arXiv subjects

Nobuto Takeuchi

Publications and source records attributed to Nobuto Takeuchi.

6 recordsLinked to original sources

arXiv2025

Generalising the Central Dogma as a cross-hierarchical principle of biology

The Central Dogma of molecular biology, as originally proposed by Crick, asserts that information passed into protein cannot flow back out. This principle has been interpreted as underpinning modern understandings of heredity and evolution, implying the unidirectionality of information flow from nucleic acids to proteins. Here, we propose a generalisation of the Central Dogma as a division of labour between the transmission and expression of information: the transmitter (nucleic acids) perpetuates information across generations, whereas the expressor (protein) enacts this information to facilitate the transmitter's function without itself perpetuating information. We argue that this generalisation offers two benefits. First, it provides a unifying perspective for comparing the Central Dogma to analogous divisions of labour observed at vastly different biological scales, including multicellular organisms, eukaryotic cells, organelles, and bacteria. Second, it offers a theoretical framework to explain the Central Dogma as an outcome of evolution. Specifically, we review a mathematical model suggesting that the Central Dogma originates through spontaneous symmetry breaking driven by evolutionary conflicts between different levels of selection. By reframing the Central Dogma as an informational relationship between components of a system, this generalisation underscores its broader relevance across the biological hierarchy and sheds light on its evolutionary origin.

q-bio.PE↗

arXiv2025

Cell differentiation can underpin the reproducibility of morphogenesis

Morphogenesis of complex body shapes is reproducible despite the noise inherent in the underlying morphogenetic processes. However, how these morphogenetic processes work together to achieve this reproducibility remains unclear. Here, we ask how morphogenetic reproducibility is realised by developing a computational model that evolves complex morphologies. We find that evolved, complex morphologies are reproducible in a sizeable fraction of simulations, despite no direct selection for reproducibility. We show that high reproducibility is caused by segregating moving cells that "shape" morphologies from stationary cells that "maintain" morphologies during morphogenesis. Strikingly, most highly reproducible morphologies also evolved cell differentiation, where proliferative, moving stem cells (i.e., progenitor cells) irreversibly differentiate into non-dividing, stationary differentiated cells. These results suggest that cell differentiation observed in natural development plays a fundamental role in morphogenesis in addition to the production of specialised cell types. This previously-unrecognised role of cell differentiation has major implications for our understanding of how morphologies are generated and regenerated.

q-bio.CB↗

arXiv2021

Error Catastrophe Can Be Avoided by Proofreading Innate to Template-Directed Polymerization

An important issue for the origins of life is ensuring the accurate maintenance of information in replicating polymers in the face of inevitable errors. Here, we investigated how this maintenance depends on reaction kinetics by incorporating the elementary steps of polymerization into the population dynamics of polymers. We found that template-directed polymerization entails an inherent error-correction mechanism akin to kinetic proofreading, generating long polymers that are more tolerant to an error catastrophe. Because this mechanism does not require enzymes, it is likely to operate under broad prebiotic conditions.

physics.bio-ph↗

arXiv2020

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 $N$) and the mutation rate of components ($m$) through mathematical analyses and computer simulations of multiple population genetics models. We first confirm a previous result that increasing $N$ or $m$ 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: $Nm^{\alpha}$ is a constant, where scaling exponent $\alpha$ depends on multiple parameters, such as the strength of selection and whether altruism is a binary or quantitative trait. This relation indicates that although $N$ and $m$ have quantitatively distinct impacts on the balance between within- and among-collective evolution, their impacts become identical if $m$ 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.

q-bio.PE↗

arXiv2019

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.

q-bio.CB↗

arXiv2017

Stronger selection can slow down evolution driven by recombination on a smooth fitness landscape

Stronger selection implies faster evolution---that is, the greater the force, the faster the change. This apparently self-evident proposition, however, is derived under the assumption that genetic variation within a population is primarily supplied by mutation (i.e.\ mutation-driven evolution). Here, we show that this proposition does not actually hold for recombination-driven evolution, i.e.\ evolution in which genetic variation is primarily created by recombination rather than mutation. By numerically investigating population genetics models of recombination, migration and selection, we demonstrate that stronger selection can slow down evolution on a perfectly smooth fitness landscape. Through simple analytical calculation, this apparently counter-intuitive result is shown to stem from two opposing effects of natural selection on the rate of evolution. On the one hand, natural selection tends to increase the rate of evolution by increasing the fixation probability of fitter genotypes. On the other hand, natural selection tends to decrease the rate of evolution by decreasing the chance of recombination between immigrants and resident individuals. As a consequence of these opposing effects, there is a finite selection pressure maximizing the rate of evolution. Hence, stronger selection can imply slower evolution if genetic variation is primarily supplied by recombination.

q-bio.PE↗