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1.  CRISPR loci reveal networks of gene exchange in archaea 
Biology Direct  2011;6:65.
Open peer review
PMCID: PMC3285040  PMID: 22188759
Biology Direct  2011;6:64.
PMCID: PMC3340325  PMID: 22185645
State estimation; data assimiliation; mathematical models; glioblastoma multiforme
3.  Purine biosynthesis in archaea: variations on a theme 
Biology Direct  2011;6:63.
PMCID: PMC3261824  PMID: 22168471
Biology Direct  2011;6:62.
Speciation corresponds to the progressive establishment of reproductive barriers between groups of individuals derived from an ancestral stock. Since Darwin did not believe that reproductive barriers could be selected for, he proposed that most events of speciation would occur through a process of separation and divergence, and this point of view is still shared by most evolutionary biologists today.
I do, however, contend that, if so much speciation occurs, the most likely explanation is that there must be conditions where reproductive barriers can be directly selected for. In other words, situations where it is advantageous for individuals to reproduce preferentially within a small group and reduce their breeding with the rest of the ancestral population. This leads me to propose a model whereby new species arise not by populations splitting into separate branches, but by small inbreeding groups "budding" from an ancestral stock. This would be driven by several advantages of inbreeding, and mainly by advantageous recessive phenotypes, which could only be retained in the context of inbreeding. Reproductive barriers would thus not arise as secondary consequences of divergent evolution in populations isolated from one another, but under the direct selective pressure of ancestral stocks. Many documented cases of speciation in natural populations appear to fit the model proposed, with more speciation occurring in populations with high inbreeding coefficients, and many recessive characters identified as central to the phenomenon of speciation, with these recessive mutations expected to be surrounded by patterns of limited genomic diversity.
Whilst adaptive evolution would correspond to gains of function that would, most of the time, be dominant, this type of speciation by budding would thus be driven by mutations resulting in the advantageous loss of certain functions since recessive mutations very often correspond to the inactivation of a gene. A very important further advantage of inbreeding is that it reduces the accumulation of recessive mutations in genomes. A consequence of the model proposed is that the existence of species would correspond to a metastable equilibrium between inbreeding and outbreeding, with excessive inbreeding promoting speciation, and excessive outbreeding resulting in irreversible accumulation of recessive mutations that could ultimately only lead to extinction.
Reviewer names
Eugene V. Koonin, Patrick Nosil (nominated by Dr Jerzy Jurka), Pierre Pontarotti
PMCID: PMC3275546  PMID: 22152499
speciation; inbreeding; saeptation; mutation load; extinction; evolution
5.  Transcription factor binding sites are highly enriched within microRNA precursor sequences 
Biology Direct  2011;6:61.
PMCID: PMC3240832  PMID: 22136256
Transcription factors; microRNA biogenesis; drosha
6.  On universal common ancestry, sequence similarity, and phylogenetic structure: the sins of P-values and the virtues of Bayesian evidence 
Biology Direct  2011;6:60.
The universal common ancestry (UCA) of all known life is a fundamental component of modern evolutionary theory, supported by a wide range of qualitative molecular evidence. Nevertheless, recently both the status and nature of UCA has been questioned. In earlier work I presented a formal, quantitative test of UCA in which model selection criteria overwhelmingly choose common ancestry over independent ancestry, based on a dataset of universally conserved proteins. These model-based tests are founded in likelihoodist and Bayesian probability theory, in opposition to classical frequentist null hypothesis tests such as Karlin-Altschul E-values for sequence similarity. In a recent comment, Koonin and Wolf (K&W) claim that the model preference for UCA is "a trivial consequence of significant sequence similarity". They support this claim with a computational simulation, derived from universally conserved proteins, which produces similar sequences lacking phylogenetic structure. The model selection tests prefer common ancestry for this artificial data set.
