Biology subjects

Erten, E. Y.

Publications and source records attributed to Erten, E. Y..

6 recordsLinked to original sources

bioRxiv2026

Internal evolutionary conflicts: a conceptual synthesis and mathematical primer

Internal evolutionary conflicts arise when elements within an organism have diverging fitness interests. Examples range from meiotic drive and cytoplasmic male sterility to transposable elements and supernumerary B chromosomes. While once treated as genetic curiosities, they are now seen as widespread and major drivers of eukaryotic genome evolution. Yet their study remains fragmented, with no clear entry point not only for those who wish to gain an overview of theoretical advances, or those who wish to construct models of their own. Here, we discuss ways in which internal evolutionary conflicts have been modelled and develop a common population genetic framework for building such models. The framework provides explicit criteria for what counts as conflict, distinguishing it from fitness trade-offs, and formalises how and when internal conflicts arise. By treating different cases within the same structure, it shows that these diverse phenomena share a common logic.

evolutionary biology↗

bioRxiv2025

Genetic variation in life-history traits is not correlated with estrogen-receptor positive breast cancer risk

Estrogen receptor-positive breast cancer (ER+ BC) is one of the most prevalent cancers, but the evolutionary processes shaping genetic variation in ER+ BC risk are poorly understood. Both evolutionary life-history theory and evidence from studies of individual ER+ BC risk variants suggest that increased genetic ER+ BC risk is associated with faster maturation, earlier reproduction, and/or increased reproductive success (i.e., there is a trade-off), but it is unclear how well this pattern is replicated when considering the polygenic architecture of these traits after controlling for potential biases. Here, we estimate genome-wide genetic correlations between ER+ BC risk and three reproductive traits (age at menarche, age at first birth, and the number of children) using genomic restricted maximum-likelihood analyses on Lifelines biobank data and linkage disequilibrium score regressions on population and family-based genome-wide association study data. Regardless of the data or method used, genetic correlations were low and not statistically significant. Further analyses decomposing genome-wide genetic variance into local regions detected only three loci exhibiting significant pleiotropy between ER+ BC risk and age at menarche, suggesting little shared genetic architecture between ER+ BC risk and reproductive traits. Thus, the role of life-history trade-offs in shaping ER+ BC risk in European populations appears, at most, small, and the evolutionary processes giving rise to this life-threatening disease remain unclear. Future studies could examine the impact of evolutionary mismatches in shaping ER+ BC risk, where conducting longitudinal studies on populations transitioning to reproductive patterns observed in contemporary European populations would be most useful.

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↗

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↗