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Biology subjects

Feldman, M. W.

Publications and source records attributed to Feldman, M. W..

At least 19 recordsLinked to original sources

Climate change, infectious disease, and the spread of microblades across the Qinling-Huaihe line

Aoki et al. (2023) proposed that the sharp difference in microblade distribution between the north and south of the Qinling-Huaihe (H-Q) line before the early Holocene could have been due to a higher frequency of pathogens in the south. Greater susceptibility to pathogen-induced disease among northerners could have effectively prevented migration across the H-Q line. Here, we explore the possibility that migration between the north and south could have been stalled by a vector-borne disease whose vector distribution was climate dependent. The original wave equation approach is extended to include climate variation in the forms of (i) a period of linear warming; (ii) a period of linear cooling; and (iii) a period of temperature oscillations. Simulations of this extended model are carried out using published estimates of the climate record for the Northern Hemisphere since the Upper Paleolithic. This analysis suggests possible time intervals during which microblades could have reached the south.

evolutionary biology↗

Evolution under Stochastic Transmission: Mutation-Rate Modifiers

In evolutionary models of large populations, it is common to analyze the effects of cyclic or random variation in the parameters that describe selection. It is less common, however, to study how stochasticity in the genetic transmission process itself affects evolutionary outcomes. Suppose that a gene locus has alleles A and a under constant selection. This locus is linked to a modifier locus with alleles M1 and M2, which control the mutation rate from A to a. The Reduction Principle states that, near a mutation-selection balance where M1 is fixed with mutation rate u1, a rare allele M2 can invade if its associated rate u2 is lower than u1. This result, valid for both haploids and diploids, assumes constant mutation rates through time. We extend this framework by allowing the mutation rate associated with M2 to fluctuate randomly across generations, denoted as u2,t. In this stochastic setting, the condition for invasion by a new modifier allele depends not only on the resident mutation rate u1 and the mean mutation rate u2 associated with the invading allele, but also on the temporal distribution of u2,t, the strength of selection at the A/a locus, and the recombination rate between M1/M2 and A/a. The analysis shows how stochasticity and recombination in transmission do not simply modify the magnitude of evolutionary change predicted under deterministic assumptions. Instead, through their interaction with selection and linkage, they can generate conditions under which the direction of modifier evolution is qualitatively reversed relative to the deterministic Reduction Principle.

evolutionary biology↗

The refinement paradox and cumulative cultural evolution: collective improvement in knowledge favors conformity, blind copying and hyper-credulity

Social learning is common in nature, yet cumulative culture (where knowledge and technology increase in complexity and diversity over time) appears restricted to humans. To understand why, we organized a computer tournament in which programmed entries specified when to learn new knowledge and when to refine (i.e. improve) existing knowledge. The tournament revealed a refinement paradox: refined behavior afforded higher payoffs as individuals converged on a small number of successful behavioral variants, but refining did not generally pay. Paradoxically, entries that refined only in certain conditions did best during behavioral improvement, while simple copying entries thrived when refinement levels were high. Cumulative cultural evolution may be rare in part because sophisticated strategies for improving knowledge and technology are initially advantageous, yet complex culture, once achieved, favors conformity, blind imitation and hyper-credulity.

evolutionary biology↗

Cultural transmission, competition for prey, and the evolution of cooperative hunting

Although cooperative hunting (CH) is widespread among animals, its benefits are unclear. When rare, CH may allow predators to escape competition and access "big prey" (BP). However, a lone CH predator cannot such catch food. Cultural transmission may allow CH to spread fast enough that cooperators can find hunting partners, but competition for BP may increase. We construct a one-predator, two-prey model in which the predators either learn to hunt "small prey" (SP) alone, or learn to hunt BP cooperatively. The predators first learn vertically and then choose partners from which they learn horizontally with probability H. CH predators only catch the BP if their partner is cooperative. We find that without horizontal learning, CH cannot evolve when initially rare. Together, a high probability of horizontal learning and competition for the SP allow CH to evolve. However, CH can only fix in the predator population if the BP is very abundant. Furthermore, a mutant that increases horizontal learning can invade whenever CH is present but not fixed, because horizontal learning allows predators to match their strategies, avoiding the situation in which a cooperator cannot find a partner. While competition for prey is important for determining the degree of CH that evolves, it is not enough for CH to emerge and spread; horizontal cultural transmission is essential. Future models may explore factors that control how horizontal transmission influences cooperative predation, and vice versa. Lessons from our model may be useful in conservation efforts and wildlife reintroduction programs.