For the real universal protein sequences, hierarchical phylogenetic structure (induced by genealogical history) is the overriding reason for why the tests choose UCA; sequence similarity is a relatively minor factor. First, for cases of conflicting phylogenetic structure, the tests choose independent ancestry even with highly similar sequences. Second, certain models, like star trees and K&W's profile model (corresponding to their simulation), readily explain sequence similarity yet lack phylogenetic structure. However, these are extremely poor models for the real proteins, even worse than independent ancestry models, though they explain K&W's artificial data well. Finally, K&W's simulation is an implementation of a well-known phylogenetic model, and it produces sequences that mimic homologous proteins. Therefore the model selection tests work appropriately with the artificial data.
For K&W's artificial protein data, sequence similarity is the predominant factor influencing the preference for common ancestry. In contrast, for the real proteins, model selection tests show that phylogenetic structure is much more important than sequence similarity. Hence, the model selection tests demonstrate that real universally conserved proteins are homologous, a conclusion based primarily on the specific nested patterns of correlations induced in genetically related protein sequences.
This article was reviewed by Rob Knight, Robert Beiko (nominated by Peter Gogarten), and Michael Gilchrist.
PMCID: PMC3314578  PMID: 22114984
7.  Extensive intron gain in the ancestor of placental mammals 
Biology Direct  2011;6:59.
Genome-wide studies of intron dynamics in mammalian orthologous genes have found convincing evidence for loss of introns but very little for intron turnover. Similarly, large-scale analysis of intron dynamics in a few vertebrate genomes has identified only intron losses and no gains, indicating that intron gain is an extremely rare event in vertebrate evolution. These studies suggest that the intron-rich genomes of vertebrates do not allow intron gain. The aim of this study was to search for evidence of de novo intron gain in domesticated genes from an analysis of their exon/intron structures.
A phylogenomic approach has been used to analyse all domesticated genes in mammals and chordates that originated from the coding parts of transposable elements. Gain of introns in domesticated genes has been reconstructed on well established mammalian, vertebrate and chordate phylogenies, and examined as to where and when the gain events occurred. The locations, sizes and amounts of de novo introns gained in the domesticated genes during the evolution of mammals and chordates has been analyzed. A significant amount of intron gain was found only in domesticated genes of placental mammals, where more than 70 cases were identified. De novo gained introns show clear positional bias, since they are distributed mainly in 5' UTR and coding regions, while 3' UTR introns are very rare. In the coding regions of some domesticated genes up to 8 de novo gained introns have been found. Intron densities in Eutheria-specific domesticated genes and in older domesticated genes that originated early in vertebrates are lower than those for normal mammalian and vertebrate genes. Surprisingly, the majority of intron gains have occurred in the ancestor of placentals.
This study provides the first evidence for numerous intron gains in the ancestor of placental mammals and demonstrates that adequate taxon sampling is crucial for reconstructing intron evolution. The findings of this comprehensive study slightly challenge the current view on the evolutionary stasis in intron dynamics during the last 100 - 200 My. Domesticated genes could constitute an excellent system on which to analyse the mechanisms of intron gain in placental mammals.
Reviewers: this article was reviewed by Dan Graur, Eugene V. Koonin and Jürgen Brosius.
PMCID: PMC3257199  PMID: 22112745
8.  Molecular musings in microbial ecology and evolution 
Biology Direct  2011;6:58.
PMCID: PMC3254073  PMID: 22074255
9.  Not all transmembrane helices are born equal: Towards the extension of the sequence homology concept to membrane proteins 
Biology Direct  2011;6:57.
Sequence homology considerations widely used to transfer functional annotation to uncharacterized protein sequences require special precautions in the case of non-globular sequence segments including membrane-spanning stretches composed of non-polar residues. Simple, quantitative criteria are desirable for identifying transmembrane helices (TMs) that must be included into or should be excluded from start sequence segments in similarity searches aimed at finding distant homologues.
