Biology subjects

Kokko, H.

Publications and source records attributed to Kokko, H..

At least 19 recordsLinked to original sources

bioRxiv2026

Competition among kin generates balancing selection in a wild population

If an individuals niche is determined by its genotype, then competition for limiting resources should be most intense among individuals of the same genotype. Theory predicts this will act to maintain genetic variation, but whether this mechanism operates under natural conditions is unclear. Using long-term observations of a population of free-living Trinidadian guppies, we asked (i) whether competition was strongest between kin, and (ii) whether this process maintained genetic variation. Competition between kin was 1.5-1.8 times stronger than that between non-kin. This contributed to balancing selection: after [~]10 generations, variation was 29% higher than expected under drift. Our results show that relatedness can play a major role in structuring ecological competition, with broader consequences for theories of inclusive fitness. One-sentence summaryHeritable variation is maintained due to resource competition being more intense among kin.

evolutionary biology↗

bioRxiv2026

Stochastic failure accumulation as a foundation for exponential mortality and selective disappearance

Most organisms become increasingly likely to die as they grow older, a phenomenon known as demographic senescence. Despite this statement saying nothing about the particular shape of a mortality curve, the Gompertz-Makeham law remains remarkably accurate in a broad range of species. We develop a general mathematical framework in which individuals are modelled as comprising a fixed number of interacting intra-organismal sub-systems, each characterised by stochastic failure and repair rates, such that the number of failed sub-systems follows a birth-death process. In many organisms, failure begets failure because sub-systems are typically interdependent. We use diffusion approximations to demonstrate that this interdependence generically produces Gompertz-Makeham mortality curves. Since individuals who die can no longer age, observed cohorts become increasingly composed of lucky individuals that avoided death by (stochastically) taking paths in failure space associated with lower mortality despite no intrinsic differences in their quality. Selective disappearance of unlucky individuals generates deviations from Gompertz-Makeham predictions at advanced ages, producing a late-life mortality plateau. We show that while these deviations must always exist, they may often be too small to detect, either because the failure accumulation process is stereotyped or because detection requires unreasonably large cohort sizes. Our work establishes Gompertz-Makeham curves arising from stochastic failure accumulation as a null expectation in organisms with many interdependent sub-systems.

ecology↗

bioRxiv2026

Beyond abstract selection coefficients: Protandry impacts the buildup of heterozygote advantage over the lifespan in a color polymorphic moth

Population genetic models excel at identifying the conditions for polymorphisms based on balancing selection but typically disregard the ecological processes that yield particular values of selection coefficients. We model a system that combines antagonistic pleiotropy, dominance reversal and heterozygote advantage: the wood tiger moth Arctia plantaginis, where alternative haplotypes at a major-effect locus determine male hindwing coloration. Yellow offers better protection against predators, while white is often associated with better mating success. The effects of mortality and reproductive success overlap in time because protandrous males can mate as long as they are alive, but they need to avoid predation for several days before the bulk of females emerge. We show that protandry aids polymorphism maintenance whenever the second-fittest genotype (after the heterozygote) is the poorly surviving but mating advantaged homozygote, while increased protandry harms polymorphism when the second-best fitness is that of the survival advantaged morph. Ecologically plausible protandry times predict that dominance reversal does not have to be strong for polymorphism to be maintained. Our study highlights the importance of timing traits in maintaining polymorphisms in Lepidoptera and showcases the benefits of deriving fitness explicitly in place of abstract selection coefficients that lack temporal components within the life cycle.

