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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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Minimal sequence set to test molecular piracy hypothesis. Seven sequences of K+ channels are from different phycodnaviruses.Six of them replicate in specific species of green algae. C. variabilis is a host for two of these viruses. The seventh phycodnavirus infects E. siliculosus, a brown alga, which is only distantly related to the green algae. The viral channels are compared to putative K+ channels from hosts and non-hosts. The host channels include all 7 K+ channels from C. variabilis and all 12 K+ channels from E. siliculosus. A K+ channel sequence from the green alga C. reinhardtii, a non-host of phycodnaviruses and a close relative of Chlorella served as a negative control.
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pone-0038826-g001: Minimal sequence set to test molecular piracy hypothesis. Seven sequences of K+ channels are from different phycodnaviruses.Six of them replicate in specific species of green algae. C. variabilis is a host for two of these viruses. The seventh phycodnavirus infects E. siliculosus, a brown alga, which is only distantly related to the green algae. The viral channels are compared to putative K+ channels from hosts and non-hosts. The host channels include all 7 K+ channels from C. variabilis and all 12 K+ channels from E. siliculosus. A K+ channel sequence from the green alga C. reinhardtii, a non-host of phycodnaviruses and a close relative of Chlorella served as a negative control.

Mentions: To investigate the evolution of the viral K+ channels and to test the ‘molecular piracy hypothesis’ in the Phycodnaviridae, we analyzed a small set of sequences, including host homologs, that recently became available (see Fig. 1). Our sequence data set contains seven K+ channels from phycodnaviruses. These viruses can be distinguished according to their host specificity. Six viruses replicate in different species of unicellular green algae. Two of these six viruses, PBCV-1 and NY-2A, specifically infect Chlorella variabilis (formerly Chlorella NC64A), two, ATCV-1 and TN603 infect Chlorella heliozoae (formerly Chlorella SAG 3.83) and two infect Micractinium conductrix (formerly Chlorella Pbi). The seventh phycodnavirus EsV-1 infects E. siliculosus, whose genomic information is also available [26]. The viral channels were compared to the K+ channels from these viral hosts and related non-host species. If gene piracy explains the presence of the viral channel genes the Kesv channel should be closely related to the EsK channels from Ectocarpus and KcvPBCV-1 and KcvNY-2A should be close to the C. variabilis channels.


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)

Minimal sequence set to test molecular piracy hypothesis. Seven sequences of K+ channels are from different phycodnaviruses.Six of them replicate in specific species of green algae. C. variabilis is a host for two of these viruses. The seventh phycodnavirus infects E. siliculosus, a brown alga, which is only distantly related to the green algae. The viral channels are compared to putative K+ channels from hosts and non-hosts. The host channels include all 7 K+ channels from C. variabilis and all 12 K+ channels from E. siliculosus. A K+ channel sequence from the green alga C. reinhardtii, a non-host of phycodnaviruses and a close relative of Chlorella served as a negative control.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3369850&req=5

pone-0038826-g001: Minimal sequence set to test molecular piracy hypothesis. Seven sequences of K+ channels are from different phycodnaviruses.Six of them replicate in specific species of green algae. C. variabilis is a host for two of these viruses. The seventh phycodnavirus infects E. siliculosus, a brown alga, which is only distantly related to the green algae. The viral channels are compared to putative K+ channels from hosts and non-hosts. The host channels include all 7 K+ channels from C. variabilis and all 12 K+ channels from E. siliculosus. A K+ channel sequence from the green alga C. reinhardtii, a non-host of phycodnaviruses and a close relative of Chlorella served as a negative control.
Mentions: To investigate the evolution of the viral K+ channels and to test the ‘molecular piracy hypothesis’ in the Phycodnaviridae, we analyzed a small set of sequences, including host homologs, that recently became available (see Fig. 1). Our sequence data set contains seven K+ channels from phycodnaviruses. These viruses can be distinguished according to their host specificity. Six viruses replicate in different species of unicellular green algae. Two of these six viruses, PBCV-1 and NY-2A, specifically infect Chlorella variabilis (formerly Chlorella NC64A), two, ATCV-1 and TN603 infect Chlorella heliozoae (formerly Chlorella SAG 3.83) and two infect Micractinium conductrix (formerly Chlorella Pbi). The seventh phycodnavirus EsV-1 infects E. siliculosus, whose genomic information is also available [26]. The viral channels were compared to the K+ channels from these viral hosts and related non-host species. If gene piracy explains the presence of the viral channel genes the Kesv channel should be closely related to the EsK channels from Ectocarpus and KcvPBCV-1 and KcvNY-2A should be close to the C. variabilis channels.

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