Biology subjects

Kumata, R.

Publications and source records attributed to Kumata, R..

6 recordsLinked to original sources

bioRxiv2026

Species-composition distributions under competition, ecological drift and immigration

Understanding how species interactions, ecological drift, and immigration jointly shape community composition is a central goal of community ecology. These processes determine not only average community composition, but also how often different community states occur. Here, we ask how competition reshapes the neutral distribution of community composition generated by drift and immigration. We analyze a stochastic two-species competition model with immigration and derive the stationary distribution of relative species composition near neutrality. The stationary distribution shows when communities are usually balanced and when they are instead dominated by one species. Species dominance can become common even when the corresponding deterministic model predicts stable coexistence, particularly in smaller communities. Balanced and dominance states can also occur together, producing a trimodal distribution. Competitive asymmetry further biases the distribution toward the competitively favored species. Thus, the interplay between competition, ecological drift, and immigration determines not only how much community composition varies, but also which community states are most likely to be observed. Our results provide an analytical bridge between neutral and competition theory and a framework for interpreting variation in community composition.

ecology↗

bioRxiv2025

Eco-evolutionary dynamics of pathogen epidemic timing in a seasonal environment

Seasonality structures the dynamics of infectious diseases, yet how pathogens evolve their seasonal timing remains unclear. Here, we develop an evolutionary epidemiology model to examine how pathogens adapt to seasonally varying environments, assuming that each strain favours a specific season for transmission. Analytical and numerical results reveal two contrasting regimes: phenological drift, where the preferred season continually advances through priority effects, and stable seasonal adaptation, where evolution converges to a fixed season. Under strong transmissibility, multiple seasonal morphs can coexist, forming polymorphic communities of epidemic timing. These outcomes result from the balance between a seasonal priority effect, rewarding early occupation of the niche, and a seasonal stabilising effect, adjusting traits to the external optimum. Our findings show that epidemic seasonality itself can evolve as a life-history trait, providing a conceptual bridge between pathogen dynamics and the broader evolution of phenology in periodic environments.

evolutionary biology↗

bioRxiv2025

The effect of spatial bottleneck on human eco-cultural range expansion

The spatial spread of humans and culture is shaped by feedback between demography and cultural accumulation, as captured by the eco-cultural range expansion model. Yet, the effect of the geographical boundaries on this process remains poorly understood. Here, we extend the model to a two dimensional space where two large habitats are connected by a narrow corridor (spatial bottleneck) with reflecting boundaries. We find that a wave of ecological invasion is unaffected by the bottleneck, whereas a cultural wave can be blocked by sufficiently narrow corridors. The maximum bottleneck width that prevents propagation depends on the domain shape, and it converges to the threshold value when the habitat to be invaded gets larger. Our results align with mathematical results on a bistable reaction-diffusion equation, particularly mean curvature flow, based on which we provide an approximate formula of the threshold bottleneck width. Applied to the Middle- Upper Paleolithic transition, the findings suggest that while the spread of modern humans was robust to spatial bottlenecks, the expansion of advanced Upper Paleolithic culture could be delayed or halted by narrow corridors. Archaeological records point to potential cases where such geographic bottlenecks constrained cultural dispersal.

ecology↗

bioRxiv2025

The ambivalent effect of spatial structure on the spread of cooperative anti-CRISPR phages

Some phages have evolved the ability to cooperate to evade the immunity triggered by their bacterial host. A first exposure to the phage may weaken the host defences and allow later infections to be successful. Because this cooperation requires sequential infections, the phage can invade the host population only if its initial density is sufficiently high in a well-mixed environment. However, most natural bacterial populations are spatially structured. Could spatial structure create more favourable conditions for viral spread? Here we study the effect of spatial structure on the dynamics of cooperative anti-CRISPR (Acr) phages spreading in a population of CRISPR-Cas resistant Pseudomonas aeruginosa bacteria. We show experimentally that spatial structure does not always promote the spread of Acr-phages. In particular, the effect of spatial structure is modulated by the efficacy of the bacterial hosts CRISPR-Cas resistance and by the efficacy of the phage Acr protein. These results are discussed in the light of a mathematical model we developed to describe the spread of the phage. The model allows us to understand the ambivalent effects of spatial structure via its effects on the reproduction and on the persistence of the phage. More generally, we find that spatial structure can have opposite effects on the epidemiological dynamics of the phage, depending on the properties of the Acr protein encoded by the phage. This joint experimental and theoretical work yields a deeper understanding of the spatial dynamics of cooperative strategies in phages.

microbiology↗

bioRxiv2022

Antigenic escape accelerated by the presence of immunocompromised hosts

The repeated emergence of SARS-CoV-2 escape mutants from host immunity has obstructed the containment of the current pandemic and poses a serious threat to humanity. Prolonged infection in immunocompromised patients has received increasing attention as a driver of immune escape, and accumulating evidence suggests that viral genomic diversity and emergence of immune-escape mutants are promoted in immunocompromised patients. However, because immunocompromised patients comprise a small proportion of the host population, whether they have a significant impact on antigenic evolution at the population level is unknown. We used an evolutionary epidemiological model combining antigenic evolution and epidemiological dynamics in host populations with heterogeneity in immune competency to determine the impact of immunocompromised patients on the pathogen evolutionary dynamics of antigenic escape from host immunity. We derived analytical formulae of the speed of antigenic evolution in heterogeneous host populations and found that even a small number of immunocompromised hosts in the population significantly accelerates antigenic evolution. Our results demonstrate that immunocompromised hosts play a key role in viral adaptation at the population level and emphasize the importance of critical care and surveillance of immunocompromised hosts.

evolutionary biology↗

bioRxiv2018

Gorilla APOBEC3 restricts SIVcpz and influences lentiviral evolution in great ape cross-species transmissions

Restriction factors including APOBEC3 family proteins have the potential prevent cross-species lentivirus transmissions. Such events as well as ensuing pathogenesis require the viral Vif protein to overcome/neutralize/degrade the APOBEC3 enzymes of the new host species. Previous investigations have focused on the molecular interaction between human APOBEC3s and HIV-1 Vif. However, the evolutionary interplay between lentiviruses and great ape (including human, chimpanzee and gorilla) APOBEC3s has not been fully investigated. Here we demonstrate that gorilla APOBEC3G plays a pivotal role in restricting lentiviral transmission from chimpanzee to gorilla. We also reveal that a sole amino acid substitution in Vif is sufficient to overcome the gorilla APOBEC3G-mediated species barrier. Moreover, the antiviral effects of gorilla APOBEC3D and APOBEC3F are considerably weaker than those of human and chimpanzee counterparts, which can result in the skewed evolution of great ape lentiviruses leading to HIV-1.\n\nHighlightsO_LISIVcpz requires M16E mutation in Vif to counteract gorilla A3G\nC_LIO_LIAcidic residue at position 16 of Vif is crucial to counteract gorilla A3G\nC_LIO_LIGorilla A3D and A3F poorly suppress lentiviral infectivity\nC_LIO_LISIVgor and related HIV-1s counteract human A3D and A3F independently of DRMR motif\nC_LI

microbiology↗