evolutionary biology↗

bioRxiv2025

A century of theories of balancing selection

Traits that affect organismal fitness are often very genetically variable. This genetic variation is vital for populations to adapt to their environments, but it is also surprising given that nature (after all) "selects" the best genotypes at the expense of those that fall short. Explaining the extensive genetic variation of fitness-related traits is thus a longstanding puzzle in evolutionary biology, with cascading implications for ecology, conservation, and human health. Balancing selection--an umbrella term for scenarios of natural selection that maintain genetic variation-- is a century-old explanation to resolve this paradox that has gained recent momentum from genome-scale methods for detecting it. Yet evaluating whether balancing selection can, in fact, resolve the paradox is challenging, given the logistical constraints of distinguishing balancing selection from alternative hypotheses and the daunting collection of theoretical models that formally underpin this debate. Here, we track the development of balancing selection theory over the last century and provide an accessible review of this rich collection of models. We first outline the range of biological scenarios that can generate balancing selection. We then examine how fundamental features of genetic systems--including non-random mating between individuals, differences in ploidy, genetic drift, and different genetic architectures of traits-- have been progressively incorporated into the theory. We end by linking these theoretical predictions to ongoing empirical efforts to understand the evolutionary processes that explain genetic variation.

evolutionary biology↗

bioRxiv2024

Infection dynamics of endosymbionts that manipulate arthropod reproduction

A large proportion of arthropod species are infected with endosymbionts, some of which selfishly alter host reproduction. The currently known forms of parasitic reproductive manipulations are male-killing, feminization, cytoplasmic incompatibility, parthenogenesis induction and distortion of sex allocation. While all of these phenomena represent adaptations that enhance parasite spread, they differ in the mechanisms involved and the consequent infection dynamics. We focus here on the latter aspect, summarizing existing theoretical literature on infection dynamics of all known reproductive manipulation types, and completing the remaining knowledge gaps where dynamics have not been modelled yet. Our unified framework includes the minimal model components required to describe the effects of each manipulation. We establish invasion criteria for all potential combinations of manipulative endosymbionts, yielding predictions for an endosymbionts increase from rarity within a host population that is initially either uninfected or infected with a different symbiont strain. We consider diplodiploid and haplodiploid hosts, as the mechanisms as well as the infection dynamics of reproductive manipulations can differ between them. Our framework reveals that endosymbionts that a priori have the best invasion prospects are not necessarily the most commonly found ones in nature; priority effects play a role too, and cytoplasmic incompatibility excels in this regard. As a whole, considerations of the ease with which a symbiont spreads have to be complemented with knowledge of how easy it is to achieve a particular manipulation, and other factors influencing host switches.

evolutionary biology↗

bioRxiv2024

Sex-specific immunocompetence: resistance and tolerance can both be futile but not under the same circumstances

Immunocompetence evolution can involve a resistance is futile scenario, if parasite encounter rates are so high that high investment in resistance only marginally delays infection. Here, we investigate two understudied aspects of futility. First, immunocompetence is usefully categorized as reducing the rate of becoming infected (resistance) or reducing the negative fitness consequences of infection once it happened (tolerance). We compare the prospects of futility for resistance, tolerance, and their joint occurrence, showing that resistance futility arises with respect to parasite encounter rates, while tolerance futility arises with respect to parasite virulence. However, if the same host trait improves pleiotropically both resistance and tolerance, futility disappears altogether and immunity investment remains profitable when increasing parasite encounter rates, virulence, or both. Second, we examine how sexual selection strength impacts these findings. If one sex (typically males) is near the faster end of a fast-slow continuum of life histories, then life history patterns reflecting futility can evolve sex-specificity. The solutions often feature sexual dimorphism in immunocompetence, but not always in the direction of strong sexual selection yielding low immunity: sexual selection can select for faster and sicker lives, but if sexual selection also causes traits that impact parasite encounter rates, the results are strongly dependent on whether futility (along any axis) plays a role. Lay SummaryIntuition suggests that investment into immunity is higher, when hosts frequently encounter parasites. While there are examples that confirm this, in other cases, hosts have been shown to abandon immune defenses under high parasite pressure. We reconcile these findings by modelling the optimal host resource allocation towards immunity under varying parasite pressure and strength of sexual selection. Our results show two axes along which immunity investments are futile and should therefore be abandoned in favor of investing into reproduction: resisting infection becomes futile under high parasite abundance, while tolerating the harmful effects of infection is not beneficial under ever increasing parasitic virulence. However, investments of organisms that are capable of both resistance and tolerance mechanisms yield fitness payoffs also when parasites are highly virulent and abundant. This work highlights the impact of parasites and immune defenses on optimal immunity investment levels in hosts, an insight which also complements theory on sex-specific immunity.

