Evolution and the complexity of bacteriophages

<p>Abstract</p> <p>Background</p> <p>The genomes of both long-genome (> 200 Kb) bacteriophages and long-genome eukaryotic viruses have cellular gene homologs whose selective advantage is not explained. These homologs add genomic and possibly biochemical complexity. U...

Full description

Bibliographic Details
Main Author: Serwer Philip
Format: Article
Language:English
Published: BMC 2007-03-01
Series:Virology Journal
Online Access:http://www.virologyj.com/content/4/1/30
id doaj-579fdc80dba54072b3869081fbddfbae
record_format Article
spelling doaj-579fdc80dba54072b3869081fbddfbae2020-11-25T02:28:09ZengBMCVirology Journal1743-422X2007-03-01413010.1186/1743-422X-4-30Evolution and the complexity of bacteriophagesSerwer Philip<p>Abstract</p> <p>Background</p> <p>The genomes of both long-genome (> 200 Kb) bacteriophages and long-genome eukaryotic viruses have cellular gene homologs whose selective advantage is not explained. These homologs add genomic and possibly biochemical complexity. Understanding their significance requires a definition of complexity that is more biochemically oriented than past empirically based definitions.</p> <p>Hypothesis</p> <p>Initially, I propose two biochemistry-oriented definitions of complexity: either decreased randomness or increased encoded information that does not serve immediate needs. Then, I make the assumption that these two definitions are equivalent. This assumption and recent data lead to the following four-part hypothesis that explains the presence of cellular gene homologs in long bacteriophage genomes and also provides a pathway for complexity increases in prokaryotic cells: (1) Prokaryotes underwent evolutionary increases in biochemical complexity after the eukaryote/prokaryote splits. (2) Some of the complexity increases occurred via multi-step, weak selection that was both protected from strong selection and accelerated by embedding evolving cellular genes in the genomes of bacteriophages and, presumably, also archaeal viruses (first tier selection). (3) The mechanisms for retaining cellular genes in viral genomes evolved under additional, longer-term selection that was stronger (second tier selection). (4) The second tier selection was based on increased access by prokaryotic cells to improved biochemical systems. This access was achieved when DNA transfer moved to prokaryotic cells both the more evolved genes and their more competitive and complex biochemical systems.</p> <p>Testing the hypothesis</p> <p>I propose testing this hypothesis by controlled evolution in microbial communities to (1) determine the effects of deleting individual cellular gene homologs on the growth and evolution of long genome bacteriophages and hosts, (2) find the environmental conditions that select for the presence of cellular gene homologs, (3) determine which, if any, bacteriophage genes were selected for maintaining the homologs and (4) determine the dynamics of homolog evolution.</p> <p>Implications of the hypothesis</p> <p>This hypothesis is an explanation of evolutionary leaps in general. If accurate, it will assist both understanding and influencing the evolution of microbes and their communities. Analysis of evolutionary complexity increase for at least prokaryotes should include analysis of genomes of long-genome bacteriophages.</p> http://www.virologyj.com/content/4/1/30
collection DOAJ
language English
format Article
sources DOAJ
author Serwer Philip
spellingShingle Serwer Philip
Evolution and the complexity of bacteriophages
Virology Journal
author_facet Serwer Philip
author_sort Serwer Philip
title Evolution and the complexity of bacteriophages
title_short Evolution and the complexity of bacteriophages
title_full Evolution and the complexity of bacteriophages
title_fullStr Evolution and the complexity of bacteriophages
title_full_unstemmed Evolution and the complexity of bacteriophages
title_sort evolution and the complexity of bacteriophages
publisher BMC
series Virology Journal
issn 1743-422X
publishDate 2007-03-01
description <p>Abstract</p> <p>Background</p> <p>The genomes of both long-genome (> 200 Kb) bacteriophages and long-genome eukaryotic viruses have cellular gene homologs whose selective advantage is not explained. These homologs add genomic and possibly biochemical complexity. Understanding their significance requires a definition of complexity that is more biochemically oriented than past empirically based definitions.</p> <p>Hypothesis</p> <p>Initially, I propose two biochemistry-oriented definitions of complexity: either decreased randomness or increased encoded information that does not serve immediate needs. Then, I make the assumption that these two definitions are equivalent. This assumption and recent data lead to the following four-part hypothesis that explains the presence of cellular gene homologs in long bacteriophage genomes and also provides a pathway for complexity increases in prokaryotic cells: (1) Prokaryotes underwent evolutionary increases in biochemical complexity after the eukaryote/prokaryote splits. (2) Some of the complexity increases occurred via multi-step, weak selection that was both protected from strong selection and accelerated by embedding evolving cellular genes in the genomes of bacteriophages and, presumably, also archaeal viruses (first tier selection). (3) The mechanisms for retaining cellular genes in viral genomes evolved under additional, longer-term selection that was stronger (second tier selection). (4) The second tier selection was based on increased access by prokaryotic cells to improved biochemical systems. This access was achieved when DNA transfer moved to prokaryotic cells both the more evolved genes and their more competitive and complex biochemical systems.</p> <p>Testing the hypothesis</p> <p>I propose testing this hypothesis by controlled evolution in microbial communities to (1) determine the effects of deleting individual cellular gene homologs on the growth and evolution of long genome bacteriophages and hosts, (2) find the environmental conditions that select for the presence of cellular gene homologs, (3) determine which, if any, bacteriophage genes were selected for maintaining the homologs and (4) determine the dynamics of homolog evolution.</p> <p>Implications of the hypothesis</p> <p>This hypothesis is an explanation of evolutionary leaps in general. If accurate, it will assist both understanding and influencing the evolution of microbes and their communities. Analysis of evolutionary complexity increase for at least prokaryotes should include analysis of genomes of long-genome bacteriophages.</p>
url http://www.virologyj.com/content/4/1/30
work_keys_str_mv AT serwerphilip evolutionandthecomplexityofbacteriophages
_version_ 1724839893849341952