Publishing type：Research paper (scientific journal)  

The preferred conditions for evolutionary innovation represent a fundamental
question, but little is known experimentally or theoretically. In this study,
we focused on the potential role of polyploidy in the evolution of novel
traits. We proposed a simple model and demonstrated that the evolutionary rate
of polyploids is similar to more much slower than that of haploids under
neutral selection or during gradual evolution. However, experiments using
polyploid cyanobacteria demonstrated that the probability of achieving
antibiotic resistance increased with the number of chromosomes and implied an
optimal number of chromosomes. Then, we investigated the dynamics of the same
model on a fitness landscape in which cells should jump over a lethal valley to
increase their fitness. The evolutionary rate could be increased in polyploidy,
and the optimal number of chromosomes was identified. Further, we proposed that
the optimization for evolutionary innovation might determine the number of
chromosomes in polyploid bacteria.

DOI： 10.1103/PRXLife.2.043021

arXiv

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Other Link： http://arxiv.org/pdf/2211.00581v1

Publishing type：Research paper (scientific journal)  

DOI： 10.1103/PhysRevResearch.6.L022024

Scopus

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Publishing type：Research paper (scientific journal)   Publisher：American Physical Society (APS)  

DOI： 10.1103/physrevlett.131.028401

PubMed

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Other Link： http://harvest.aps.org/v2/journals/articles/10.1103/PhysRevLett.131.028401/fulltext

Publishing type：Research paper (scientific journal)   Publisher：Public Library of Science (PLoS)  

In physics of living systems, a search for relationships of a few macroscopic variables that emerge from many microscopic elements is a central issue. We evolved gene regulatory networks so that the expression of core genes (partial system) is insensitive to environmental changes. Then, we found the expression levels of the remaining genes autonomously increase to provide a plastic (sensitive) response. A feedforward structure from the non-core to core genes evolved autonomously. Negative proportionality was observed between the average changes in core and non-core genes, reflecting reciprocity between the macroscopic robustness of homeostatic genes and plasticity of regulator genes. The proportion coefficient between those genes is represented by their number ratio, as in the “lever principle”, whereas the decrease in the ratio results in a transition from perfect to partial adaptation, in which only a portion of the core genes exhibits robustness against environmental changes. This reciprocity between robustness and plasticity was satisfied throughout the evolutionary course, imposing an evolutionary constraint. This result suggests a simple macroscopic law for the adaptation characteristic in evolved complex biological networks.

DOI： 10.1371/journal.pone.0277181

PubMed

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Publishing type：Research paper (scientific journal)   Publisher：Biophysical Society of Japan  

DOI： 10.2142/biophys.63.316

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Publishing type：Research paper (scientific journal)   Publisher：Public Library of Science (PLoS)  

Cellular adaptation to stressful environments such as starvation is essential to the survival of microbial communities, but the uniform response of the cell community may lead to entire cell death or severe damage to their fitness. Here, we demonstrate an elaborate response of the yeast community against glucose depletion, in which the first adapted cells kill the latecomer cells. During glucose depletion, yeast cells release autotoxins, such as leucic acid and L-2keto-3methylvalerate, which can even kill the clonal cells of the ones producing them. Although these autotoxins were likely to induce mass suicide, some cells differentiated to adapt to the autotoxins without genetic changes. If nondifferentiated latecomers tried to invade the habitat, autotoxins damaged or killed the latecomers, but the differentiated cells could selectively survive. Phylogenetically distant fission and budding yeast shared this behavior using the same autotoxins, suggesting that latecomer killing may be the universal system of intercellular communication, which may be relevant to the evolutional transition from unicellular to multicellular organisms.

DOI： 10.1371/journal.pbio.3001844

PubMed

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Publishing type：Research paper (scientific journal)   Publisher：American Physical Society ({APS})  

DOI： 10.1103/PhysRevResearch.4.L022008

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Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