evolutionary biology↗

bioRxiv2022

Positive fitness effects help explain the broad range of Wolbachia prevalences in natural populations

The bacterial endosymbiont Wolbachia is best known for its ability to modify its hosts reproduction by inducing cytoplasmic incompatibility (CI) to facilitate its own spread. Classical models predict either near-fixation of costly Wolbachia once the symbiont has overcome a threshold frequency (invasion barrier), or Wolbachia extinction if the barrier is not overcome. However, natural populations do not all follow this pattern: Wolbachia can also be found at low frequencies (below one half) that appear stable over time. Wolbachia is known to have pleiotropic fitness effects (beyond CI) on its hosts. Existing models typically focus on the possibility that these are negative. Here we consider the possibility that the symbiont provides direct benefits to infected females (e.g. resistance to pathogens) in addition to CI. We discuss an underappreciated feature of Wolbachia dynamics: that CI with additional fitness benefits can produce low-frequency (< 1/2) stable equilibria. Additionally, without a direct positive fitness effect, any stable equilibrium close to one half will be sensitive to perturbations, which make such equilibria unlikely to sustain in nature. The results hold for both diplodiploid and different haplodiploid versions of CI. We suggest that insect populations showing low-frequency Wolbachia infection might host CI-inducing symbiotic strains providing additional (hidden or known) benefits to their hosts, especially when classical explanations (ongoing invasion, source-sink dynamics) have been ruled out.

ecology↗

bioRxiv2022

Extrinsic mortality and senescence: a guide for the perplexed

Do environments or species traits that lower the mortality of individuals create selection for delaying senescence? Reading the literature creates an impression that mathematically oriented biologists cannot agree on the validity of George Williams prediction (who claimed yes). The abundance of models and opinions may bewilder those that are new to the field. Here we provide heuristics as well as simple models that outline when the Williams prediction holds, why there is a null model where extrinsic mortality does not change the evolution of senescence at all, and why it is also possible to expect the opposite of Williams prediction, where increased extrinsic mortality favours slower senescence. We hope to offer intuition by quantifying how much delaying the placement of an offspring into the population reduces its expected contribution to the gene pool of the future. Our first example shows why sometimes increased extrinsic mortality has no effect (the null result), and why density dependence can change that. Thereafter, a model with ten different choices for population regulation shows that high extrinsic mortality favours fast life histories (Williams) if increasing density harms the production of juveniles or their chances to recruit into the population. If instead increasing density harms the survival of older individuals in a population, then high extrinsic mortality favours slow life histories (anti-Williams). We discuss the possibility that empirically found Williams-like patterns provide indirect evidence for population regulation operating via harming the production or fitness prospects of juveniles, as opposed to the survival of established breeders.

evolutionary biology↗

bioRxiv2021

Sex differences in the strength of selection under facultative sex

Facultative sex, the ability to reproduce both sexually and asexually, is widespread across the tree of life. In anisogamous species, the frequency of sex modulates selection on traits with sex-specific expression. Current theory on conditional gene expression posits that the strength of selection on loci only expressed by a subset of individuals, and/or in a subset of environments, is proportional to the frequency of expressers in the population. We show here that this assumption does not hold when the subsets in question are males or females (because of the Fisher condition) and is most important in facultatively sexual populations. In this case, the proportion of sexually produced offspring is not determined by male frequency (sex ratio), but on relative female investment in sexual versus asexual reproduction. This breaks the link between the frequency of expressers and selection for loci with sex-specific expression. However, certain conditions can re-establish this link, for example male traits that predict mating success better under strong male-male competition, and sex ratio affecting the relative fecundity of sexual versus asexual females. Our work highlights the importance of the Fisher condition for understanding the efficiency of selection and has implications for differences in the genetic load among sexes.