We found that there are two types of TMs in membrane-associated proteins. On the one hand, there are so-called simple TMs with elevated hydrophobicity, low sequence complexity and extraordinary enrichment in long aliphatic residues. They merely serve as membrane-anchoring device. In contrast, so-called complex TMs have lower hydrophobicity, higher sequence complexity and some functional residues. These TMs have additional roles besides membrane anchoring such as intra-membrane complex formation, ligand binding or a catalytic role. Simple and complex TMs can occur both in single- and multi-membrane-spanning proteins essentially in any type of topology. Whereas simple TMs have the potential to confuse searches for sequence homologues and to generate unrelated hits with seemingly convincing statistical significance, complex TMs contain essential evolutionary information.
For extending the homology concept onto membrane proteins, we provide a necessary quantitative criterion to distinguish simple TMs (and a sufficient criterion for complex TMs) in query sequences prior to their usage in homology searches based on assessment of hydrophobicity and sequence complexity of the TM sequence segments.
This article was reviewed by Shamil Sunyaev, L. Aravind and Arcady Mushegian.
PMCID: PMC3217874  PMID: 22024092
10.  Probable presence of an ubiquitous cryptic mitochondrial gene on the antisense strand of the cytochrome oxidase I gene 
Biology Direct  2011;6:56.
Presentation of the hypothesis
Testing the hypothesis
Implications of the hypothesis
PMCID: PMC3214167  PMID: 22024028
Mitochondrial DNA; cox-1 gene; ubiquitous gene; overprinting; genome evolution; janolog
11.  The rhizome of Reclinomonas americana, Homo sapiens, Pediculus humanus and Saccharomyces cerevisiae mitochondria 
Biology Direct  2011;6:55.
Mitochondria are thought to have evolved from eubacteria-like endosymbionts; however, the origin of the mitochondrion remains a subject of debate. In this study, we investigated the phenomenon of chimerism in mitochondria to shed light on the origin of these organelles by determining which species played a role in their formation. We used the mitochondria of four distinct organisms, Reclinomonas americana, Homo sapiens, Saccharomyces cerevisiae and multichromosome Pediculus humanus, and attempted to identify the origin of each mitochondrial gene.
Our results suggest that the origin of mitochondrial genes is not limited to the Rickettsiales and that the creation of these genes did not occur in a single event, but through multiple successive events. Some of these events are very old and were followed by events that are more recent and occurred through the addition of elements originating from current species. The points in time that the elements were added and the parental species of each gene in the mitochondrial genome are different to the individual species. These data constitute strong evidence that mitochondria do not have a single common ancestor but likely have numerous ancestors, including proto-Rickettsiales, proto-Rhizobiales and proto-Alphaproteobacteria, as well as current alphaproteobacterial species. The analysis of the multichromosome P. humanus mitochondrion supports this mechanism.
The most plausible scenario of the origin of the mitochondrion is that ancestors of Rickettsiales and Rhizobiales merged in a proto-eukaryotic cell approximately one billion years ago. The fusion of the Rickettsiales and Rhizobiales cells was followed by gene loss, genomic rearrangements and the addition of alphaproteobacterial elements through ancient and more recent recombination events. Each gene of each of the four studied mitochondria has a different origin, while in some cases, multichromosomes may allow for enhanced gene exchange. Therefore, the tree of life is not sufficient to explain the chimeric structure of current genomes, and the theory of a single common ancestor and a top-down tree does not reflect our current state of knowledge. Mitochondrial evolution constitutes a rhizome, and it should be represented as such.
This article was revised by William Martin, Arcady Mushegian and Eugene V. Koonin.
PMCID: PMC3214132  PMID: 22014084
12.  Phylogenetic analysis reveals wide distribution of globin X 
Biology Direct  2011;6:54.
The vertebrate globin gene repertoire consists of seven members that differ in terms of structure, function and phyletic distribution. While hemoglobin, myoglobin, cytoglobin, and neuroglobin are present in almost all gnathostomes examined so far, other globin genes, like globin X, are much more restricted in their phyletic distribution. Till today, globin X has only been found in teleost fish and Xenopus. Here, we report that globin X is also present in the genomes of the sea lamprey, ghost shark and reptiles. Moreover, the identification of orthologs of globin X in crustacean, insects, platyhelminthes, and hemichordates confirms its ancient origin.
