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Given the ubiquitous nature of love, numerous theories have been proposed to explain its existence. One such theory refers to love as a commitment device, suggesting that romantic love evolved to foster commitment between partners and enhance their reproductive success. In the present study, we investigated this hypothesis using a large-scale sample of 86,310 individual responses collected across 90 countries. If romantic love is universally perceived as a force that fosters commitment between long-term partners, we expected that individuals likely to suffer greater losses from the termination of their relationships-including people of lower socioeconomic status, those with many children, and women-would place a higher value on romantic love compared to people with higher status, those with fewer children, and men. These predictions were supported. Additionally, we observed that individuals from countries with a higher (vs. lower) Human Development Index placed a greater level of importance on romantic love, suggesting that modernization might influence how romantic love is evaluated. On average, participants worldwide were unwilling to commit to a long-term romantic relationship without love, highlighting romantic love's universal importance., Competing Interests: Declarations. Ethics Statement and Informed Consent: The study’s procedure received approval from the first author’s Institutional Review Board (IRB) at the Institute of Psychology, University of Wrocław. Before collecting data, all team members either received ethical approval from their local IRBs or acted on the ethical approval of the first author’s IRB. All participants provided informed consent prior to participating in the survey. Conflict of Interest: The authors declare that they have no conflict of interest., (© 2024. The Author(s).)

Misinformation represents an evolutionary paradox: despite its harmful impact on society, it persists and evolves, thriving in the information-rich environment of the digital age. This paradox challenges the conventional expectation that detrimental entities should diminish over time. The persistence of misinformation, despite advancements in fact-checking and verification tools, suggests that it possesses adaptive qualities that enable it to survive and propagate. This paper explores how misinformation, as a blend of truth and fiction, continues to resonate with audiences. The role of narratives in human history, particularly in the evolution of Homo narrans, underscores the enduring influence of storytelling on cultural and social cohesion. Despite the increasing ability of individuals to verify the accuracy of sources, misinformation remains a significant challenge, often spreading rapidly through digital platforms. Current behavioral research tends to treat misinformation as completely irrational, static, finite entities that can be definitively debunked, overlooking their dynamic and evolving nature. This approach limits our understanding of the behavioral and societal factors driving the transformation of misinformation over time. The persistence of misinformation can be attributed to several factors, including its role in fostering social cohesion, its perceived short-term benefits, and its use in strategic deception. Techniques such as extrapolation, intrapolation, deformation, cherry-picking, and fabrication contribute to the production and spread of misinformation. Understanding these processes and the evolutionary advantages they confer is crucial for developing effective strategies to counter misinformation. By promoting transparency, critical thinking, and accurate information, society can begin to address the root causes of misinformation and create a more resilient information environment., (©Nicola Luigi Bragazzi, Sergio Garbarino. Originally published in JMIR Infodemiology (https://infodemiology.jmir.org), 27.12.2024.)

Supergenes are genetic architectures resulting in the segregation of alternative combinations of alleles underlying complex phenotypes. The co-segregation of alleles at linked loci is often facilitated by polymorphic chromosomal rearrangements suppressing recombination locally. Supergenes are involved in many complex polymorphisms, including sexual, colour or behavioural polymorphisms in numerous plants, fungi, mammals, fish, and insects. Despite a long history of empirical and theoretical research, the formation of supergenes remains poorly understood. Here, using a two-island population genetic model, we explore how gene flow and the evolution of overdominant chromosomal inversions may jointly lead to the formation of supergenes. We show that the evolution of inversions in differentiated populations, both under disruptive selection, leads to an increase in frequency of poorly adapted, immigrant haplotypes. Indeed, rare allelic combinations, such as immigrant haplotypes, are more frequently reshuffled by recombination than common allelic combinations, and therefore benefit from the recombination suppression generated by inversions. When an inversion capturing a locally adapted haplotype spreads but is associated with a fitness cost hampering its fixation (e.g. a recessive mutation load), the maintenance of a non-inverted haplotype in the population is enhanced; under certain conditions, the immigrant haplotype persists alongside the inverted local haplotype, while the standard local haplotype disappears. This establishes a stable, local polymorphism with two non-recombining haplotypes encoding alternative adaptive strategies, that is, a supergene. These results bring new light to the importance of local adaptation, overdominance, and gene flow in the formation of supergenes and inversion polymorphisms in general., (© 2024 John Wiley & Sons Ltd.)

Infinitely many distinct trait values may arise in populations bearing quantitative traits, and modeling their population dynamics is thus a formidable task. While classical models assume fixed or infinite population size, models in which the total population size fluctuates due to demographic noise in births and deaths can behave qualitatively differently from constant or infinite population models due to density-dependent dynamics. In this paper, I present a stochastic field theory for the eco-evolutionary dynamics of finite populations bearing one-dimensional quantitative traits. I derive stochastic field equations that describe the evolution of population densities, trait frequencies, and the mean value of any trait in the population. These equations recover well-known results such as the replicator-mutator equation, Price equation, and gradient dynamics in the infinite population limit. For finite populations, the equations describe the intricate interplay between natural selection, noise-induced selection, eco-evolutionary feedback, and neutral genetic drift in determining evolutionary trajectories. My work uses ideas from statistical physics, calculus of variations, and SPDEs, providing alternative methods that complement the measure-theoretic martingale approach that is more common in the literature., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author. Published by Elsevier Inc. All rights reserved.)

Human fascination with art has deep evolutionary roots, yet its role remains a puzzle for evolutionary theory. Although its widespread presence across cultures suggests a potential adaptive function, determining its evolutionary origins requires more comprehensive evidence beyond mere universality or assumed survival benefits. This paper introduces and tests the Collector Hypothesis, which suggests that artworks serve as indicators of collectors' surplus wealth and social status, offering greater benefits to collectors than to artists in mating and reproductive contexts. Our study among Indigenous Papuan communities provides preliminary support for the Collector Hypothesis, indicating that, compared to artists, collectors are perceived as having higher social status and greater attractiveness to women. These findings provide unique insights into Papuan communities and contribute to the ongoing discussion about art's adaptive significance of art by suggesting that artistic capacities may benefit not only creators but also those who accumulate and display art. Further research in diverse cultural contexts is needed for a comprehensive understanding of this interplay., Competing Interests: Declarations Ethics approval and consent to participate The Institutional Ethics Committee at the University of Wroclaw approved the study’s protocols and gave ethical approval for conducting the study. The local community leaders also approved the study. Conflict of Interest Authors declare no conflict of interest., (© 2024. The Author(s).)

The biopsychosocial model remains a key paradigm for healthcare, despite widely recognised scientific and philosophical shortcomings. Here we report on recent updates integrating evolutionary theory with the biopsychosocial model to provide a more comprehensive and scientifically complete approach to understanding the multiple relevant levels of causation of medical and psychiatric problems.