evolutionary biology↗

bioRxiv2021

Balancing quality and quantity of social relationships in volatile social environments

Cooperation does not occur in a vacuum: interactions develop over time in social groups that undergo demographic changes. Intuition suggests that stable social environments favour developing few but strong reciprocal relationships (a focused strategy), while volatile social environments favour the opposite: more but weaker social relationships (a diversifying strategy). We model reciprocal investments under a quality-quantity tradeoff for social relationships. We find that volatility, counterintuitively, can favour a focused strategy. This result becomes explicable through applying the theory of antagonistic pleiotropy, originally developed for senescence, to social life. Diversifying strategies show superior performance later in life, but with costs paid at young ages while the social network is slowly being built. Under volatile environments, many individuals die before reaching sufficiently old ages to reap the benefits. Social strategies that do well early in life are then favoured: a focused strategy leads individuals to form their first few social bonds quickly and to make strong use of existing bonds. Our model highlights the importance of pleiotropy and population age structure for the evolution of cooperative strategies and other social traits, and shows that it is not sufficient to reflect on the fate of survivors only, when evaluating the benefits of social strategies.

evolutionary biology↗

bioRxiv2021

Parthenogenesis and the Evolution of Anisogamy

Recently, it was pointed out [1] that classic models for the evolution of anisogamy do not take into account the possibility of parthenogenetic reproduction, even though sex is facultative in many relevant taxa (e.g. algae) that harbour both anisogamous and isogamous species. Here we complement the analysis of [1] with an approach where we assume that the relationship between progeny size and its survival may differ between parthenogenetically and sexually produced progeny, favouring either the former or the latter. We show that the findings of [1], that parthenogenesis can stabilise isogamy relative to the obligate sex case, extend to our scenarios. We additionally investigate two different ways for one mating type to take over the entire population. First, parthenogenesis can lead to biased sex ratios that are sufficiently extreme that one type can displace the other, leading to de facto asexuality for the remaining type that now lacks partners to fuse with. This process involves positive feedback: microgametes, being numerous, lack opportunities for syngamy, and should they proliferate parthenogenetically, the next generation makes this asexual route even more prominent for microgametes. Second, we consider mutations to strict asexuality in producers of micro- or macrogametes, and show that the prospects of asexual invasion depend strongly on the mating type in which the mutation arises. Perhaps most interestingly, we also find scenarios in which parthenogens have an intrinsic survival advantage yet facultatively sexual isogamous populations are robust to the invasion of asexuals, despite us assuming no genetic benefits of recombination. Here equal contribution from both mating types to zygotes that are sufficiently well provisioned can outweigh the additional costs associated with syngamy.

evolutionary biology↗

bioRxiv2021

Selfish migrants: How a meiotic driver is selected to increase dispersal

Meiotic drivers are selfish genetic elements that manipulate meiosis to increase their transmission to the next generation to the detriment of the rest of the genome. One example is the t haplotype in house mice, which is a naturally occurring meiotic driver with deleterious traits--poor fitness in polyandrous matings and homozygote inviability or infertility--that prevent its fixation. Recently, we discovered and validated a novel effect of t in a long-term field study on free-living wild house mice and with experiments: t-carriers are more likely to disperse. Here, we ask what known traits of the t haplotype can select for a difference in dispersal between t-carriers and wildtype mice. To that end, we built individual-based models with dispersal loci on the t and the homologous wildtype chromosomes. We also allow for density-dependent expression of these loci. The t haplotype consistently evolves to increase the dispersal propensity of its carriers, particularly at high densities. By examining variants of the model that modify different costs caused by t, we show that the increase in dispersal is driven by the deleterious traits of t, disadvantage in polyandrous matings and lethal homozygosity or male sterility. Finally, we show that an increase in driver-carrier dispersal can evolve across a range of values in driver strength and disadvantages.