PMCID: PMC3206486  PMID: 22004552
13.  A network-based approach to classify the three domains of life 
Biology Direct  2011;6:53.
Identifying group-specific characteristics in metabolic networks can provide better insight into evolutionary developments. Here, we present an approach to classify the three domains of life using topological information about the underlying metabolic networks. These networks have been shown to share domain-independent structural similarities, which pose a special challenge for our endeavour. We quantify specific structural information by using topological network descriptors to classify this set of metabolic networks. Such measures quantify the structural complexity of the underlying networks. In this study, we use such measures to capture domain-specific structural features of the metabolic networks to classify the data set. So far, it has been a challenging undertaking to examine what kind of structural complexity such measures do detect. In this paper, we apply two groups of topological network descriptors to metabolic networks and evaluate their classification performance. Moreover, we combine the two groups to perform a feature selection to estimate the structural features with the highest classification ability in order to optimize the classification performance.
By combining the two groups, we can identify seven topological network descriptors that show a group-specific characteristic by ANOVA. A multivariate analysis using feature selection and supervised machine learning leads to a reasonable classification performance with a weighted F-score of 83.7% and an accuracy of 83.9%. We further demonstrate that our approach outperforms alternative methods. Also, our results reveal that entropy-based descriptors show the highest classification ability for this set of networks.
Our results show that these particular topological network descriptors are able to capture domain-specific structural characteristics for classifying metabolic networks between the three domains of life.
PMCID: PMC3226542  PMID: 21995640
14.  Xenorhodopsins, an enigmatic new class of microbial rhodopsins horizontally transferred between archaea and bacteria 
Biology Direct  2011;6:52.
PMCID: PMC3198991  PMID: 21985229
15.  Fish the ChIPs: a pipeline for automated genomic annotation of ChIP-Seq data 
Biology Direct  2011;6:51.
High-throughput sequencing is generating massive amounts of data at a pace that largely exceeds the throughput of data analysis routines. Here we introduce Fish the ChIPs (FC), a computational pipeline aimed at a broad public of users and designed to perform complete ChIP-Seq data analysis of an unlimited number of samples, thus increasing throughput, reproducibility and saving time.
Starting from short read sequences, FC performs the following steps: 1) quality controls, 2) alignment to a reference genome, 3) peak calling, 4) genomic annotation, 5) generation of raw signal tracks for visualization on the UCSC and IGV genome browsers. FC exploits some of the fastest and most effective tools today available. Installation on a Mac platform requires very basic computational skills while configuration and usage are supported by a user-friendly graphic user interface. Alternatively, FC can be compiled from the source code on any Unix machine and then run with the possibility of customizing each single parameter through a simple configuration text file that can be generated using a dedicated user-friendly web-form. Considering the execution time, FC can be run on a desktop machine, even though the use of a computer cluster is recommended for analyses of large batches of data. FC is perfectly suited to work with data coming from Illumina Solexa Genome Analyzers or ABI SOLiD and its usage can potentially be extended to any sequencing platform.
Compared to existing tools, FC has two main advantages that make it suitable for a broad range of users. First of all, it can be installed and run by wet biologists on a Mac machine. Besides it can handle an unlimited number of samples, being convenient for large analyses. In this context, computational biologists can increase reproducibility of their ChIP-Seq data analyses while saving time for downstream analyses.
This article was reviewed by Gavin Huttley, George Shpakovski and Sarah Teichmann.
PMCID: PMC3201895  PMID: 21978789
16.  Evolution of vacuolar proton pyrophosphatase domains and volutin granules: clues into the early evolutionary origin of the acidocalcisome 
Biology Direct  2011;6:50.
PMCID: PMC3198990  PMID: 21974828
17.  Structural analysis of hubs in human NR-RTK network 
Biology Direct  2011;6:49.