In the article, mainly based on the reference to the entries in the diary of Th. Dobzhansky, a geneticist and one of the founders of the "synthetic theory of evolution", examines how Dobzhansky tried to combine science, primarily evolutionary theory, and religion. It is argued that although Dobxzhansky was a believer during whole his life, he became a peculiar believer who revised for himself and for others the former, primarily religious answers to the "ultimate questions" of existence, and posed these questions in a new, evolutionary way. Even more, he tried to substantiate and justify religion and his belief in God through the evolutionary theory, to demonstrate that science and religion are not incompatible, and to offer his believe in the usefulness of science and religion to each other. This Dobzhansky's attempt was perceived and evaluated ambiguously by both scientists and religious figures. In addition, Dobzhansky owing to his search for these answers, made a number of world outlook and general cultural conclusions for himself and presented these conclusions in articles and books written not only for colleagues in the scientific community, but also for other people., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Whole-genome duplication (polyploidy) poses many complications but is an important driver for eukaryotic evolution. To experimentally study how many challenges from the cellular (including gene expression) to the life history levels are overcome in polyploid evolution, a system in which polyploidy can be reliably induced and sustained over generations is crucial. Until now, this has not been possible with animals, as polyploidy notoriously causes first-generation lethality. The parasitoid wasp Nasonia vitripennis emerges as a stunningly well-suited model. Polyploidy can be induced in this haplodiploid system through (1) silencing genes in the sex determination cascade and (2) by colchicine injection to induce meiotic segregation failure. Nasonia polyploids produce many generations in a short time, making them a powerful tool for experimental evolution studies. The strong variation observed in Nasonia polyploid phenotypes aids the identification of polyploid mechanisms that are the difference between evolutionary dead ends and successes. Polyploid evolution research benefits from decades of Nasonia research that produced extensive reference-omics data sets, facilitating the advanced studies of polyploid effects on the genome and transcriptome. It is also possible to create both inbred lines (to control for genetic background effects) and outbred lines (to conduct polyploid selection regimes). The option of interspecific crossing further allows to directly contrast autopolyploidy (intraspecific polyploidy) to allopolyploidy (hybrid polyploidy). Nasonia can also be used to investigate the nascent field of using polyploidy in biological control to improve field performance and lower ecological risk. In short, Nasonia polyploids are an exceptional tool for researching various biological paradigms., Competing Interests: We have no conflict of interest to declare., (© 2024 The Author(s). Evolutionary Applications published by John Wiley & Sons Ltd.)

Pairwise host-parasite relationships are typically embedded in broader networks of ecological interactions, which have the potential to shape parasite evolutionary trajectories. Understanding this 'community context' of pathogen evolution is vital for wildlife, agricultural and human systems alike, as pathogens typically infect more than one host-and these hosts may have independent ecological relationships. Here, we introduce an eco-evolutionary model examining ecological feedback across a range of host-host interactions. Specifically, we analyse a model of the evolution of virulence of a parasite infecting two hosts exhibiting competitive, mutualistic or exploitative relationships. We first find that parasite specialism is necessary for inter-host interactions to impact parasite evolution. Furthermore, we find generally that increasing competition between hosts leads to higher shared parasite virulence while increasing mutualism leads to lower virulence. In exploitative host-host interactions, the particular form of parasite specialization is critical-for instance, specialization in terms of onward transmission, host tolerance or intra-host pathogen growth rate lead to distinct evolutionary outcomes under the same host-host interactions. Our work provides testable hypotheses for multi-host disease systems, predicts how changing interaction networks may impact virulence evolution and broadly demonstrates the importance of looking beyond pairwise relationships to understand evolution in realistic community contexts.

Background: Social anxiety (SA) is characterized by concerns about the expected occurrence (probability) and anticipated distress (cost) of social threats. Unclear is whether SA correlates specifically with biased expectations of belongingness or status threats., Aims: We aimed to discern if SA is uniquely tied to biased expectancies of either belongingness or status threats., Materials and Methods: We assessed 757 participants' perceptions of exclusion and put-down scenarios, analysing associations between SA and threat perceptions., Discussion: Our findings support the status-sensitivity hypothesis, suggesting individuals with high SA are particularly attuned to the perceived cost of status threats, potentially informing treatment approaches., Conclusion: Understanding SA's link to status concerns enhances therapeutic strategies, emphasizing the need to address status-related situations, cognitions, and emotions in interventions., (© 2024 The Authors. British Journal of Clinical Psychology published by John Wiley & Sons Ltd on behalf of British Psychological Society.)

RNA and protein expressed from the same gene can have diverse isoforms due to various post-transcriptional and post-translational modifications. For the vast majority of alternative isoforms, It is unknown whether they are adaptive or simply biological noise. As we cannot experimentally probe the function of each isoform, we can ask whether the distribution of isoforms across genes and across species is consistent with expectations from different evolutionary processes. However, there is currently no theoretical framework that can generate such predictions. To address this, we developed a mathematical model where isoform abundances are determined collectively by cis -acting loci, trans -acting factors, gene expression levels, and isoform decay rates to predict isoform abundance distributions across species and genes in the face of mutation, genetic drift, and selection. We found that factors beyond selection, such as effective population size and the number of cis -acting loci, significantly influence evolutionary outcomes. Notably, suboptimal phenotypes are more likely to evolve when the population is small and/or when the number of cis -loci is large. We also explored scenarios where modification processes have both beneficial and detrimental effects, revealing a non-monotonic relationship between effective population size and optimization, demonstrating how opposing selection pressures on cis - and trans -acting loci can constrain the optimization of gene product diversity. As a demonstration of the power of our theory, we compared the expected distribution of A-to-I RNA editing levels in coleoids and found this to be largely consistent with non-adaptive explanations.

Plus, minus, and double-strand RNA viruses are all found in nature. We use computational models to study the relative success of these strategies. We consider translation, replication, and virion assembly inside one cell, and transmission of virions between cells. For viruses which do not incorporate a polymerase in the capsid, transmission of only plus strands is the default strategy because virions containing minus strands are not infectious. Packaging only plus strands has a significant advantage if the number of RNA strands produced per cell is larger than the number of capsids. In this case, by not packaging minus strands, the virus produces more plus-strand virions. Therefore, plus-strand viruses are selected at low multiplicity of infection. However, at high multiplicity of infection, it is preferable to package both strands because the additional minus virions produced are helpful when there are multiple infections per cell. The fact that plus-strand viruses are widespread while viruses that package both strands are not seen in nature suggests that RNA strands are indeed produced in excess over capsids, and that the multiplicity of infection is not sufficiently high to favor the production of both kinds of virions. For double-strand viruses, we show that it is advantageous to produce only plus strands from the double strand within the cell, as is observed in real viruses. The reason for the success of minus-strand viruses is more puzzling initially. For viruses that incorporate a polymerase in the virion, minus virions are infectious. However, this is not sufficient to explain the success of minus-strand viruses, because in this case, viruses that package both strands outcompete those that package only minus or only plus. Real minus-strand viruses make use of replicable strands that are coated by a nucleoprotein, and separate translatable plus strands that are uncoated. Here we show that when there are distinct replicable and translatable strands, minus-strand viruses are selected.