evolutionary biology↗

Addictions may be driven by competition-induced microbiome dysbiosis

Recent studies revealed mechanisms by which the microbiome affects its hosts brain, behavior and wellbeing, and that dysbiosis - persistent microbiome-imbalance - is associated with the onset and progress of various chronic diseases, including addictive behaviors. Yet, understanding of the ecological and evolutionary processes that shape the host-microbiome ecosystem and affect the host state, is still limited. Here we propose that competition dynamics within the microbiome, associated with host-microbiome mutual regulation, may promote dysbiosis and aggravate addictive behaviors. We constructed a mathematical framework, modeling the dynamics of the host-microbiome ecosystem in response to alterations. We find that when this ecosystem is exposed to substantial perturbations, the microbiome may shift towards a composition that reinforces the new host state. Such positive feedback loop augments post-perturbation imbalances, hindering attempts to return to the initial equilibrium, thus promoting relapse episodes and prolonged addictions. We also find that the initial microbiome composition is a key factor: a diverse microbiome enhances the ecosystems resilience, whereas lower microbiome diversity is more prone to reach dysbiosis, exacerbating addictions. This framework provides novel evolutionary and ecological perspectives on host-microbiome interactions and their implications for host behavior and health, while offering verifiable predictions with potential relevance to clinical treatments.

microbiology↗

Oblique Transmission, Conformity, and Preference in the Evolution of Altruism

The evolution of altruism is frequently studied using models of non-random assortment, including kin selection. In genetic kin selection models, under certain assumptions including additive costs and benefits, the criterion for altruism to invade a population is Hamiltons rule. Deviations from Hamiltons rule occur when vertical transmission has cultural and genetic components, or when costs and benefits are combined multiplicatively. Here, we include oblique and vertical cultural transmission and genetic transmission in four models--two forms of parent-to-offspring altruism, sibling-to-sibling altruism, and altruism between offspring that meet assortatively--under additive or multiplicative assumptions. Oblique transmission may be conformist (anti-conformist), where the probability that an individual acquires a more common cultural variant is greater (less) than its frequency. Inclusion of conformist or anti-conformist oblique transmission may reduce or increase the threshold for invasion by altruism relative to Hamiltons rule. Thresholds for invasion by altruism are lower with anti-conformity than with conformity, and lower or the same with additive rather than multiplicative fitness components. Invasion by an allele that increases the preference for altruism does not depend on oblique phenotypic transmission, and with sibling-to-sibling altruism, this alleles invasion threshold can be higher with additive rather than multiplicative fitnesses.

evolutionary biology↗

Non-Vertical Cultural Transmission, Assortment, and the Evolution of Cooperation

Cultural evolution of cooperation under vertical and non-vertical cultural transmission is studied, and conditions are found for fixation and coexistence of cooperation and defection. The evolution of cooperation is facilitated by its horizontal transmission and by an association between social interactions and horizontal transmission. The effect of oblique transmission depends on the horizontal transmission bias. Stable polymorphism of cooperation and defection can occur, and when it does, reduced association between social interactions and horizontal transmission evolves, which leads to a decreased frequency of cooperation and lower population mean fitness. The deterministic conditions are compared to outcomes of stochastic simulations of structured populations. Parallels are drawn with Hamiltons rule incorporating assortment and effective relatedness.