Currently a huge amount of protein-protein interaction data is available therefore extracting meaningful ones are a challenging task. In a protein-protein interaction network, hubs are considered as key proteins maintaining function and stability of the network. Therefore, studying protein-protein complexes from a structural perspective provides valuable information for predicted interactions.
In this study, we have predicted by comparative modelling and docking methods protein-protein complexes of hubs of human NR-RTK network inferred from our earlier study. We found that some interactions are mutually excluded while others could occur simultaneously. This study revealed by structural analysis the key role played by Estrogen receptor (ESR1) in mediating the signal transduction between human Receptor Tyrosine kinases (RTKs) and nuclear receptors (NRs).
Although the methods require human intervention and judgment, they can identify the interactions that could occur together or ones that are mutually exclusive. This adds a fourth dimension to interaction network, that of time, and can assist in obtaining concrete predictions consistent with experiments.
Open peer review
This article was reviewed by Dr. Anthony Almudevar, Prof. James Faeder and Prof. Eugene Koonin. For the full reviews, please go to the Reviewers' comments.
PMCID: PMC3220635  PMID: 21974810
18.  Sequence variability of Rhizobiales orthologs and relationship with physico-chemical characteristics of proteins 
Biology Direct  2011;6:48.
Chromosomal orthologs can reveal the shared ancestral gene set and their evolutionary trends. Additionally, physico-chemical properties of encoded proteins could provide information about functional adaptation and ecological niche requirements.
We analyzed 7080 genes (five groups of 1416 orthologs each) from Rhizobiales species (S. meliloti, R. etli, and M. loti, plant symbionts; A. tumefaciens, a plant pathogen; and B. melitensis, an animal pathogen). We evaluated their phylogenetic relationships and observed three main topologies. The first, with closer association of R. etli to A. tumefaciens; the second with R. etli closer to S. meliloti; and the third with A. tumefaciens and S. meliloti as the closest pair. This was not unusual, given the close relatedness of these three species. We calculated the synonymous (dS) and nonsynonymous (dN) substitution rates of these orthologs, and found that informational and metabolic functions showed relatively low dN rates; in contrast, genes from hypothetical functions and cellular processes showed high dN rates. An alternative measure of sequence variability, percentage of changes by species, was used to evaluate the most specific proportion of amino acid residues from alignments. When dN was compared with that measure a high correlation was obtained, revealing that much of evolutive information was extracted with the percentage of changes by species at the amino acid level. By analyzing the sequence variability of orthologs with a set of five properties (polarity, electrostatic charge, formation of secondary structures, molecular volume, and amino acid composition), we found that physico-chemical characteristics of proteins correlated with specific functional roles, and association of species did not follow their typical phylogeny, probably reflecting more adaptation to their life styles and niche preferences. In addition, orthologs with low dN rates had residues with more positive values of polarity, volume and electrostatic charge.
These findings revealed that even when orthologs perform the same function in each genomic background, their sequences reveal important evolutionary tendencies and differences related to adaptation.
This article was reviewed by: Dr. Purificación López-García, Prof. Jeffrey Townsend (nominated by Dr. J. Peter Gogarten), and Ms. Olga Kamneva.
PMCID: PMC3198989  PMID: 21970442
rhizobia; comparative genomics; evolutionary rates; nonsynonymous substitution; adaptation
19.  Biased gene transfer and its implications for the concept of lineage 
Biology Direct  2011;6:47.
PMCID: PMC3191353  PMID: 21943000
20.  A mathematical model for targeting chemicals to tissues by exploiting complex degradation 
Biology Direct  2011;6:46.
In many biological and therapeutic contexts, it is highly desirable to target a chemical specifically to a particular tissue where it exerts its biological effect. In this paper, we present a simple, generic, mathematical model that elucidates a general method for targeting a chemical to particular tissues. The model consists of coupled reaction-diffusion equations to describe the evolution within the tissue of the concentrations of three chemical species: a (concentration of free chemical), b (binding protein) and their complex, c (chemical bound to binding protein). We assume that all species are free to diffuse, and that a and b undergo a reversible reaction to form c. In addition, the complex, c, can be broken down by a process (e.g. an enzyme in the tissue) that results in the release of the chemical, a, which is then free to exert its biological action.