Organisms gain by anticipating future changes in the environment. Those environmental changes often follow stochastic trends. The steeper the slope of the trend, the more likely the trend's momentum carries the future trend in the same direction. This article presents a simple biological circuit that measures the momentum, providing a prediction about future trend. The circuit calculates the momentum by the difference between a short-term and a long-term exponential moving average. The time lengths of the two moving averages can be adjusted by changing the decay rates of state variables. Different time lengths for those averages trade off between errors caused by noise and errors caused by lags in predicting a change in the direction of the trend. Prior studies have emphasized circuits that make similar calculations about trends. However, those prior studies embedded their analyses in the details of particular applications, obscuring the simple generality and wide applicability of the approach. The model here contributes to the topic by clarifying the great simplicity and generality of anticipation for stochastic trends. This article also notes that, in financial analysis, the difference between moving averages is widely used to predict future trends in asset prices. The financial measure is called the moving average convergence-divergence indicator. Connecting the biological problem to financial analysis opens the way for future studies in biology to exploit the variety of highly developed trend models in finance., (© The Author(s) 2024. Published by Oxford University Press on behalf of The Society for the Study of Evolution (SSE) and European Society for Evolutionary Biology (ESEN).)

Evolutionary biology provides a unifying theory for testing hypotheses about the relationship between hormones and person perception. Person perception usually receives attention from the perspective of sexual selection. However, because person perception is one trait in a suite regulated by hormones, univariate approaches are insufficient. In this Perspectives article, quantitative genetics is presented as an important but underutilized framework for testing evolutionary hypotheses within this literature. We note tacit assumptions within the current literature on psychiatric genetics, which imperil the interpretation of findings thus far. As regulators of a diverse manifold of traits, hormones mediate tradeoffs among an array of functions. Hormonal pleiotropy also provides the basis of correlational selection, a process whereby selection on one trait in a hormone-mediated suite generates selection on the others. This architecture provides the basis for conflicts between sexual and natural selection within hormone-mediated suites. Due to its role in person perception, psychiatric disorders, and reproductive physiology, the sex hormone estrogen is highlighted as an exemplar here. The implications of this framework for the evolution of person perception are discussed. Empirical quantification of selection on traits within hormone-mediated suites remains an important gap in this literature with great potential to illuminate the fundamental nature of psychiatric disorders., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Gurguis, Kimm and Pigott.)

With the rapid evolution of SARS-CoV-2, the emergence of new strains is an intriguing question. This paper presents an evolutionary theory to analyze the mutations of the virus and identify the conditions that lead to the generation of new strains. We represent the virus variants using a 4-letter sequence based on amino acid mutations on the spike protein and employ an n-distance algorithm to derive a variant phylogenetic tree. We show that the theoretically-derived tree aligns with experimental data on virus evolution. Additionally, we propose an A-X model, utilizing the set of existing mutation sites (A) and a set of randomly generated sites (X), to calculate the emergence of new strains. Our findings demonstrate that a sufficient number of random iterations can predict the generation of new macro-lineages when the number of sites in X is large enough. These results provide a crucial theoretical basis for understanding the evolution of SARS-CoV-2., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Evolutionary theory has typically focused on pairwise interactions, such as those between hosts and parasites, with relatively little work having been carried out on more complex interactions including hyperparasites: parasites of parasites. Hyperparasites are common in nature, with the chestnut blight fungus virus CHV-1 a well-known natural example, but also notably include the phages of important human bacterial diseases. We build a general modeling framework for the evolution of hyperparasites that highlights the central role that the ability of a hyperparasite to be transmitted with its parasite plays in their evolution. A key result is that hyperparasites which transmit with their parasite hosts (hitchhike) will be selected for lower virulence, trending towards hypermutualism or hypercommensalism. We examine the impact on the evolution of hyperparasite systems of a wide range of host and parasite traits showing, for example, that high parasite virulence selects for higher hyperparasite virulence resulting in reductions in parasite virulence when hyperparasitized. Furthermore, we show that acute parasite infection will also select for increased hyperparasite virulence. Our results have implications for hyperparasite research, both as biocontrol agents and for their role in shaping community ecology and evolution and moreover emphasize the importance of understanding evolution in the context of multitrophic interactions., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

The book of Patrick Matthew (1790-1874) 'On Naval Timber and Arboriculture' has regularly thwarted readers' attempts of interpretation. The problems seem to extend beyond analysing and interpreting its evolutionary passages. Building upon previous studies, this analysis presents evidence that the book's structure itself may have contributed significantly to its reception by sundry readers as somehow either clear or obscure, consequently leading to a diversity of interpretations. First, the book does not have a consistent literary form. Second, it presents a miscellany of juxtaposed contents. Third, its readers approach it from different contexts. Internal evidence shows that Patrick Matthew added a lot of material, while the manuscript was already in the proof-reading or press stage. This explains why it provides no consistent literary form or integrated content that would have helped interpretation. Hence readers have been left to their own devices, and their interpretation depended more strongly than usual on their own contexts.

Since the Origin of Species, it has been known that evolution depends on what Darwin called the "strong principle of inheritance." Highly accurate replication of cellular phenotype is a universal phenomenon in all of life since LUCA and is often taken for granted as a constant in evolutionary theory. It is not known how self-replication arose during the origin of life. In this report I use the simple mathematics of evolutionary theory to investigate the dynamics of self-replication accuracy and allelic selection. Results indicate that the degree of self-replication accuracy must be greater than a threshold related to the selection coefficients of the alleles in a population in order for evolution to occur. Accurate replication of cellular phenotype and of the molecules involved in genotype/phenotype linkage is necessary for the origin of evolution and may be considered the fundamental principle of life., Competing Interests: Declaration of competing interest The author has no competing interests to declare., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Populations declining toward extinction can persist via genetic adaptation in a process called evolutionary rescue. Predicting evolutionary rescue has applications ranging from conservation biology to medicine, but requires understanding and integrating the multiple effects of a stressful environmental change on population processes. Here we derive a simple expression for how generation time, a key determinant of the rate of evolution, varies with population size during evolutionary rescue. Change in generation time is quantitatively predicted by comparing how intraspecific competition and the source of maladaptation each affect the rates of births and deaths in the population. Depending on the difference between two parameters quantifying these effects, the model predicts that populations may experience substantial changes in their rate of adaptation in both positive and negative directions, or adapt consistently despite severe stress. These predictions were then tested by comparison to the results of individual-based simulations of evolutionary rescue, which validated that the tolerable rate of environmental change varied considerably as described by analytical results. We discuss how these results inform efforts to understand wildlife disease and adaptation to climate change, evolution in managed populations and treatment resistance in pathogens.

