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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 Universit├Ąt 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

The consensus sequence of viral K+ channel pore is similar to protein LAP from proteobacterium Labrenzia alexandrii DFL-11.(A) Consensus sequence of viral K+ channels. (B) Alignment of K+ channel KcvATCV-1 with protein LAP from L. alexandrii DFL-11 (data bank ZP_05113853). Identical amino acids are indicated by (*), conserved or semi-conserved amino acids are indicated by (:) and (.) respectively. Note that the consensus sequence of K+ channel selectivity filter (grey box) is only partially conserved in the bacterial protein.
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pone-0038826-g007: The consensus sequence of viral K+ channel pore is similar to protein LAP from proteobacterium Labrenzia alexandrii DFL-11.(A) Consensus sequence of viral K+ channels. (B) Alignment of K+ channel KcvATCV-1 with protein LAP from L. alexandrii DFL-11 (data bank ZP_05113853). Identical amino acids are indicated by (*), conserved or semi-conserved amino acids are indicated by (:) and (.) respectively. Note that the consensus sequence of K+ channel selectivity filter (grey box) is only partially conserved in the bacterial protein.

Mentions: The fact that all of the viral K+ channel proteins group together in a common clade prompted us to identify a consensus sequence (Fig. 7A) from the viral channels using the standard procedure in the Biopython software (http://biopython.org/wiki/Main_Page) that could be used in a BLAST search to hunt for similar channel proteins. The search resulted in one hit, albeit with only moderate significance, to a protein (labeled LPA) from the marine proteobacterium Labrenzia alexandrii DFL-11 (GenBank: NZ_EQ973121).


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)

The consensus sequence of viral K+ channel pore is similar to protein LAP from proteobacterium Labrenzia alexandrii DFL-11.(A) Consensus sequence of viral K+ channels. (B) Alignment of K+ channel KcvATCV-1 with protein LAP from L. alexandrii DFL-11 (data bank ZP_05113853). Identical amino acids are indicated by (*), conserved or semi-conserved amino acids are indicated by (:) and (.) respectively. Note that the consensus sequence of K+ channel selectivity filter (grey box) is only partially conserved in the bacterial protein.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0038826-g007: The consensus sequence of viral K+ channel pore is similar to protein LAP from proteobacterium Labrenzia alexandrii DFL-11.(A) Consensus sequence of viral K+ channels. (B) Alignment of K+ channel KcvATCV-1 with protein LAP from L. alexandrii DFL-11 (data bank ZP_05113853). Identical amino acids are indicated by (*), conserved or semi-conserved amino acids are indicated by (:) and (.) respectively. Note that the consensus sequence of K+ channel selectivity filter (grey box) is only partially conserved in the bacterial protein.
Mentions: The fact that all of the viral K+ channel proteins group together in a common clade prompted us to identify a consensus sequence (Fig. 7A) from the viral channels using the standard procedure in the Biopython software (http://biopython.org/wiki/Main_Page) that could be used in a BLAST search to hunt for similar channel proteins. The search resulted in one hit, albeit with only moderate significance, to a protein (labeled LPA) from the marine proteobacterium Labrenzia alexandrii DFL-11 (GenBank: NZ_EQ973121).

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 Universit├Ąt 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