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While biological evolution is a well-defined and accepted phenomenon, the notion of conceptual evolution, however implicit in biomedical progress, remains less well-defined and accepted. Frameworks are provided which portray conceptual evolution in terms of the spatio-temporal and hierarchical cognitive embrace of the human external and internal environments.
This article discusses the conceptual basis of the different mechanisms of adaptive evolution. It is argued that only two such mechanisms may conceivably exist, Lamarckism and Darwinism. Darwinism is the fundamental process generating the diversity of species. Some aspects of the gene-centered approach to Darwinism are questioned, since they do not account for the generation of biological diversity. Diversity in biological design must be explained in relation to the diversity of interactions of organisms (or other higher-level units) with their environment. This aspect is usually overlooked in gene-centered views of evolution. A variant of the gene-selectionist approach has been proposed to account for the spread of cultural traits in human societies. Alternatively, I argue that social evolution is rather driven by what I call pseudo-Lamarckian inheritance. Finally, I argue that Lamarckian and pseudo-Lamarckian inheritance are just special cases of faithful replication which are found in the development of some higher-order units, such as multicellular organisms and human societies.
The modern study of human evolution must take into account physical anthropology, which examines phenotypic expression, and molecular evolution, which examines genotypic change. Recent independent investigations have shown that the process of genetic imprinting, defined as parental-dependent transmission of genetic traits, plays a pivotal role in human evolution. We draw on data from various scientific disciplines to support the hypothesis that maternal lineage via preferential genetic contribution, plays a decisive role in this regard. This concept is of more than theoretical interest, in that, current human disease states can be better understood and studied in the context of loss of genetically-defined evolutionary advantage.
Molecular genetics, which has its roots mainly in the development of microbial genetics in the middle of this century, not only greatly facilitates investigations of essential cellular functions, but also offers a means to better understand evolutionary progress. Spontaneous mutagenesis, the driving force of biological evolution, depends on a multitude of mechanistically distinct processes, many of which are already quite well understood. Often, enzymes act as variation generators, and natural gene vectors help to spread functional domains, entire genes and groups of genes across natural isolation barriers. In this overview, particular attention is given to comparing three selected natural strategies for the generation of genetic diversity: nucleotide substitution, DNA rearrangements, and gene acquisition. All of these mechanisms, as well as many others, appear to fulfill their specific roles in microbial evolution. Rather than being the result of an accumulation of errors, biological evolution may depend on a multitude of specific biological functions, as well as on a certain degree of intrinsic structural flexibility of biological molecules.
We have previously demonstrated that the C-terminal regions of the rat and human pancreatic polypeptide (PPP) precursors exhibit a high degree of divergence, whereas the N-terminal regions are highly conserved. This blend of structural conservation and divergence in the precursors appears to be caused by splice junction sliding and translational frameshift in the 3'-region of the PPP gene [Yonekura et al., J. Biol. Chem. 263 (1988) 2990-2997]. In the present study, we determined the nucleotide (nt) sequences of the chicken PPP (cPPP) cDNA and gene, and compared them with those of the mammals. In cPPP, the C-terminal region of the precursor is quite heterologous with respect to the rat (rPPP) and human (hPPP) precursors, and this heterogeneity is accentuated by the large deletion in exon 3 of cPPP. Furthermore, mutational accumulation during evolution caused the structural organization of the 3'-region of cPPP to change; cPPP is terminated in exon 3, whereas rPPP and hPPP are terminated in exon 4. Thus, our previous observation regarding the possibility of 'mosaic evolution' [Yamamoto et al., J. Biol. Chem. 261 (1986) 6156-6159] of PPP has been extended and confirmed by this study. Available evidence suggests that 'mosaic evolution' is a phenomenon unique to PPP, and not to the genes encoding the other members of the PPP family, neuropeptide-Y and peptide-YY.