The role of evolutionary theory at the origin of life is an extensively debated topic. The origin and early development of life is usually separated into a prebiotic phase and a protocellular phase, ultimately leading to the Last Universal Common Ancestor. Most likely, the Last Universal Common Ancestor was subject to Darwinian evolution, but the question remains to what extent Darwinian evolution applies to the prebiotic and protocellular phases. In this review, we reflect on the current status of evolutionary theory in origins of life research by bringing together philosophy of science, evolutionary biology, and empirical research in the origins field. We explore the various ways in which evolutionary theory has been extended beyond biology; we look at how these extensions apply to the prebiotic development of (proto)metabolism; and we investigate how the terminology from evolutionary theory is currently being employed in state-of-the-art origins of life research. In doing so, we identify some of the current obstacles to an evolutionary account of the origins of life, as well as open up new avenues of research.

Background: Despite the practical importance of addressing the drug user's sleep problems to enhance the efficacy of treatment and rehabilitation, little is known about whether and how history of childhood maltreatment relates to this issue. This study takes an evolutionary perspective to investigate the associations between history of childhood maltreatment and sleep problems in adults with drug abuse via their emotion regulation difficulties, future-oriented coping, and anxiety. Methods: Participants were 604 male adults with drug abuse between the ages of 18-58 years ( M  = 36.20, SD  = 8.17) in a drug rehabilitation centre in China. In addition to bivariate correlation analysis, path analysis was conducted to examine goodness-of-fit of the conceptual model, controlling for the effect of demographic characteristics. Results: Thirty-two percent of participants ( n  = 194) reported poor sleep quality (PSQI > 5), whereas sleep disturbance (81.3%), daytime dysfunction (77.3%), and sleep latency (66.5%) were the three most common problems among them. Correlation analysis supported the hypothesised positive correlations between poor sleep quality and childhood maltreatment, emotion regulation difficulties, and anxiety, and a negative correlation with future-oriented coping. Results of path analysis showed a significant indirect effect of childhood maltreatment on sleep problems via both emotion regulation difficulties and anxiety, whereas such effects via both future-oriented coping and anxiety were statistically nonsignificant. Conclusions: The findings suggest life history theory is applicable to understanding drug users' sleep problems, and interventions regarding both emotion regulation difficulties and anxiety can lessen the risk posed by childhood maltreatment on sleep problems.

In a recent reply to Takacs and Bourrat's article (Biol Philos 37:12, 2022), Autzen and Okasha (Biol Philos 37:37, 2022) question our characterization of the relationship between the geometric mean and arithmetic mean measures of fitness. We here take issue with the claim that our characterization falls prey to the mistakes they highlight. Briefly revisiting what Takacs and Bourrat (Biol Philos 37:12, 2022) accomplished reveals that the key issue of difference concerns cases of deterministic but nonconstant growth. Restricting focus to such cases shows that there is in fact no reason for disagreement., Competing Interests: Conflict of interestThe authors have no competing interests to declare that are relevant to the content of this article., (© The Author(s) 2024.)

Sir Richard Peto is well known for proposing puzzling paradoxes in cancer biology-some more well-known than others. In a 1984 piece, Peto proposed that after decades of molecular biology in cancer research, we are still ignorant of the biology underpinning cancer. Cancer is a product of somatic mutations. How do these mutations arise and what are the mechanisms? As an epidemiologist, Peto asked if we really need to understand mechanisms in order to prevent cancer? Four decades after Peto's proposed ignorance in cancer research, we can simply ask, are we still ignorant? Did the great pursuit to uncover mechanisms of cancer eclipse our understanding of causes and preventions? Or can we get closer to treating and preventing cancer by understanding the underlying mechanisms that make us most vulnerable to this disease?, (© 2022. The Author(s).)

Social interactions among viruses occur whenever multiple viral genomes infect the same cells, hosts, or populations of hosts. Viral social interactions range from cooperation to conflict, occur throughout the viral world, and affect every stage of the viral lifecycle. The ubiquity of these social interactions means that they can determine the population dynamics, evolutionary trajectory, and clinical progression of viral infections. At the same time, social interactions in viruses raise new questions for evolutionary theory, providing opportunities to test and extend existing frameworks within social evolution. Many opportunities exist at this interface: Insights into the evolution of viral social interactions have immediate implications for our understanding of the fundamental biology and clinical manifestation of viral diseases. However, these opportunities are currently limited because evolutionary biologists only rarely study social evolution in viruses. Here, we bridge this gap by (1) summarizing the ways in which viruses can interact socially, including consequences for social evolution and evolvability; (2) outlining some open questions raised by viruses that could challenge concepts within social evolution theory; and (3) providing some illustrative examples, data sources, and conceptual questions, for studying the natural history of social viruses., (© 2023 The Authors. Journal of Evolutionary Biology published by John Wiley & Sons Ltd on behalf of European Society for Evolutionary Biology.)

Understanding the interplay between ecological processes and the evolutionary dynamics of quantitative traits in natural systems remains a major challenge. Two main theoretical frameworks are used to address this question, adaptive dynamics and quantitative genetics, both of which have strengths and limitations and are often used by distinct research communities to address different questions. In order to make progress, new theoretical developments are needed that integrate these approaches and strengthen the link to empirical data. Here, we discuss a novel theoretical framework that bridges the gap between quantitative genetics and adaptive dynamics approaches. 'Oligomorphic dynamics' can be used to analyse eco-evolutionary dynamics across different time scales and extends quantitative genetics theory to account for multimodal trait distributions, the dynamical nature of genetic variance, the potential for disruptive selection due to ecological feedbacks, and the non-normal or skewed trait distributions encountered in nature. Oligomorphic dynamics explicitly takes into account the effect of environmental feedback, such as frequency- and density-dependent selection, on the dynamics of multi-modal trait distributions and we argue it has the potential to facilitate a much tighter integration between eco-evolutionary theory and empirical data., (© 2023 The Authors. Ecology Letters published by John Wiley & Sons Ltd.)

