Serwer Philip
Department of Biochemistry, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229-3900, USA.
Virol J. 2007 Mar 13;4:30. doi: 10.1186/1743-422X-4-30.
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.
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.
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.
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.
长基因组（>200 kb）噬菌体和长基因组真核病毒的基因组都含有细胞基因同源物，但其选择优势尚不清楚。这些同源物增加了基因组以及可能的生化复杂性。要理解它们的意义，需要一个比以往基于经验的定义更偏向生化层面的复杂性定义。
首先，我提出两个基于生化的复杂性定义：一是随机性降低，二是编码信息增加但并非满足即时需求。然后，我假设这两个定义是等效的。这一假设和近期数据引出了以下四点假设，该假设解释了长噬菌体基因组中细胞基因同源物的存在，也为原核细胞的复杂性增加提供了一条途径：（1）真核生物与原核生物分化后，原核生物在生化复杂性上经历了进化增加。（2）部分复杂性增加是通过多步骤、弱选择发生的，这种选择既受到强选择的保护，又通过将不断进化的细胞基因嵌入噬菌体基因组以及大概还有古菌病毒基因组中而加速（一级选择）。（3）病毒基因组中保留细胞基因的机制是在额外的、更强的长期选择下进化而来的（二级选择）。（4）二级选择基于原核细胞对改良生化系统的更多获取。当DNA转移将进化程度更高的基因及其更具竞争力和更复杂的生化系统转移到原核细胞时，就实现了这种获取。
我提议通过微生物群落中的受控进化来验证这一假设，以（1）确定删除单个细胞基因同源物对长基因组噬菌体及其宿主的生长和进化的影响，（2）找出选择细胞基因同源物存在的环境条件，（3）确定为维持同源物而选择的噬菌体基因（如果有的话），以及（4）确定同源物进化的动态过程。
这一假设总体上解释了进化飞跃。如果正确，它将有助于理解和影响微生物及其群落的进化。至少对于原核生物而言，对进化复杂性增加的分析应包括对长基因组噬菌体基因组的分析。