The insulin-like growth factor binding proteins (IGFBPs) have conserved characteristics of their genomic organization, including similar locations of exon borders relative to nucleotides encoding conserved cysteine residues. Furthermore, the human IGFBP genes, as well as the human homeobox (HOX) genes, are localized to chromosomes 2, 7, 12, and 17. Although little is known about the evolution of the IGFBP genes, the association of human IGFBP and homeobox (HOX) genes at four chromosomal loci may indicate that their ancestral genes were linked prior to the first duplication of chromosomal DNA containing the ancestral HOX cluster. The hypothesis that IGFBPs are ancient proteins is supported by the reported detection of IGFBP activity in serum from the Agnathan species, Geotria australis, a primitive vertebrate. Further studies of IGFBPs in different species are needed to understand the evolution of this protein/gene family. Chicken provides a good intermediate model, since birds diverged from mammals approximately 300 million years ago. A complementary DNA (cDNA) clone encoding chicken insulin-like growth factor binding protein-5 (cIGFBP-5) was isolated. The deduced amino acid sequence is 83% identical to human IGFBP-5 and encodes a mature polypeptide of 251 amino acids. The conservation of IGFBP-5 primary structure across vertebrate species suggests maintenance of important functions during evolution.
The rates and patterns of evolution at silent sites in codons reveal much about the basic features of molecular evolution. Recent increases in the amount of sequence data available for various species and more precise knowledge of the chromosomal locations of those sequences, coming in particular from genome projects, reveal that some features of molecular evolution vary around the genome.
BACKGROUND: Catalytic RNAs, or ribozymes, possessing both a genotype and a phenotype, are ideal molecules for evolution experiments in vitro. A large, heterogeneous pool of RNAs can be subjected to multiple rounds of selection, amplification and mutation, leading to the development of variants that have some desired phenotype. Such experiments allow the investigator to correlate specific genetic changes with quantifiable alterations of the catalytic properties of the RNA. In addition, patterns of evolutionary change can be discerned through a detailed examination of the genotypic composition of the evolving RNA population. RESULTS: Beginning with a pool of 10(13) variants of the Tetrahymena ribozyme, we carried out in vitro evolution experiments that led to the generation of ribozymes with the ability to cleave an RNA substrate in the presence of Ca2+ ions, an activity that does not exist for the wild-type molecule. Over the course of 12 generations, a seven-error variant emerged that has substantial Ca(2+)-dependent RNA-cleavage activity. Advantageous mutations increased in frequency in the population according to three distinct dynamics--logarithmic, linear and transient. Through a comparative analysis of 31 individual variants, we infer how certain mutations influence the catalytic properties of the ribozyme. CONCLUSIONS: In vitro evolution experiments make it possible to elucidate important aspects of both evolutionary biology and structural biochemistry on a reasonable short time scale.
We have cloned a 4-kb region encompassing the Cu,Zn superoxide dismutase (Sod) gene from a genomic library of the Mediterranean fruit fly, Ceratitis capitata, using a cDNA probe from Drosophila melanogaster. The coding sequence of 462 bases is equally as long as that in Drosophila species. The rate of amino acid replacement over the past 100 million years is approximately the same in the Diptera and in mammals, thus excluding the hypothesis (proposed to account for an apparent acceleration in rate of evolution of Sod over geological time) that the evolution of the SOD protein is much higher in the mammals than in other organisms. The coding region is interrupted by two introns in Ceratitis, whereas only one occurs in Drosophila. Phylogenetic comparisons indicate that the second intron was present in the common dipteran ancestor, but was lost shortly after the divergence of the Drosophila lineage from other Diptera. Analysis of the exon/intron structure of Sod in various animal phyla, plants, and fungi indicates that intron insertions as well as deletions have occurred in the evolution of the Sod gene.