Effective bioinspiration requires dialogue between designers and biologists, and this dialogue must be rooted in a shared scientific understanding of living systems. To support learning from "nature's overarching design lessons" the Biomimicry Institute has produced ten "Unifying Patterns of Nature". These patterns have been developed to engage with those interested in finding biologically inspired solutions to human challenges. Yet, although well-intentioned and appealing, they are likely to dishearten biologists. The aim of this paper is to identify why and propose alternative principles based on evolutionary theory.

The notion that mutations are random relative to their fitness effects is central to the Neo-Darwinian view of evolution. However, a recent interpretation of the patterns of mutation accumulation in the genome of Arabidopsis thaliana has challenged this notion, arguing for the presence of a targeted DNA repair mechanism that causes a nonrandom association of mutation rates and fitness effects. Specifically, this mechanism was suggested to cause a reduction in the rates of mutations on essential genes, thus lowering the rates of deleterious mutations. Central to this argument were attempts to rule out selection at the population level. Here, we offer an alternative and parsimonious interpretation of the patterns of mutation accumulation previously attributed to mutation bias, showing how they can instead or additionally be caused by developmental selection, that is selection occurring at the cellular level during the development of a multicellular organism. Thus, the depletion of deleterious mutations in A. thaliana may indeed be the result of a selective process, rather than a bias in mutation. More broadly, our work highlights the importance of considering development in the interpretation of population-genetic analyses of multicellular organisms, and it emphasizes that efforts to identify mechanisms involved in mutational biases should explicitly account for developmental selection., (© The Author(s) 2023. Published by Oxford University Press on behalf of Society for Molecular Biology and Evolution.)

Variation in gene expression across lineages is thought to explain much of the observed phenotypic variation and adaptation. The protein is closer to the target of natural selection but gene expression is typically measured as the amount of mRNA. The broad assumption that mRNA levels are good proxies for protein levels has been undermined by a number of studies reporting moderate or weak correlations between the two measures across species. One biological explanation for this discrepancy is that there has been compensatory evolution between the mRNA level and regulation of translation. However, we do not understand the evolutionary conditions necessary for this to occur nor the expected strength of the correlation between mRNA and protein levels. Here, we develop a theoretical model for the coevolution of mRNA and protein levels and investigate the dynamics of the model over time. We find that compensatory evolution is widespread when there is stabilizing selection on the protein level; this observation held true across a variety of regulatory pathways. When the protein level is under directional selection, the mRNA level of a gene and the translation rate of the same gene were negatively correlated across lineages but positively correlated across genes. These findings help explain results from comparative studies of gene expression and potentially enable researchers to disentangle biological and statistical hypotheses for the mismatch between transcriptomic and proteomic data., (© The Author(s) 2023. Published by Oxford University Press on behalf of Society for Molecular Biology and Evolution.)

The short life of Hungarian paleontologist and Albanologist, Franz Baron Nopcsa (1877-1933) is reviewed with an eye on his discoveries of the dinosaurs of Transylvania and their dwarfed nature, as well as his interest in the people of Albania, especially their social organization, laws, history, and ethnography during the first and second Balkan Wars. He also engaged in espionage in Romania during World War I. In addition to his research on the dwarfed dinosaurs and their insular context, his paleontological work also focused on neo-Lamarckian evolutionary theory, the origin of avian flight, and growth and sexual dimorphism in dinosaurs based on osteology and bone microstructure., (© 2022 American Association for Anatomy.)

Since the ENCODE project published its final results in a series of articles in 2012, there is no consensus on what its implications are. ENCODE's central and most controversial claim was that there is essentially no junk DNA: most sections of the human genome believed to be «junk» are functional. This claim was met with many reservations. If researchers disagree about whether there is junk DNA, they have first to agree on a concept of function and how function, given a particular definition, can be discovered. The ENCODE debate centered on a notion of function that assumes a strong dichotomy between evolutionary and non-evolutionary function and causes, prevalent in the Modern Evolutionary Synthesis. In contrast to how the debate is typically portrayed, both sides share a commitment to this distinction. This distinction is, however, much debated in alternative approaches to evolutionary theory, such as the EES. We show that because the ENCODE debate is grounded in a particular notion of function, it is unclear how it connects to broader debates about what is the correct evolutionary framework. Furthermore, we show how arguments brought forward in the controversy, particularly arguments from mathematical population genetics, are deeply embedded in their particular disciplinary contexts, and reflect substantive assumptions about the evolution of genomes. With this article, we aim to provide an anatomy of the ENCODE debate that offers a new perspective on the notions of function both sides employed, as well as to situate the ENCODE debate within wider debates regarding the forces operating in evolution., (Copyright: © 2023 by Fabrizio Serra editore, Pisa · Roma.)

An individual's optimal investment in parental care potentially depends on many variables, including its future fitness prospects, the expected costs of providing care and its partner's expected or observed parental behaviour. Previous models suggested that low-quality parents could evolve to exploit their high-quality partners by reducing care, leading to the paradoxical prediction that low-quality parents could have higher fitness than their high-quality partners. However, these studies lacked a complete and consistent life-history model. Here, we challenge this result, developing a consistent analytical model of parental care strategies given individual variation in quality, and checking our results using agent-based simulations. In contrast to previous models, we predict that high-quality individuals always outcompete low-quality individuals in fitness terms. However, care effort may differ between high- and low-quality parents in either direction: low-quality individuals care more than high-quality individuals if their baseline mortality is higher, but less if their mortality increases more steeply with increasing care. We also highlight the ambiguity of the term 'quality' and stress the need for 'genealogical consistency' in evolutionary models., (© 2023 The Authors. Journal of Evolutionary Biology published by John Wiley & Sons Ltd on behalf of European Society for Evolutionary Biology.)

It has been hypothesized that horizontal gene transfer on plasmids can facilitate the evolution of cooperation, by allowing genes to jump between bacteria, and hence increase genetic relatedness at the cooperative loci. However, we show theoretically that horizontal gene transfer only appreciably increases relatedness when plasmids are rare, where there are many plasmid-free cells available to infect (many opportunities for horizontal gene transfer). In contrast, when plasmids are common, there are few opportunities for horizontal gene transfer, meaning relatedness is not appreciably increased, and so cooperation is not favored. Plasmids, therefore, evolve to be rare and cooperative, or common and noncooperative, meaning plasmid frequency and cooperativeness are never simultaneously high. The overall level of plasmid-mediated cooperation, given by the product of plasmid frequency and cooperativeness, is therefore consistently negligible or low., (© The Author(s) 2023. Published by Oxford University Press on behalf of The Society for the Study of Evolution (SSE) and European Society for Evolutionary Biology (ESEN).)