Abstract

Metabolic behaviours of proliferating cells are often explained as a consequence of rational optimization of cellular growth rate, whereas microeconomics formulates consumption behaviours as optimization problems. Here, we pushed beyond the analogy to precisely map metabolism onto the theory of consumer choice. We thereby revealed the correspondence between long-standing mysteries in both fields: the Warburg effect, a seemingly wasteful but ubiquitous strategy where cells favour aerobic glycolysis over more energetically efficient oxidative phosphorylation, and Giffen behaviour, the unexpected consumer behaviour where a good is demanded more as its price rises. We identified the minimal, universal requirements for the Warburg effect: a trade-off between oxidative phosphorylation and aerobic glycolysis and complementarity, i.e. impossibility of substitution for different metabolites. Thus, various hypotheses for the Warburg effect are integrated into an identical optimization problem with the same universal structure. Besides, the correspondence between the Warburg effect and Giffen behaviour implies that oxidative phosphorylation is counter-intuitively stimulated when its efficiency is decreased by metabolic perturbations such as drug administration or mitochondrial dysfunction; the concept of Giffen behaviour bridges the Warburg effect and the reverse Warburg effect. This highlights that the application of microeconomics to metabolism can offer new predictions and paradigms for both biology and economics.

DOI： 10.1007/s11538-021-00952-x

PubMed

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Other Link： https://link.springer.com/article/10.1007/s11538-021-00952-x/fulltext.html

Publisher：Cold Spring Harbor Laboratory  

When organisms face crises, such as starvation, every individual should adapt to environmental changes (1, 2), or the community alters their behaviour (3–5). Because a stressful environment reduces the carrying capacity (6), the population size of unicellular organisms shrinks in such conditions (7, 8). However, the uniform stress response of the cell community may lead to overall extinction or severely damage their entire fitness. How microbial communities accommodate this dilemma remains poorly understood. Here, we demonstrate an elaborate strategy of the yeast community against glucose starvation, named the voluntary triage. During starvation, yeast cells release some autotoxins, such as leucic acid and L-2keto-3methylvalerate, which can even kill the cells producing them. Although it may look like mass suicide at first glance, cells use epigenetic “tags” to adapt to the autotoxin inheritably. If non-tagged latecomers, regardless of whether they are closely related, try to invade the habitat, autotoxins kill them and inhibit their growth, but the tagged cells can selectively survive. Phylogenetically distant fission and budding yeast (9) share this strategy using the same autotoxins, which implies that the universal system of voluntary triage may be relevant to the major evolutional transition from unicellular to multicellular organisms (10).

DOI： 10.1101/2020.10.17.344093

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Publishing type：Research paper (scientific journal)  

DOI： 10.1101/2020.06.12.148304

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Publishing type：Research paper (scientific journal)  

DOI： 10.1103/PhysRevResearch.2.012005

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Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1128/mBio.00510-19

Web of Science

PubMed

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Publishing type：Research paper (scientific journal)  

DOI： 10.1371/journal.pcbi.1005847

Web of Science

PubMed

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Publishing type：Research paper (scientific journal)  

DOI： 10.1103/physreve.95.030201

Web of Science

PubMed

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Other Link： http://harvest.aps.org/v2/journals/articles/10.1103/PhysRevE.95.030201/fulltext

Publishing type：Research paper (scientific journal)  

DOI： 10.1371/journal.pcbi.1005434

Web of Science

PubMed

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Publishing type：Research paper (scientific journal)  

DOI： 10.1103/physrevlett.115.218101

Web of Science

PubMed

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Other Link： http://harvest.aps.org/v2/journals/articles/10.1103/PhysRevLett.115.218101/fulltext

Publishing type：Research paper (scientific journal)  

DOI： 10.1371/journal.pcbi.1003784

Web of Science

PubMed

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Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.febslet.2014.05.015

Web of Science

PubMed

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Publishing type：Research paper (scientific journal)  

DOI： 10.1073/pnas.1120711109

Web of Science

PubMed

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Publishing type：Research paper (scientific journal)  

DOI： 10.1073/pnas.1019612108

Web of Science

PubMed

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J-GLOBAL

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Language：Japanese   Publisher：The Biophysical Society of Japan General Incorporated Association  

<p>Robustness and plasticity are important characteristics common to a variety of biological systems and have attracted much attention not only from biologists but also from physicists interested in biosystems. Whereas robustness concerns insensitivity to perturbations against external changes, plasticity concerns changeability upon external inputs. How these two properties are compatible with each other is an important question to be addressed. Recently we have uncovered universal reciprocity relationship between the robustness of period and plasticity of phase in biochemical oscillators such as circadian clocks. We review this relationship and discuss its theoretical origin and biological relevance.</p>

DOI： 10.2142/biophys.57.186

J-GLOBAL

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Language：Japanese   Publisher：The Physical Society of Japan (JPS)  

CiNii Books

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Language：Japanese  

J-GLOBAL

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