Mitochondria are derived from free-living alpha-proteobacteria that were engulfed by eukaryotic host cells through the process of endosymbiosis, and therefore have their own DNA which is organized using basic proteins to form organelle nuclei (nucleoids). Mitochondria divide and are split amongst the daughter cells during cell proliferation. Their division can be separated into two main events: division of the mitochondrial nuclei and division of the matrix (the so-called mitochondrial division, or mitochondriokinesis). In this review, we first focus on the cytogenetical relationships between mitochondrial nuclear division and mitochondriokinesis. Mitochondriokinesis occurs after mitochondrial nuclear division, similar to bacterial cytokinesis. We then describe the fine structure and dynamics of the mitochondrial division ring (MD ring) as a basic morphological background for mitochondriokinesis. Electron microscopy studies first identified a small electron-dense MD ring in the cytoplasm at the constriction sites of dividing mitochondria in the slime mold Physarum polycephalum, and then two large MD rings (with outer cytoplasmic and inner matrix sides) in the red alga Cyanidioschyzon merolae. Now MD rings have been found in all eukaryotes. In the third section, we describe the relationships between the MD ring and the FtsZ ring descended from ancestral bacteria. Other than the GTPase, FtsZ, mitochondria have lost most of the proteins required for bacterial cytokinesis as a consequence of endosymbiosis. The FtsZ protein forms an electron transparent ring (FtsZ or Z ring) in the matrix inside the inner MD ring. For the fourth section, we describe the dynamic association between the outer MD ring with a ring composed of the eukaryote-specific GTPase dynamin. Recent studies have revealed that eukaryote-specific GTPase dynamins form an electron transparent ring between the outer membrane and the MD ring. Thus, mitochondriokinesis is thought to be controlled by a mitochondrial division (MD) apparatus including a dynamic trio, namely the FtsZ, MD and dynamin rings, which consist of a chimera of rings from bacteria and eukaryotes in primitive organisms. Since the genes for the MD ring and dynamin rings are not found in the prokaryotic genome, the host genomes may make these rings to actively control mitochondrial division. In the fifth part, we focus on the dynamic changes in the formation and disassembly of the FtsZ, MD and dynamin rings. FtsZ rings are digested during a later period of mitochondrial division and then finally the MD and dynamin ring apparatuses pinched off the daughter mitochondria, supporting the idea that the host genomes are responsible for the ultimate control of mitochondrial division. We discuss the evolution, from the original vesicle division (VD) apparatuses to VD apparatuses including classical dynamin rings and MD apparatuses. It is likely that the MD apparatuses involving the dynamic trio evolved into the plastid division (PD) apparatus in Bikonta, while in Opisthokonta, the MD apparatus was simplified during evolution and may have branched into the mitochondrial fusion apparatus. Finally, we describe the possibility of intact isolation of large MD/PD apparatuses, the identification of all their proteins and their related genes using C. merolae genome information and TOF-MS analyses. These results will assist in elucidating the universal mechanism and evolution of MD, PD and VD apparatuses.
Respiratory sinus arrhythmia (RSA, or high-frequency heart-rate variability) is frequently employed as an index of cardiac vagal tone or even believed to be a direct measure of vagal tone. However, there are many significant caveats regarding vagal tone interpretation: 1. Respiratory parameters can confound relations between RSA and cardiac vagal tone.2. Although intraindividual relations between RSA and cardiac vagal control are often strong, interindividual associations may be modest.3. RSA measurement is profoundly influenced by concurrent levels of momentary physical activity, which can bias estimation of individual differences in vagal tone.4. RSA magnitude is affected by beta-adrenergic tone.5. RSA and cardiac vagal tone can dissociate under certain circumstances.6. The polyvagal theory contains evolution-based speculations that relate RSA, vagal tone and behavioral phenomena. We present evidence that the polyvagal theory does not accurately depict evolution of vagal control of heart-rate variability, and that it ignores the phenomenon of cardiac aliasing and disregards the evolution of a functional role for vagal control of the heart, from cardiorespiratory synchrony in fish to RSA in mammals. Unawareness of these issues can lead to misinterpretation of cardiovascular autonomic mechanisms. On the other hand, RSA has been shown to often provide a reasonable reflection of cardiac vagal tone when the above-mentioned complexities are considered. Finally, a recent hypothesis is expanded upon, in which RSA plays a primary role in regulation of energy exchange by means of synchronizing respiratory and cardiovascular processes during metabolic and behavioral change.