The delineation of the subtypes of automatically reinforced self-injurious behavior improved the utility of functional analysis results in predicting treatment efficacy. However, the mechanisms underlying subtype differences remain unclear and difficult to study in clinical populations. Morris and McDowell (2021) attempted to elucidate subtype differences by developing and evaluating models of the subtypes within the evolutionary theory of behavior dynamics. In the current study, we applied techniques from precision medicine to further evaluate the models developed by Morris and McDowell. This evaluation highlighted shortcomings of the existing models and suggested ways they could be improved. Thus, we conducted more extended modeling within the framework of precision medicine to identify models that were more quantitatively similar to available clinical data. Improved models that more closely approximate clinical data were identified. The implications of these models for research, practice, and further applications of the evolutionary theory of behavior dynamics are discussed., (© 2023 Society for the Experimental Analysis of Behavior (SEAB).)

A foundational idea of evo-devo is that morphological variation is not isotropic, that is, it does not occur in all directions. Instead, some directions of morphological variation are more likely than others from DNA-level variation and these largely depend on development. We argue that this evo-devo perspective should apply not only to morphology but to evolution at all phenotypic levels. At other phenotypic levels there is no development, but there are processes that can be seen, in analogy to development, as constructing the phenotype (e.g., protein folding, learning for behavior, etc.). We argue that to explain the direction of evolution two types of arguments need to be combined: generative arguments about which phenotypic variation arises in each generation and selective arguments about which of it passes to the next generation. We explain how a full consideration of the two types of arguments improves the explanatory power of evolutionary theory. Also see the video abstract here: https://youtu.be/Egbvma_uaKc., (© 2023 Wiley Periodicals LLC.)

The Appraisal-Disruption Model (ADM) suggests that individuals use alcohol as a means of dampening negative self-talk. Relationship-contingent self-esteem (RCSE) emerges from validating one's self-esteem depending on one's romantic relationship(s) and is known to predict alcohol-related problems. We hypothesized that RCSE indirectly predicts drinking outcomes through the mediating mechanism(s) of stress and impaired control over alcohol (IC; drinking to excess beyond one's own intentions). We fit a multiple-group structural equation model with self-report survey data from 479 college students. We used a 20,000 bootstrap technique to examine possible mediated pathways. Consistent with evolutionary theory, our model was moderated by sex: more variance in alcohol-related problems was explained for women (R 2 = 0.479) than for men (R 2 = 0.280). RCSE was directly linked to more stress. Furthermore, higher levels of RCSE were indirectly linked to more IC through increased stress, and in turn, more heavy episodic drinking and alcohol-related problems for both men and women. Consistent with the ADM, those with higher levels of RCSE experienced more stress and, in turn, more IC and subsequent adverse alcohol outcomes. Thus, therapists targeting alcohol use disorders (AUDs) may wish to determine if their client's self-esteem changes dramatically based on their moment-to-moment appraisal of their intimate relationships.

Evolutionary theory has made large impacts on our understanding and management of the world, in part because it has been able to incorporate new data and new insights successfully. Nonetheless, there is currently a tension between certain biological phenomena and mainstream evolutionary theory. For example, how does the inheritance of molecular epigenetic changes fit into mainstream evolutionary theory? Is niche construction an evolutionary process? Is local adaptation via habitat choice also adaptive evolution? These examples suggest there is scope (and perhaps even a need) to broaden our views on evolution. We identify three aspects whose incorporation into a single framework would enable a more generalised approach to the understanding and study of adaptive evolution: (i) a broadened view of extended phenotypes; (ii) that traits can respond to each other; and (iii) that inheritance can be non-genetic. We use causal modelling to integrate these three aspects with established views on the variables and mechanisms that drive and allow for adaptive evolution. Our causal model identifies natural selection and non-genetic inheritance of adaptive parental responses as two complementary yet distinct and independent drivers of adaptive evolution. Both drivers are compatible with the Price equation; specifically, non-genetic inheritance of parental responses is captured by an often-neglected component of the Price equation. Our causal model is general and simplified, but can be adjusted flexibly in terms of variables and causal connections, depending on the research question and/or biological system. By revisiting the three examples given above, we show how to use it as a heuristic tool to clarify conceptual issues and to help design empirical research. In contrast to a gene-centric view defining evolution only in terms of genetic change, our generalised approach allows us to see evolution as a change in the whole causal structure, consisting not just of genetic but also of phenotypic and environmental variables., (© 2022 The Authors. Biological Reviews published by John Wiley & Sons Ltd on behalf of Cambridge Philosophical Society.)

Cellular life exhibits order and complexity, which typically increase over the course of evolution. Cell polarization is a well-studied example of an ordering process that breaks the internal symmetry of a cell by establishing a preferential axis. Like many cellular processes, polarization is driven by self-organization, meaning that the macroscopic pattern emerges as a consequence of microscopic molecular interactions at the biophysical level. However, the role of self-organization in the evolution of complex protein networks remains obscure. In this Review, we provide an overview of the evolution of polarization as a self-organizing process, focusing on the model species Saccharomyces cerevisiae and its fungal relatives. Moreover, we use this model system to discuss how self-organization might relate to evolutionary change, offering a shift in perspective on evolution at the microscopic scale., Competing Interests: Competing interests The authors declare no competing or financial interests., (© 2023. Published by The Company of Biologists Ltd.)

We explore the interpersonal origins of human culture, arguing that culture emerges as a necessary consequence of our helplessness in infancy, which in turn requires a greater degree of collaboration and social organization than is necessary for other mammals. We propose a model of cultural transmission that depends on a dyadic interpersonal process whose vicissitudes can have a lifelong impact. We explore the role played by imagining subjectively experienced psychological states and processes in others, which we have defined as mentalizing , in the process of cultural transmission, and propose that mentalizing is key to the establishment of epistemic trust-that is to say, an experience of trust that enables the individual to absorb and use the knowledge they are being offered. We suggest that psychoanalysis can be viewed as a paradigmatic example of a process of transferring knowledge from one human being (the teacher, the caregiver, the analyst) to another (the learner, the young person, the patient) and argue that the mechanisms of psychic change in analysis cannot be fully understood without appreciating this aspect of the biological/evolutionary origins of our essential humanity. Finally, we discuss the clinical implications of the model we are proposing for the psychoanalytic process.