For simplicity, we consider a one-dimensional geometry. In the special case where the rate of complex formation is small (compared to the diffusion timescale of the species within the tissue) the system can be solved analytically. This analytic solution allows us to show how the concentration of free chemical, a, in the tissue can be increased over the concentration of free chemical at the tissue boundary. We show that, under certain conditions, the maximum concentration of a can occur at the centre of the tissue, and give an upper bound on this maximum level. Numerical simulations are then used to determine how the behaviour of the system changes when the assumption of negligible complex formation rate is relaxed.
We have shown, using our mathematical model, how complex degradation can potentially be exploited to target a chemical to a particular tissue, and how the level of the active chemical depends on factors such as the diffusion coefficients and degradation/production rates of each species. The biological significance of these results in terms of potential applications in cartilage tissue engineering and chemotherapy is discussed. In particular, we believe these results may be of use in determining the most promising prodrug candidates.
PMCID: PMC3197567  PMID: 21936951
Solute transport; Tissue; Mathematical model; Prodrug; Insulin-like Growth factor (IGF); proteases
21.  A Rooted Net of Life 
Biology Direct  2011;6:45.
W. Ford Doolittle, Eric Bapteste and Robert Beiko.
PMCID: PMC3189188  PMID: 21936906
22.  Families of transposable elements, population structure and the origin of species 
Biology Direct  2011;6:44.
Eukaryotic genomes harbor diverse families of repetitive DNA derived from transposable elements (TEs) that are able to replicate and insert into genomic DNA. The biological role of TEs remains unclear, although they have profound mutagenic impact on eukaryotic genomes and the origin of repetitive families often correlates with speciation events. We present a new hypothesis to explain the observed correlations based on classical concepts of population genetics.
Presentation of the hypothesis
The main thesis presented in this paper is that the TE-derived repetitive families originate primarily by genetic drift in small populations derived mostly by subdivisions of large populations into subpopulations. We outline the potential impact of the emerging repetitive families on genetic diversification of different subpopulations, and discuss implications of such diversification for the origin of new species.
Testing the hypothesis
Several testable predictions of the hypothesis are examined. First, we focus on the prediction that the number of diverse families of TEs fixed in a representative genome of a particular species positively correlates with the cumulative number of subpopulations (demes) in the historical metapopulation from which the species has emerged. Furthermore, we present evidence indicating that human AluYa5 and AluYb8 families might have originated in separate proto-human subpopulations. We also revisit prior evidence linking the origin of repetitive families to mammalian phylogeny and present additional evidence linking repetitive families to speciation based on mammalian taxonomy. Finally, we discuss evidence that mammalian orders represented by the largest numbers of species may be subject to relatively recent population subdivisions and speciation events.
Implications of the hypothesis
The hypothesis implies that subdivision of a population into small subpopulations is the major step in the origin of new families of TEs as well as of new species. The origin of new subpopulations is likely to be driven by the availability of new biological niches, consistent with the hypothesis of punctuated equilibria. The hypothesis also has implications for the ongoing debate on the role of genetic drift in genome evolution.
This article was reviewed by Eugene Koonin, Juergen Brosius and I. King Jordan.
PMCID: PMC3183009  PMID: 21929767
23.  Expression levels of microRNAs are not associated with their regulatory activities 
Biology Direct  2011;6:43.
MicroRNAs (miRNAs) regulate their targets by triggering mRNA degradation or translational repression. The negative relationship between miRNAs and their targets suggests that the regulatory effect of a miRNA could be determined from the expression levels of its targets. Here, we investigated the relationship between miRNA activities determined by computational programs and miRNA expression levels by using data in which both mRNA and miRNA expression from the same samples were measured. We found that different from the intuitive expectation one might have, miRNA activity shows very weak correlation with miRNA expression, which indicates complex regulating mechanisms between miRNAs and their target genes.