Progress in miniature chip-design raises demands for implantable power sources in health care applications such as continuous glucose monitoring of diabetic patients. Pioneered by Adam Heller, miniaturized enzymatic biofuel cells (mBCs) convert blood sugars into electrical energy by employing for example glucose oxidase (GOx) on the anode and bilirubin oxidase on the cathode. To match application demands it is crucial to increase lifetime and power output of mBCs. The power output has been limited by the performance of GOx on the anode. We developed a glucose oxidase detection assay (GODA) as medium-throughput screening system for improving GOx properties by directed protein evolution. GODA is a reaction product detection assay based on coupled enzymatic reactions leading to NADPH formation which is recorded at 340 nm. The main advantage of the assay is that it detects the production of d-gluconolactone instead of the side-product hydrogen peroxide and enables to improve bioelectrochemical properties of GOx. For validating the screening system, a mutagenic library of GOx from Aspergillus niger (EC 1.1.3.4) was generated and screened for improved activity using Saccharomyces cerevisiae as host. Directed evolution resulted in a GOx mutant I115V with 1.4-1.5-fold improved activity for beta-d-glucose (Vmax from 7.94 to 10.81 micromol min(-1) mg(-1); Km approximately 19-21 mM) and oxygen consumption kinetics correlate well [Vmax (O2) from 5.94 to 8.34 micromol min(-1) mg(-1); Km (O2) from 700 to 474 microM]. The developed mutagenic protocol and GODA represent a proof-of-principle that GOx can be evolved by directed evolution in S. cerevisiae for putative use in biofuel cells.
Adaptive behavior in unicellular organisms (i.e., bacteria) depends on highly organized networks of proteins governing purposefully the myriad of molecular processes occurring within the cellular system. For instance, bacteria are able to explore the environment within which they develop by utilizing the motility of their flagellar system as well as a sophisticated biochemical navigation system that samples the environmental conditions surrounding the cell, searching for nutrients or moving away from toxic substances or dangerous physical conditions. In this paper we discuss how proteins of the intervening signal transduction network could be modeled as artificial neurons, simulating the dynamical aspects of the bacterial taxis. The model is based on the assumption that, in some important aspects, proteins can be considered as processing elements or McCulloch-Pitts artificial neurons that transfer and process information from the bacterium's membrane surface to the flagellar motor. This simulation of bacterial taxis has been carried out on a hardware realization of a McCulloch-Pitts artificial neuron using an operational amplifier. Based on the behavior of the operational amplifier we produce a model of the interaction between CheY and FliM, elements of the prokaryotic two component system controlling chemotaxis, as well as a simulation of learning and evolution processes in bacterial taxis. On the one side, our simulation results indicate that, computationally, these protein 'switches' are similar to McCulloch-Pitts artificial neurons, suggesting a bridge between evolution and learning in dynamical systems at cellular and molecular levels and the evolutive hardware approach. On the other side, important protein 'tactilizing' properties are not tapped by the model, and this suggests further complexity steps to explore in the approach to biological molecular computing.
This paper continues a theme of exploring algorithms based on principles of biological development for tasks such as pattern generation, machine learning and robot control. Previous work has investigated the use of genes expressed as fractal proteins to enable greater evolvability of gene regulatory networks (GRNs). Here, the evolution of such GRNs is investigated further to determine whether evolution exhibits natural tendencies towards efficiency and graceful degradation of developmental programs. Experiments where "perfect" GRNs are evolved for a further thousand generations without the addition of any further selection pressure, confirm this hypothesis. After further evolution, the perfect GRNs operate in a more efficient manner (using fewer proteins) and show an improved ability to function correctly with missing genes. When the algorithm is applied to applications (e.g. robot control) this equates to efficient and fault-tolerant controllers.
In this study, we review data on the existence of comparable divisions and subdivisions in the telencephalon of different groups of tetrapods based on expression of some developmental regulatory genes, having a particular focus in the comparison of the anuran amphibian Xenopus and the mouse. The available data on Xenopus, mouse, chick and turtle indicate that apparently all tetrapod groups possess the same molecularly distinct divisions and subdivisions in the telencephalon. This basic organization was likely present in the telencephalon of stem tetrapods. Each division/subdivision is characterized by expression of a unique combination of developmental regulatory genes, and appears to represent a self-regulated and topologically constant histogenetic brain compartment that gives rise to specific groups of cells. This interpretation has an important consequence for searching homologies, since a basic condition for cell groups in different vertebrates to be considered homologous is that they originate in the same compartment. However, evolution may allow individual cell groups derived from comparable (field homologous) subdivisions to be either similar or dissimilar across the vertebrate groups, giving rise to several possible scenarios of evolution, which include both the evolutionary conservation of similar (homologous) cells or the production of novel cell groups. Finally, available data in the lamprey, a jawless fish, suggest that not all telencephalic subdivisions were present at the origin of vertebrates, raising important questions about their evolution.