Paleoanthropology's relationship with evolutionary theory has not been entirely happy. The anatomists who dominated paleoanthropology for its first century had little interest in biological diversity and its causes, or in hominins' place in that diversity, or in the rules and principles of zoological nomenclature - which they basically ignored entirely. When, as the twentieth century passed its midpoint, Ernst Mayr introduced theory to paleoanthropology in the form of the gradualist Modern Evolutionary Synthesis (in its most hardened form), he shocked students of human evolution not only into a strictly linear evolutionary mindset, but into a taxonomic minimalism that would for years obscure the signal of phylogenetic diversity and vigorous evolutionary experimentation among hominins that was starting to emerge from a rapidly enlarging hominin fossil record. Subsequently, the notion of episodic as opposed to gradualist evolution re-established phylogenies as typically branching, and species as bounded entities with births, histories, and deaths; but the implications of this revised perspective were widely neglected by paleoanthropologists, who continued to reflexively cram diverse new morphologies into existing taxonomic pigeonholes. For Pleistocene hominins, the effective systematic algorithm became, "if it isn't Australopithecus, it must be Homo" (or vice versa), thereby turning both taxa into wastebaskets. The recent development of the "Extended Evolutionary Synthesis" has only exacerbated the resulting caricature of phylogenetic structure within Homininae, by offering developmental/phenotypic plasticity as an excuse for associating wildly differing morphologies within the same taxon. Homo erectus has been a favorite victim of this foible. Biological species are indeed morphologically variable. But they are only variable within limits; and until we stop brushing diverse morphologies under the rug of developmental plasticity, paleoanthropology will remain at a major impasse.

How cooperation evolves in the presence of selfishness is a core problem in evolutionary biology. Selfish individuals tend to benefit themselves, which makes it harder to maintain cooperation between unrelated individuals and for living systems to evolve towards complex organizations. The general evolutionary model presented here identifies that non-kin selection is the root cause for cooperation between unrelated individuals and can enable and maintain higher complexity of biological organizations (the coexistence of more individuals of different types). The maintained number of genotypes within a cooperation organization is shown to follow a universal exponential law as a quantitative function of the population size and non-kin selection strength, showing a gene-pool-size invariance. Our results highlight that non-kin selection may be a hallmark of biological evolution, and play an important role in shaping life's potentials., Competing Interests: Conflict of interest The authors declare no conflict of interest., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

AbstractThe adaptive potential of nonheritable somatic mutations has received limited attention in traditional evolutionary theory because heritability is a fundamental pillar of Darwinian evolution. We hypothesized that the ability of a germline genotype to express a novel phenotype via nonheritable somatic mutations can be selectively advantageous and that this advantage will channel evolving populations toward germline genotypes that constitutively express the phenotype. We tested this hypothesis by simulating evolving populations of developing organisms with an impermeable germline-soma separation navigating a minimal fitness landscape. The simulations revealed the conditions under which nonheritable somatic mutations promote adaptation. Specifically, this can occur when the somatic mutation supply is high, when few cells with the advantageous somatic mutation are required to increase organismal fitness, and when the somatic mutation also confers a selective advantage at the cellular level. We therefore provide proof of principle that nonheritable somatic mutations can promote adaptive evolution via a process we call "somatic genotypic exploration." We discuss the biological plausibility of this phenomenon as well as its evolutionary implications.

The mutualistic interactions between Riftia pachyptila and its endosymbiont Candidatus Endoriftia persephone (short Endoriftia) have been extensively researched. However, the closed Endoriftia genome is still lacking. Here, by employing single-molecule real-time sequencing we present the closed chromosomal sequence of Endoriftia. In contrast to theoretical predictions of enlarged and mobile genetic element-rich genomes related to facultative endosymbionts, the closed Endoriftia genome is streamlined with fewer than expected coding sequence regions, insertion-, prophage-sequences and transposase-coding sequences. Automated and manually curated functional analyses indicated that Endoriftia is more versatile regarding sulphur metabolism than previously reported. We identified the presence of two identical rRNA operons and two long CRISPR regions in the closed genome. Additionally, pangenome analyses revealed the presence of three types of secretion systems (II, IV and VI) in the different Endoriftia populations indicating lineage-specific adaptations. The in depth mobilome characterization identified the presence of shared genomic islands in the different Endoriftia drafts and in the closed genome, suggesting that the acquisition of foreign DNA predates the geographical dispersal of the different endosymbiont populations. Finally, we found no evidence of epigenetic regulation in Endoriftia, as revealed by gene screenings and absence of methylated modified base motifs in the genome. As a matter of fact, the restriction-modification system seems to be dysfunctional in Endoriftia, pointing to a higher importance of molecular memory-based immunity against phages via spacer incorporation into CRISPR system. The Endoriftia genome is the first closed tubeworm endosymbiont to date and will be valuable for future gene oriented and evolutionary comparative studies., (© 2022 The Authors. Molecular Ecology Resources published by John Wiley & Sons Ltd.)

Background and Objectives: The situation-symptom congruence hypothesis (SSCH; (Keller & Nesse, 2006), grounded in evolutionary theory, argues that different types of adversity should lead to distinct patterns of depressive symptoms that help individuals deal with adaptive challenges. Situation-symptom congruence hypotheses were tested in this study using experience sampling methodology., Methods: Two hundred and sixty-five individuals, including 54% who scored at least 16 on the Center for Epidemiologic Studies Revised Depression Scale, responded to text prompts daily for up to 9 days, reporting depressive symptoms as well as the most stressful event or issue they had experienced or focused on within the past 24 h., Results: Multilevel modeling analyses indicated that the relationships between stressors and depressive symptom patterns were largely consistent with SSCH predictions. All stressors were significantly associated with symptoms hypothesized to be adaptive in response to those stressors. Moreover, in separate analyses, nine of the ten symptoms examined were either predicted by the stressors hypothesized to lead to that symptom or negatively related to stressors hypothesized to not elicit those symptoms., Limitations: It is unclear whether the results generalize to those diagnosed with a major depressive disorder; the study did not assess actual life events., Conclusions: Findings suggest that depressive symptoms may, in part, be adaptations that have evolved through natural selection to help individuals cope with adverse situations., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Evolutionary biology is paying increasing attention to the mechanisms that enable phenotypic plasticity, evolvability, and extra-genetic inheritance. Yet, there is a concern that these phenomena remain insufficiently integrated within evolutionary theory. Understanding their evolutionary implications would require focusing on phenotypes and their variation, but this does not always fit well with the prevalent genetic representation of evolution that screens off developmental mechanisms. Here, we instead use development as a starting point, and represent it in a way that allows genetic, environmental and epigenetic sources of phenotypic variation to be independent. We show why this representation helps to understand the evolutionary consequences of both genetic and non-genetic phenotype determinants, and discuss how this approach can instigate future areas of empirical and theoretical research., (© 2022 The Authors. BioEssays published by Wiley Periodicals LLC.)

