. conductrix, and KcvATCV-1 and KcvTN603 from viruses that replicate in C. heliozoae. The channel Kesv is from virus EsV-1, which replicates in E. siliculosus. The selectivity filter sequence is in black; aromatic amino acids upstream of the filter are marked in grey and the transmembrane domains are underlined.
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pone-0038826-g002: Multiple sequence alignment of K+ channel proteins from different phycodnaviruses.The genes that code for these proteins, originate from viruses with different host specificities. KcvPBCV-1 and KcvNY-2A are from viruses that replicate in C. variabilis, KcvMT325 and KcvCVM-1 from viruses that replicate in M. conductrix, and KcvATCV-1 and KcvTN603 from viruses that replicate in C. heliozoae. The channel Kesv is from virus EsV-1, which replicates in E. siliculosus. The selectivity filter sequence is in black; aromatic amino acids upstream of the filter are marked in grey and the transmembrane domains are underlined.

Mentions: The sequences for 7 virus-encoded channel proteins are shown in Fig. 2. For six of them have already been shown to function as K+ channels in heterologous systems [7], [17]–[19]. The amino acid sequences of the viral K+ channel proteins vary among each other and this variability is apparent even within the same species. For example, a genomic analysis of 40 virus isolates from a single species, all of which replicate in C. variabilis, revealed that the channel proteins differed by as many as 16 amino acids from the reference channel KcvPBCV-1[19], [35]. The channel protein from C. variabilis virus NY-2A (KcvNY-2A) is also included in the alignment in Fig. 2. Ortholog channel proteins from viruses that replicate in either C. heliozoae or M. conductrix are also each represented by two viruses.


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)

Multiple sequence alignment of K+ channel proteins from different phycodnaviruses.The genes that code for these proteins, originate from viruses with different host specificities. KcvPBCV-1 and KcvNY-2A are from viruses that replicate in C. variabilis, KcvMT325 and KcvCVM-1 from viruses that replicate in M. conductrix, and KcvATCV-1 and KcvTN603 from viruses that replicate in C. heliozoae. The channel Kesv is from virus EsV-1, which replicates in E. siliculosus. The selectivity filter sequence is in black; aromatic amino acids upstream of the filter are marked in grey and the transmembrane domains are underlined.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0038826-g002: Multiple sequence alignment of K+ channel proteins from different phycodnaviruses.The genes that code for these proteins, originate from viruses with different host specificities. KcvPBCV-1 and KcvNY-2A are from viruses that replicate in C. variabilis, KcvMT325 and KcvCVM-1 from viruses that replicate in M. conductrix, and KcvATCV-1 and KcvTN603 from viruses that replicate in C. heliozoae. The channel Kesv is from virus EsV-1, which replicates in E. siliculosus. The selectivity filter sequence is in black; aromatic amino acids upstream of the filter are marked in grey and the transmembrane domains are underlined.
Mentions: The sequences for 7 virus-encoded channel proteins are shown in Fig. 2. For six of them have already been shown to function as K+ channels in heterologous systems [7], [17]–[19]. The amino acid sequences of the viral K+ channel proteins vary among each other and this variability is apparent even within the same species. For example, a genomic analysis of 40 virus isolates from a single species, all of which replicate in C. variabilis, revealed that the channel proteins differed by as many as 16 amino acids from the reference channel KcvPBCV-1[19], [35]. The channel protein from C. variabilis virus NY-2A (KcvNY-2A) is also included in the alignment in Fig. 2. Ortholog channel proteins from viruses that replicate in either C. heliozoae or M. conductrix are also each represented by two viruses.

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