evolutionary biology↗

Complex dynamics induced by delayed adaptive behavior during outbreaks

The COVID-19 pandemic has posed a significant dilemma for governments across the globe. The public health consequences of inaction are catastrophic; but the economic consequences of drastic action are likewise catastrophic. Governments must therefore strike a balance in the face of these trade-offs. But with critical uncertainty about how to find such a balance, they are forced to experiment with their interventions and await the results of their experimentation. Models have proved inaccurate because behavioral response patterns are either not factored in or are hard to predict. One crucial behavioral response in a pandemic is adaptive social contact: potentially infectious contact between people is deliberately reduced either individually or by fiat; and this must be balanced against the economic cost of having fewer people in contact and therefore active in the labor force. We develop a model for adaptive optimal control of the effective social contact rate within a Susceptible-Infectious-Susceptible (SIS) epidemic model using a dynamic utility function with delayed information. This utility function trades off the population-wide contact rate with the expected cost and risk of increasing infections. Our analytical and computational analysis of this simple discrete-time deterministic model reveals the existence of a non-zero equilibrium, oscillatory dynamics around this equilibrium under some parametric conditions, and complex dynamic regimes that shift under small parameter perturbations. These results support the supposition that infectious disease dynamics under adaptive behavior-change may have an indifference point, may produce oscillatory dynamics without other forcing, and constitute complex adaptive systems with associated dynamics. Implications for COVID-19 include an expectation of fluctuations, for a considerable time, around a quasi-equilibrium that balances public health and economic priorities, that shows multiple peaks and surges in some scenarios, and that implies a high degree of uncertainty in mathematical projections. Author summaryEpidemic response in the form of social contact reduction, such as has been utilized during the ongoing COVID-19 pandemic, presents inherent tradeoffs between the economic costs of reducing social contacts and the public health costs of neglecting to do so. Such tradeoffs introduce an interactive, iterative mechanism which adds complexity to an infectious disease system. Consequently, infectious disease modeling typically has not included dynamic behavior change that must address such a tradeoff. Here, we develop a theoretical model that introduces lost or gained economic and public health utility through the adjustment of social contact rates with delayed information. We find this model produces an equilibrium, a point of indifference where the tradeoff is neutral, and at which a disease will be endemic for a long period of time. Under small perturbations, this model exhibits complex dynamic regimes, including oscillatory behavior, runaway exponential growth, and eradication. These dynamics suggest that for epidemic response that relies on social contact reduction, secondary waves and surges with accompanied business re-closures and shutdowns may be expected, and that accurate projection under such circumstances is unlikely.

systems biology↗

Loss of genetic variation in the two-locus multiallelic haploid model

In the evolutionary biology literature, it is generally assumed that in deterministic haploid selection models, in the absence of variation-generating mechanisms such as mutation, no polymorphic equilibrium can be stable. However, results corroborating this claim are scarce and almost always depend upon additional assumptions. Using ideas from game theory, we establish a condition on the fitness parameters of haplotypes formed by two loci such that a monomorphism is a global attractor. Further, we show that no isolated equilibrium exists, at which an unequal number of alleles from two loci is present. Under the assumption of convergence of trajectories to equilirium points, we settle the two-locus three-allele case for a fitness scheme formally equivalent to the classical symmetric viability model.

evolutionary biology↗

Designing gene drives to limit spillover to non-target populations

The prospect of utilizing CRISPR-based gene-drive technology for controlling populations, such as invasive and disease-vector species, has generated much excitement. However, the potential for spillovers of gene drive alleles from the target population to non-target populations -- events that may be ecologically catastrophic -- has raised concerns. Here, using two-population mathematical models, we investigate the possibility of limiting spillovers and impact on non-target populations by designing differential-targeting gene drives, in which the expected equilibrium gene drive allele frequencies are high in the target population but low in the non-target population. We find that achieving differential targeting is possible with certain configurations of gene drive parameters. Most of these configurations ensure differential targeting only under relatively low migration rates between target and non-target populations. Under high migration, differential targeting is possible only in a narrow region of the parameter space. When migration is increased, differential-targeting states can sharply transition to states of global fixation or global loss of the gene drive. Because fixation of the gene drive in the non-target population could severely disrupt ecosystems, we outline possible ways to avoid this outcome. Our results emphasize that, although gene drive technology is promising, understanding the potential consequences for populations other than the targets requires detailed analysis of gene-drive spillovers, and that ways to limit the unintended effects of gene drives to non-target populations should be explored prior to the application of gene drives in natural settings.