Mutational meltdown describes an eco-evolutionary process in which the accumulation of deleterious mutations causes a fitness decline that eventually leads to the extinction of a population. Possible applications of this concept include medical treatment of RNA virus infections based on mutagenic drugs that increase the mutation rate of the pathogen. To determine the usefulness and expected success of such an antiviral treatment, estimates of the expected time to mutational meltdown are necessary. Here, we compute the extinction time of a population under high mutation rates, using both analytical approaches and stochastic simulations. Extinction is the result of three consecutive processes: (a) initial accumulation of deleterious mutations due to the increased mutation pressure; (b) consecutive loss of the fittest haplotype due to Muller's ratchet; (c) rapid population decline toward extinction. We find accurate analytical results for the mean extinction time, which show that the deleterious mutation rate has the strongest effect on the extinction time. We confirm that intermediate-sized deleterious selection coefficients minimize the extinction time. Finally, our simulations show that the variation in extinction time, given a set of parameters, is surprisingly small., Competing Interests: The authors declare no conflict of interest., (© 2022 The Authors. Ecology and Evolution published by John Wiley & Sons Ltd.)

Females and males often have markedly different mortality rates and life spans, but it is unclear why these forms of sexual dimorphism evolve. The unguarded X hypothesis contends that dimorphic life spans arise from sex differences in X or Z chromosome copy number (i.e., one copy in the "heterogametic" sex; two copies in the "homogametic" sex), which leads to a disproportionate expression of deleterious mutations by the heterogametic sex (e.g., mammalian males; avian females). Although data on adult sex ratios and sex-specific longevity are consistent with predictions of the unguarded X hypothesis, direct experimental evidence remains scant, and alternative explanations are difficult to rule out. Using a simple population genetic model, we show that the unguarded X effect on sex differential mortality is a function of several reasonably well-studied evolutionary parameters, including the proportion of the genome that is sex linked, the genomic deleterious mutation rate, the mean dominance of deleterious mutations, the relative rates of mutation and strengths of selection in each sex, and the average effect of mutations on survival and longevity relative to their effects on fitness. We review published estimates of these parameters, parameterize our model with them, and show that unguarded X effects are too small to explain observed sex differences in life span across species. For example, sex differences in mean life span are known to often exceed 20% (e.g., in mammals), whereas our parameterized models predict unguarded X effects of a few percent (e.g., 1-3% in Drosophila and mammals). Indeed, these predicted unguarded X effects fall below statistical thresholds of detectability in most experiments, potentially explaining why direct tests of the hypothesis have generated little support for it. Our results suggest that evolution of sexually dimorphic life spans is predominantly attributable to other mechanisms, potentially including "toxic Y" effects and sexual dimorphism for optimal investment in survival versus reproduction., Competing Interests: The authors declare no conflict of interest., (© 2022 The Authors. Evolution Letters published by Wiley Periodicals LLC on behalf of Society for the Study of Evolution (SSE) and European Society for Evolutionary Biology (ESEB).)

Background: Early women's marriage is associated with adverse outcomes for mothers and their offspring, including reduced human capital and increased child undernutrition and mortality. Despite preventive efforts, it remains common in many populations and is often favored by cultural norms. A key question is why it remains common, given such penalties. Using an evolutionary perspective, a simple mathematical model was developed to explore women's optimal marriage age under different circumstances, if the sole aim were to maximize maternal or paternal lifetime reproductive fitness (surviving offspring)., Methods: The model was based on several assumptions, supported by empirical evidence, regarding relationships between women's marital age and parental and offspring outcomes. It assumes that later marriage promotes women's autonomy, enhancing control over fertility and childcare, but increases paternity uncertainty. Given these assumptions, optimal marriage ages for maximizing maternal and paternal fitness were calculated. The basic model was then used to simulate environmental changes or public health interventions, including shifts in child mortality, suppression of women's autonomy, or promoting women's contraception or education., Results: In the basic model, paternal fitness is maximized at lower women's marriage age than is maternal fitness, with the paternal optimum worsening child undernutrition and mortality. A family planning intervention delays marriage age and reduces child mortality and undernutrition, at a cost to paternal but not maternal fitness. Reductions in child mortality favor earlier marriage but increase child undernutrition, whereas ecological shocks that increase child mortality favor later marriage but reduce fitness of both parents. An education intervention favors later marriage and reduces child mortality and undernutrition, but at a cost to paternal fitness. Efforts to suppress maternal autonomy substantially increase fitness of both parents, but only if other members of the household provide compensatory childcare., Conclusion: Early women's marriage maximizes paternal fitness despite relatively high child mortality and undernutrition, by increasing fertility and reducing paternity uncertainty. This tension between the sexes over the optimal marriage age is sensitive to ecological stresses or interventions. Education interventions seem most likely to improve maternal and child outcomes, but may be resisted by males and their kin as they may reduce paternal fitness., Competing Interests: The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Wells.)

Developing a low-carbon economy is the only way for countries to achieve sustainable development. Carbon emission reduction policies and low-carbon technology (LCT) innovation play key roles in developing low-carbon economy. Under government reward and punishment regulations, based on the bilateral matching and evolutionary theories, this paper constructs an evolution model consisting of a manufacturer investing LCT and a supplier offering LCT to analyze multi-phase LCT investment strategies. Firstly, the profit optimization model of a green supply chain is constructed from the perspectives of centralized-matching (CM), decentralized-matching (DM), and mismatching (MM), and the spatial information internal evolution law of multi-phase LCT investment is described by the Markov chain. Then, a bilateral matching algorithm is proposed to solve the equilibrium solutions, and the evolution process of the three modes is analyzed by numerical simulation. Finally, based on the product green degree, we analyze the impact of subsidies and taxes on investment-production decisions. Analytical results show that the matching mechanism proposed in this paper can help supply chain firms to obtain stable matching and has a significant effect on the realization of "triple wins" of society, economy, and environment. The investment utility of CM is higher than that of DM and MM. Manufacturers are inclined to adopt LCT, and the investment level tends to be stable over time. Government reward and punishment regulations are helpful to motivate supply chain firms to invest in LCT, and the synergistic effect of subsidies and taxes is better than that of a single policy., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

In 1909, Italian zoologist Daniele Rosa (1857-1944) proposed a radical new evolutionary theory: hologenesis, or simultaneous, pan-terrestrial creation and evolution driven primarily by internal factors. Hologenesis was widely ignored or rejected outside Italy, but Swiss-French anthropologist George Montandon (1879-1944) eagerly embraced and developed the theory. An ambitious careerist, Montandon's deep investment in an obscure and unpopular theory is puzzling. Today, Montandon is best known for his virulent antisemitism and active collaboration with the Nazi occupation of France at the end of his career. By that point, however, he had quietly moved away from hologenesis. This shift has gone unnoticed or been left unexplained in existing research. This article reexamines Montandon's theoretical outlook and reasons for championing Rosa's forgotten theory. It argues that while Montandon's adoption of hologenesis arose from a complex blend of scientific and personal factors, his previously overlooked early fieldwork with the Ainu played a key role. In contrast, hologenesis did not inform Montandon's later public antisemitism.