This review summarizes the work from our laboratory investigating mechanisms of opioid analgesia using the Northern grass frog, Rana pipiens. Over the last dozen years, we have accumulated data on the characterization of behavioral effects after opioid administration on radioligand binding by using opioid agonist and antagonist ligands in amphibian brain and spinal cord homogenates, and by cloning and sequencing opioid-like receptor cDNA from amphibian central nervous system (CNS) tissues. The relative analgesic potency of mu, delta, and kappa opioids is highly correlated between frogs and other mammals, including humans. Radioligand binding studies using selective opioid agonists show a similar selectivity profile in amphibians and mammals. In contrast, opioid antagonists that are highly selective for mammalian mu, delta, and kappa opioid receptors were not selective in behavioral and binding studies in amphibians. Three opioid-like receptor cDNAs were cloned and sequenced from amphibian brain tissues and are orthologs to mammalian mu, delta, and kappa opioid receptors. Bioinformatics analysis of the three types of opioid receptor cDNAs from all vertebrate species with full datasets gave a pattern of the molecular evolution of opioid receptors marked by the divergence of mu, delta, and kappa opioid receptor sequences during vertebrate evolution. This divergence in receptor amino acid sequence in later-evolved vertebrates underlies the hypothesis that opioid receptors are more type-selective in mammals than in nonmammalian vertebrates. The apparent order of receptor type evolution is kappa, then delta, and, most recently, the mu opioid receptor. Finally, novel bioinformatics analyses suggest that conserved extracellular receptor domains determine the type selectivity of vertebrate opioid receptors.
The method of minimum evolution reconstructs a phylogenetic tree T for n taxa given dissimilarity data d. In principle, for every tree W with these n leaves an estimate for the total length of W is made, and T is selected as the W that yields the minimum total length. Suppose that the ordinary least-squares formula S(W)(d) is used to estimate the total length of W. A theorem of Rzhetsky and Nei shows that when d is positively additive on a completely resolved tree T, then for all W not =T it will be true that S(W)(d)>S(T)(d). The same will be true if d is merely sufficiently close to an additive dissimilarity function. This paper proves that as n grows large, even if the shortest branch length in the true tree T remains constant and d is additive on T, then the difference S(W)(d) - S(T)(d) can go to zero. It is also proved that, as n grows large, there is a tree T with n leaves, an additive distance function d(T) on T with shortest edge epsilon, a distance function d, and a tree W with the same n leaves such that d differs from d(T) by only approximately epsilon/4, yet minimum evolution incorrectly selects the tree W over the tree T. This result contrasts with the method of neighbor-joining, for which Atteson showed that incorrect selection of W required a deviation at least epsilon/2. It follows that, for large n, minimum evolution with ordinary least-squares can be only half as robust as neighbor-joining.
Comparative physiology traditionally relies on unusual animals to explore the mechanistic basis or evolution of physiological processes. Despite his credentials as a comparative physiologist, much of the recent work by Peter Hochachka relied upon humans as "comparative" models. Technological advances in clinical analyses and expanding databases of genomic diversity have made humans a very "convenient" model to study the evolution of metabolism. For example, a growing number of metabolic diseases have been shown to have a genetic basis. Obesity, type II diabetes, metabolic syndrome X may each have linkages to polymorphisms in genes encoding transcriptional regulators of bioenergetic genes. Genetic polymorphisms and gene families for these important transcription factors inspire questions about the evolution of energy metabolism in other animals. Thus, these biomedical studies provide important direction for researchers interested in exploring the regulatory basis of interspecies variations in bioenergetics.