evolutionary biology↗

bioRxiv2021

Cancer risk and sexual conflict as constraints to body size evolution

Selection often favours large bodies, visible as Copes rule over macroevolutionary time -- but size increases are not inevitable. One understudied cost of large bodies is the high number of cell divisions and the associated risk of oncogenic mutations. Our elasticity analysis shows that selection against a proportional increase in size becomes ever more intense with increasing body size if cancer is the sole selective agent. Thus cancer potentially halts body size increases even if no other constraint does so. We then provide multicellular realism with potentially sexually dimorphic body sizes and traits that control cell populations from zygote to maturity and beyond (ontogenetic management). This shows sexual conflict to extend to ontogeny; sexual dimorphism in mortalities and other life history measures may evolve even in the absence of any ecological causes underlying size- or sex-dependent mortality. Coadaptation of ontogenetic management and body size is required for substantial increases in size.

evolutionary biology↗

bioRxiv2020

Bird size with dinosaur-level cancer defences: can evolutionary lags during miniaturisation explain cancer robustness in birds?

An increased appreciation of the ubiquity of cancer risk across the tree of life means we also need to understand the more robust cancer defences some species seem to have. Petos paradox, the finding that large-bodied species do not suffer from more cancer even if their lives require far more cell divisions than those of small species, can be explained if large size selects for better cancer defences. Since birds live longer than non-flying mammals of an equivalent body size, and birds are descendants of moderate-sized dinosaurs, we ask whether ancestral cancer defence innovations are retained if body size shrinks in an evolutionary lineage. Our model derives selection coefficients and fixation events for gains and losses of cancer defence innovations over macroevolutionary time, based on known relationships between body size, intrinsic cancer risk, extrinsic mortality (modulated by flight ability) and effective population size. We show that evolutionary lags can, under certain assumptions, explain why birds, descendants of relatively large bodied dinosaurs, retain low cancer risk. Counterintuitively, it is possible for a bird to be too robust for its own good: excessive cancer suppression can take away from reproductive success. On the other hand, an evolutionary history of good cancer defences may also enable birds to reap the lifespan-increasing benefits of other innovations such as flight.

evolutionary biology↗

bioRxiv2020

Transmissible cancers do not easily select for sexual reproduction

The predominance of sexual reproduction in eukaryotes remains paradoxical in evolutionary theory. Of the hypotheses proposed to resolve this paradox, the "Red Queen hypothesis" emphasizes the potential of antagonistic interactions to cause fluctuating selection, which favours the evolution and maintenance of sex. While empirical and theoretical developments have focused on host-parasite interactions, the premises of the Red Queen theory apply equally well to any type of antagonistic interactions. Recently, it has been suggested that early multicellular organisms with basic anticancer defenses were presumably plagued by antagonistic interactions with transmissible cancers, and that this could have played a pivotal role in the evolution of sex. Here, we dissect this argument using a population genetic model. One fundamental aspect distinguishing transmissible cancers from other parasites is the continual production of cancerous cell lines from hosts own tissues. We show that this influx dampens fluctuating selection and therefore makes the evolution of sex more difficult than in standard Red Queen models. Although coevolutionary cycling can remain sufficient to select for sex under some parameter regions of our model, we show that the size of those regions shrinks once we account for epidemiological constraints. Altogether, our results suggest that horizontal transmission of cancerous cells is unlikely to cause fluctuating selection favouring sexual reproduction. Nonetheless, we confirm that vertical transmission of cancerous cells can promote the evolution of sex through a separate mechanism, known as similarity selection, that does not depend on coevolutionary fluctuations.

evolutionary biology↗

bioRxiv2020

RPA-PCR couple: an approach to expedite plant diagnostics and overcome PCR inhibitors