evolutionary biology↗

Reconsidering the management paradigm of fragmented populations

Habitat fragmentation and population declines call for informed management of many endangered species. The dominant paradigm for such management focuses on avoiding deleterious inbreeding effects in separated populations, by facilitating migration to maintain connectivity between them, an approach epitomized by the \"one migrant per generation\" rule. We show that this paradigm fails to take into account two important factors. First, it ignores an inherent trade-off: maintaining within-population genetic diversity is at the expense of maintaining global diversity. Migration increases local within-population genetic diversity, but also homogenizes the meta-population, which may lead to erosion of global genetic diversity. Second, this paradigm does not consider that because many fragmented species have declined in numbers only within the last century, they still carry much of the high genetic diversity characteristic of the historically large population. The conservation of a species global diversity, crucial for evolutionarily adaptation to ecological challenges such as epidemics, industrial pollutants, or climate change, is paramount to a species long-term survival. Here we discuss how consideration of these factors can inform management of fragmented populations and provide a framework to assess the impact on genetic diversity of different management strategies. We also propose two alternative management strategies to replace the \"one migrant per generation\" dogma.

ecology↗

Hunter-gatherer genomes reveal diverse demographic trajectories following the rise of farming in East Africa

A major outstanding question in human prehistory is the fate of hunting and gathering populations following the rise of agriculture and pastoralism. Genomic analysis of ancient and contemporary Europeans suggests that autochthonous groups were either absorbed into or replaced by expanding farmer populations. Many of the hunter-gatherer populations persisting today live in Africa, perhaps because agropastoral transitions occurred later on the continent. Here, we present the first genomic data from the Chabu, a relatively isolated and marginalized hunting-and-gathering group from the Southwestern Ethiopian highlands. The Chabu are a distinct genetic population that carry the highest levels of Southwestern Ethiopian ancestry of any extant population studied thus far. This ancestry has been in situ for at least 4,500 years. We show that the Chabu are undergoing a severe population bottleneck which began around 40 generations ago. We also study other Eastern African populations and demonstrate divergent patterns of historical population size change over the past 60 generations between even closely related groups. We argue that these patterns demonstrate that, unlike in Europe, Africans hunter-gatherers responded to agropastoralism with diverse strategies.

genetics↗

Disease and introgression explain the long-lasting contact zone of Modern Humans and Neanderthals and its eventual destabilization

Neanderthals and modern humans both occupied the Levant for tens of thousands of years prior to modern humans spread into the rest of Eurasia and their replacement of the Neanderthals. That the inter-species boundary remained geographically localized for so long is a puzzle, particularly in light of the rapidity of its subsequent movement. We propose that disease dynamics can explain the localization and persistence of the inter-species boundary; in this view, each species carried pathogens to which it was largely immune and tolerant, but that could spread to the other, vulnerable, species, inducing a significant disease burden. Epidemics and endemic diseases along the interspecies boundary would have mitigated against bands of one species migrating into regions dominated by the other species. Together with decreased population densities and limited inter-group interactions due to disease burden, this mechanism could have resulted in a fixed and narrow contact-zone. We further propose, and support with results from dynamical systems models, that genetic introgression, including transmission of alleles related to the immune system, would have gradually allowed the two species to overcome this barrier to pervasive inter-species interaction, leading to the eventual release of the inter-species boundary from its geographic localization. Asymmetries between the two species in the initial size of their associated \"pathogen package\" could have created feedback loops that influenced the rates at which immunity to and tolerance of the novel pathogens were acquired. These asymmetries could have allowed modern humans to overcome the disease burden earlier than Neanderthals, giving them a significant advantage in their subsequent spread into Eurasia, particularly upon interaction with Neanderthal populations that had previously been far from the original contact zone in the Levant.