This manuscript was reviewed by an anonymous reviewer and Dr Yuriy Gusev.
PMCID: PMC3189187  PMID: 21929766
MicroRNA; microRNA activity; microRNA expression
24.  Kinetics of the viral cycle influence pharmacodynamics of antiretroviral therapy 
Biology Direct  2011;6:42.
More and more antiretroviral therapies are being developed for treatment of HIV infection. The in-vivo efficacy of these drugs is commonly predicted based on in-vitro measures of antiviral effect. One primary in-vitro measure is the IC50, the amount of drug required for 50% inhibition of viral replication. We have previously shown that HIV life-cycle kinetics impact clinically observed HIV viral dynamics. Here we present a mathematical model of how they affect the pharmacodynamics of antiretroviral drugs.
We find that experimentally measured antiretroviral IC50s are determined by three factors: (i) intrinsic drug properties (e.g. drug-target binding), (ii) kinetics of the HIV life cycle, and (iii) kinetics of drug-inhibited infected cells. Our model predicts that the IC50 is a declining function of the duration of the drug-susceptible stage in the host cell. We combine our model with known viral life-cycle kinetics to derive a measure of intrinsic properties, reflecting drug action, for known antiretroviral drugs from previously measured IC50s. We show that this measure of intrinsic drug property correlates very well with in vitro-measured antiviral activity, whereas experimentally measured IC50 does not.
Our results have implications for understanding pharmacodynamics of and improving activity of antiretroviral drugs. Our findings predict that drug activity can be improved through co-administration of synergistic drugs that delay the viral life cycle but are not inhibitory by themselves. Moreover, our results may easily extend to treatment of other pathogens.
This article was reviewed by Dr. Ruy Ribeiro, Dr. Ha Youn Lee, Dr. Alan Perelson and Dr. Christoph Adami.
PMCID: PMC3203257  PMID: 21910865
HIV; viral dynamics; HAART; antiretroviral therapy; viral life cycle; pharmacodynamics; IC50
25.  The public goods hypothesis for the evolution of life on Earth 
Biology Direct  2011;6:41.
It is becoming increasingly difficult to reconcile the observed extent of horizontal gene transfers with the central metaphor of a great tree uniting all evolving entities on the planet. In this manuscript we describe the Public Goods Hypothesis and show that it is appropriate in order to describe biological evolution on the planet. According to this hypothesis, nucleotide sequences (genes, promoters, exons, etc.) are simply seen as goods, passed from organism to organism through both vertical and horizontal transfer. Public goods sequences are defined by having the properties of being largely non-excludable (no organism can be effectively prevented from accessing these sequences) and non-rival (while such a sequence is being used by one organism it is also available for use by another organism). The universal nature of genetic systems ensures that such non-excludable sequences exist and non-excludability explains why we see a myriad of genes in different combinations in sequenced genomes. There are three features of the public goods hypothesis. Firstly, segments of DNA are seen as public goods, available for all organisms to integrate into their genomes. Secondly, we expect the evolution of mechanisms for DNA sharing and of defense mechanisms against DNA intrusion in genomes. Thirdly, we expect that we do not see a global tree-like pattern. Instead, we expect local tree-like patterns to emerge from the combination of a commonage of genes and vertical inheritance of genomes by cell division. Indeed, while genes are theoretically public goods, in reality, some genes are excludable, particularly, though not only, when they have variant genetic codes or behave as coalition or club goods, available for all organisms of a coalition to integrate into their genomes, and non-rival within the club. We view the Tree of Life hypothesis as a regionalized instance of the Public Goods hypothesis, just like classical mechanics and euclidean geometry are seen as regionalized instances of quantum mechanics and Riemannian geometry respectively. We argue for this change using an axiomatic approach that shows that the Public Goods hypothesis is a better accommodation of the observed data than the Tree of Life hypothesis.
PMCID: PMC3179745  PMID: 21861918

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