Plant diseases are often diagnosed by the method of DNA extraction followed by PCR. DNA extraction from plant tissue can be a recalcitrant and lengthy process, and sometimes ends up with inhibitors that reduce PCR amplification efficiency. Here we present a unique approach, RPA-PCR couple, to exclude the DNA extraction step from the standard plant diagnostic process. The process crudely macerates plant tissue in water for a few minutes, and then transfers the macerate supernatant to a Recombinase Polymerase Amplification (RPA) reaction. Following an incubation of 20 minutes at 39 {degrees}C, the RPA reaction can be directly utilized in PCR amplification. In RPA-PCR couple, the RPA reaction is run at slower reaction kinetics to promotes amplification of long amplicons and the slower reaction kinetics are achieved by lowering RPA components concentrations. In this proof of concept study, we targeted Phytophthora intergenic mitochondrial spacer between atp9 and nad9 genes and the two common Phytophthora pathogens of strawberry: P. fragariae and P. cactorum. We presented coupling of RPA with real time TaqMan and SYBR Green PCR assays, and conventional PCR amplification aimed at Sanger sequencing. We found the RPA-PCR couple specific and capable of detecting as low as 10 fg of Phytophthora genomic DNA. Moreover, comparing RPA-PCR couple with the routine method of DNA extraction followed by PCR generated comparable results for the field samples. The idea of RPA-PCR couple to exclude DNA extraction may have vast application in different fields such as clinical diagnostics, food inspection and soil sciences.

molecular biology↗

bioRxiv2020

Sex ratio and sexual conflict in a collective action problem

The maintenance of cooperation is difficult whenever collective action problems are vulnerable to freeriding (reaping the benefits without contributing to the maintenance of the good). We identify a novel factor that can make a system tolerate an extent of freeriding. If a population consists of discrete types with demographically distinct roles, such that the success of one type does not imply it can spread to replace other types in the population, then collective goods may persist in the presence of free-riders because they are necessarily kept in a minority role. Biased sex ratios (e.g. in haplodiploids) create conditions where individuals of one sex are a minority. We show that this can make the less common sex contribute less to a public good in a setting where the relevant life-history stage -- larval group defence against predators -- does not feature any current breeding opportunities that might lead to confounding reasons behind sex-specific behaviour. We test our model with haplodiploid pine sawfly larvae, showing that female larvae are the main contributors to building the antipredator defence against predators. Significance statementIndividuals in groups can cooperate to achieve something together, but with an evolutionary difficulty: if benefits of cooperation are shared equally among all, freeriders get the same benefit as others while paying less for it. We propose a novel reason why freeriding does not automatically spread until the collectively beneficial outcome is destroyed: sometimes groups consist of individuals of distinct categories, limiting freerider spread. If, for example, there are always fewer males than females, then even if every male becomes a freerider, the whole group still survives simply because not everyone can be male. Pine sawfly larvae defend against predators by regurgitating sticky fluids, but females contribute more to this common defence, and we show this example fits our model.

evolutionary biology↗

bioRxiv2019

From zygote to a multicellular soma: body size affects optimal growth strategies under cancer risk

Multicellularity evolved independently in multiple lineages, yielding organisms with a wide range of adult sizes. Building an intact soma is not a trivial task, when dividing cells accumulate damage. Here, we study ontogenetic management strategies, i.e. rules of dividing, differentiating and killing somatic cells, to examine two questions. First, do these rules evolve differently for organisms differing in the target mature body size, and second, how well a strategy evolved in small-bodied organisms performs if implemented in a large body - and vice versa ( large-evolved strategies in small bodies). We model the growth and mature lifespan of an organism starting from a single cell and optimize, using a genetic algorithm, trait combinations across a range of target sizes, with seven evolving traits: 1) probability of asymmetric division, 2) probability of differentiation (per symmetric cell division), 3) Hayflick limit, 4) damage response threshold, 5) damage response strength, 6) number of differentiation steps, 7) division propensity of cells relative to stemness. Some, but not all traits, evolve differently depending on body size: large-bodied organisms perform best with a smaller probability of differentiation, a larger number of differentiation steps on the way to form a tissue, and a higher threshold of cellular damage to trigger cell death, than small organisms. Strategies evolved in large organisms are more robust: they maintain high performance across a wide range of body sizes, while those that evolved in smaller organisms fail when attempting to create a large body. This highlights an asymmetry: under various risks of developmental failure and cancer, it is easier for a lineage to become miniaturized (should selection otherwise favour this) than to increase in size.

evolutionary biology↗