evolutionary biology↗

Evolution of resilience in protein interactomes across the tree of life

Phenotype robustness to environmental fluctuations is a common biological phenomenon. Although most phenotypes involve multiple proteins that interact with each other, the basic principles of how such interactome networks respond to environmental unpredictability and change during evolution are largely unknown. Here we study interactomes of 1,840 species across the tree of life involving a total of 8,762,166 protein-protein interactions. Our study focuses on the resilience of interactomes to network failures and finds that interactomes become more resilient during evolution, indicating that a species position in the tree of life is predictive of how robust its interactome is to network failures. In bacteria, we find that a more resilient interactome is in turn associated with the greater ability of the organism to survive in a more complex, variable and competitive environment. We find that at the protein family level, proteins exhibit a coordinated rewiring of interactions over time and that a resilient interactome arises through gradual change of the network topology. Our findings have implications for understanding molecular network structure both in the context of evolution and environment.\n\nSignificance StatementThe interactome network of protein-protein interactions captures the structure of molecular machinery that underlies organismal complexity. The resilience to network failures is a critical property of the interactome as the breakdown of interactions may lead to cell death or disease. By studying interactomes from 1,840 species across the tree of life, we find that evolution leads to more resilient interactomes, providing evidence for a longstanding hypothesis that interactomes evolve favoring robustness against network failures. We find that a highly resilient interactome has a beneficial impact on the organisms survival in complex, variable, and competitive habitats. Our findings reveal how interactomes change through evolution and how these changes affect their response to environmental unpredictability.

systems biology↗

Cryptic selection forces and dynamic heritability in generalized phenotypic evolution

Individuals with different phenotypes can have widely-varying responses to natural selection, yet many classical approaches to evolutionary dynamics emphasize how a populations average phenotype increases in fitness over time. However, recent experimental results have produced examples of populations that have multiple fitness peaks, or that experience frequency-dependence that affects the direction and strength of selection on certain individuals. Here, we extend classical fitness gradient formulations of natural selection in order to describe the dynamics of a phenotype distribution in terms of its moments--such as the mean, variance, skewness, etc. The number of governing equations in our model can be adjusted in order to capture different degrees of detail about the population. We compare our simplified model to direct Wright-Fisher simulations of evolution in several canonical fitness landscapes, we find that our model provides a low-dimensional description of complex dynamics not typically explained by classical theory, such as cryptic selection forces due to selection on trait ranges, time-variation of the heritability, and nonlinear responses to stabilizing or disruptive selection due to asymmetric trait distributions. In addition to providing a framework for extending general understanding of common qualitative concepts in phenotypic evolution--such as fitness gradients, selection pressures, and heritability--our approach has practical importance for studying evolution in contexts in which genetic analysis is infeasible.

evolutionary biology↗

Who is the host of the host-associated microbiome? Colony-level dynamics overshadow individual-level characteristics in the fur microbiome of a social mammal, the Egyptian fruit-bat

In the first longitudinal study of bat microbiomes, we find that unlike the pattern described in humans and other mammals, the prominent dynamics in Egyptian fruit bats fur microbiomes are those of change over time at the level of the colony as a whole. Thus, on average, a pair of fur microbiome samples from different individuals in the same colony collected on the same date are more similar to one another than a pair of samples from the same individual collected at different time points. This pattern suggests that the whole colony may be the appropriate biological unit for understanding some of the roles of the host microbiome in social bats ecology and evolution. This pattern of synchronized colony changes over time is also reflected in the profile of volatile compounds in the bats fur, but differs from the more individualized pattern found in the bats gut microbiome.

ecology↗

Generation of Variation and Mean Fitness Increase: Necessity is the Mother of Genetic Invention

Generation of variation may be detrimental in well-adapted populations evolving under constant selection. In a constant environment, genetic modifiers that reduce the rate at which variation is generated by processes such as mutation and migration, succeed. However, departures from this reduction principle have been demonstrated. Here we analyze a general model of evolution under constant selection where the rate at which variation is generated depends on the individual. We find that if a modifier allele increases the rate at which individuals of below-average fitness generate variation, then it will increase in frequency and increase the population mean fitness. This principle applies to phenomena such as stress-induced mutagenesis and condition-dependent dispersal, and exemplifies \"Necessity is the mother of genetic invention.\"

evolutionary biology↗

Evolution of vertical and oblique transmission under fluctuating selection

Vertical and oblique cultural transmission of a dichotomous phenotype is studied under constant, periodic cycling, and randomly fluctuating selection. Conditions are derived for the existence of a stable polymorphism in a periodically cycling selection regime. Under such a selection regime, the fate of a genetic modifier of the rate of vertical transmission depends on the length of the cycle and the strength of selection. In general, the evolutionarily stable rate of vertical transmission differs markedly from the rate that maximizes the geometric mean fitness of the population. The evolution of rules of transmission has dramatically different dynamics from the more frequently studied modifiers of recombination, mutation, or migration.

evolutionary biology↗