657 research outputs found
A scaling law of multilevel evolution: how the balance between within- and among-collective evolution is determined
Numerous living systems are hierarchically organised, whereby replicating
components are grouped into reproducing collectives -- e.g., organelles are
grouped into cells, and cells are grouped into multicellular organisms. In such
systems, evolution can operate at two levels: evolution among collectives,
which tends to promote selfless cooperation among components within collectives
(called altruism), and evolution within collectives, which tends to promote
cheating among components within collectives. The balance between within- and
among-collective evolution thus exerts profound impacts on the fitness of these
systems. Here, we investigate how this balance depends on the size of a
collective (denoted by ) and the mutation rate of components () through
mathematical analyses and computer simulations of multiple population genetics
models. We first confirm a previous result that increasing or
accelerates within-collective evolution relative to among-collective evolution,
thus promoting the evolution of cheating. Moreover, we show that when within-
and among-collective evolution exactly balance each other out, the following
scaling relation generally holds: is a constant, where scaling
exponent depends on multiple parameters, such as the strength of
selection and whether altruism is a binary or quantitative trait. This relation
indicates that although and have quantitatively distinct impacts on the
balance between within- and among-collective evolution, their impacts become
identical if is scaled with a proper exponent. Our results thus provide a
novel insight into conditions under which cheating or altruism evolves in
hierarchically-organised replicating systems.Comment: Accepted in Genetics after a minor revision. Revised based on referee
reports. Added results on a binary-trait model. Conclusions do not chang
<Book Reviews>Peter Post, William H. Frederick, Iris Heidebrink, and Shigeru Sato, eds. The Encyclopedia of Indonesia in the Pacific War: In Cooperation with the Netherlands Institute for War Documentation. Leiden: Brill Academic Publishers, 2010, xxix+684p.
Horizontal transfer between loose compartments stabilizes replication of fragmented ribozymes
The emergence of replicases that can replicate themselves is a central issue
in the origin of life. Recent experiments suggest that such replicases can be
realized if an RNA polymerase ribozyme is divided into fragments short enough
to be replicable by the ribozyme and if these fragments self-assemble into a
functional ribozyme. However, the continued self-replication of such replicases
requires that the production of every essential fragment be balanced and
sustained. Here, we use mathematical modeling to investigate whether and under
what conditions fragmented replicases achieve continued self-replication. We
first show that under a simple batch condition, the replicases fail to display
continued self-replication owing to positive feedback inherent in these
replicases. This positive feedback inevitably biases replication toward a
subset of fragments, so that the replicases eventually fail to sustain the
production of all essential fragments. We then show that this inherent
instability can be resolved by small rates of random content exchange between
loose compartments (i.e., horizontal transfer). In this case, the balanced
production of all fragments is achieved through negative frequency-dependent
selection operating in the population dynamics of compartments. This selection
mechanism arises from an interaction mediated by horizontal transfer between
intracellular and intercellular symmetry breaking. The horizontal transfer also
ensures the presence of all essential fragments in each compartment, sustaining
self-replication. Taken together, our results underline compartmentalization
and horizontal transfer in the origin of the first self-replicating replicases.Comment: 14 pages, 4 figures, and supplemental materia
Metallosupramolecular Structures Derived from a Series of Diphosphine-bridged Digold (I) Metalloligands with Terminal D-Penicillamine
This is the accepted version of the following article: N. Yoshinari and T. Konno, "Metallosupramolecular Structures Derived from a Series of Diphosphine-bridged Digold(I) Metalloligands with Terminal d-Penicillamine," Chem. Rec., 16(3), 1647–1663, John Wiley & Sons, 2016, which has been published in final form at http://dx.doi.org/10.1002/tcr.201600026. This article may be used for non-commercial purposes in accordance with the Wiley Self-Archiving Policy
Development of a multipurpose hand controller for JEMRMS
A prototype multipurpose hand controller for the JEMRMS (Japanese Experiment Module Remote Manipulator System) was developed. The hand controller (H/C) is an orthogonal type, with 6 degrees of freedom (DOF) and small size. The orthogonal type H/C is very simple for coordinate transformations and can easily control any type of manipulators. In fact, the JEMRMS is planned to have two manipulators controlled by a common H/C at this stage. The H/C was able to be used as a rate control joystick and a force reflection master arm, using an experimental 6 DOF manipulator. Good maneuverability was confirmed in the verification test. The orthogonal type H/C is suitable for use as a common H/C for the two manipulators of the JEMRMS
Error-threshold exists in fitness landscapes with lethal mutants
BACKGROUND: One of the important insights of quasi-species theory is an error-threshold. The error-threshold is the error rate of replication above which the sudden onset of the population delocalization from the fittest genotype occurs despite Darwinian selection; i.e., the break down of evolutionary optimization. However, a recent article by Wilke in this journal, after reviewing the previous studies on the error-threshold, concluded that the error-threshold does not exist if lethal mutants are taken into account in a fitness landscape. Since lethal mutants obviously exist in reality, this has a significant implication about biological evolution. However, the study of Wagner and Krall on which Wilke's conclusion was based considered mutation-selection dynamics in one-dimensional genotype space with the assumption that a genotype can mutate only to an adjoining genotype in the genotype space. In this article, we study whether the above conclusion holds in high-dimensional genotype space without the assumption of the adjacency of mutations, where the consequences of mutation-selection dynamics can be qualitatively different. RESULTS: To examine the effect of mutant lethality on the existence of the error-threshold, we extend the quasi-species equation by taking the lethality of mutants into account, assuming that lethal genotypes are uniformly distributed in the genotype space. First, with the simplification of neglecting back mutations, we calculate the error-threshold as the maximum allowable mutation rate for which the fittest genotype can survive. Second, with the full consideration of back mutations, we study the equilibrium population distribution and the ancestor distribution in the genotype space as a function of error rate with and without lethality in a multiplicative fitness landscape. The results show that a high lethality of mutants actually introduces an error-threshold in a multiplicative fitness landscape in sharp contrast to the conclusion of Wilke. Furthermore, irrespective of the lethality of mutants, the delocalization of the population from the fittest genotype occurs for an error rate much smaller than random replication. Finally, the results are shown to extend to a system of finite populations. CONCLUSION: High lethality of mutants introduces an error-threshold in a multiplicative fitness landscape. Furthermore, irrespective of the lethality of mutants, the break down of evolutionary optimization happens for an error rate much smaller than random replication
A histochemical study on hydrolytic and oxidative enzymes in human sarcomas
Histochemical evaluations of human sarcomas such as reticulum cell sarcoma, fibrosarcoma, lymphosarcoma and neurofibrosarcoma, were carried out with five hydrolytic enzymes and eight oxidative enzymes. The activities of acid phosphatase and beta-glucuronidase were slightly positive in the neoplastic cells observed. Beta-esterase activity was also positive but varied according to the kind of sarcomas. Alkaline phosphatase activity was faint or negative in sarcoma cells, though positive in capillary walls. Leucine aminopeptidase activity was negative giving not any appreciable coloration of the cell as far as the method employed is concerned. Among the activities of dehydrogenases, the most intense activity was observed in lactic dehydrogenase. The activities of succinic and beta-hydroxybutyric dehydrogenases were slight. The activities of alpha-glycerophosphate, glutamic and betahydroxybutyric
dehydrogenases were faint or slight. The activities of NADPlinked dehydrogenases, glucose-6-phosphate and isocitric dehydrogenase were all faint or slight in these sarcoma cells.</p
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