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Biology subjects

Omole, A. D.

Publications and source records attributed to Omole, A. D..

2 recordsLinked to original sources

A population genetics model explaining overdispersion in active transposable elements

Active transposable element (TE) families often show overdispersion (variance greater than the mean), which is in contrast to the predictions of classical Poisson-based models and related theories built on the same approximation. To address this gap, we develop a diploid stochastic model of TE dynamics under free recombination, based on a biparental Moran model with transposition, excision, purifying selection, and derive mean and variance dynamics of TE copy numbers at two stages of the life cycle: before and after transposition and excision. We show that overdispersion arises naturally through transposition generating positive linkage disequilibrium between TE insertion sites with the disequilibrium persisting even under free recombination. The higher the transposition rate, the stronger the resulting overdispersion. Underdispersion and Poisson-like variation are instead stage-dependent: neither is expected after transposition and excision, while both remain possible beforehand, governed by the curvature of the fitness function. We further show that maintaining positive equilibrium copy numbers, and thus sustaining overdispersion, requires the net transposition rate to remain below roughly 0.5 insertions per copy per generation, a constraint satisfied by observed natural populations to maintain genome stability. A qualitative comparison with the DPGP3 Zambian Drosophila melanogaster dataset, focusing on TE insertions in high-recombination euchromatic regions shows that most TE families are overdispersed and that many also exhibit the predicted right-skewness and excess-kurtosis patterns, which are predicted by our model. These results identify overdispersion as a natural outcome of active TE dynamics and provide a mechanistic framework for understanding the full distribution of TE copy numbers in highly recombining regions.

genetics↗

Maintenance of long-term transposable element activity in genomes through regulation by nonautonomous elements

Transposable elements are DNA sequences that can move and replicate within genomes. Broadly, there are two types: autonomous elements, which encode the necessary enzymes for transposition, and nonautonomous elements which rely on the enzymes produced by autonomous elements for their transposition. Nonautonomous elements have been proposed to regulate the numbers of transposable elements, which is a possible explanation for the persistence of transposition activity over long evolutionary times. However, previous modeling studies indicate that interactions between autonomous and nonautonomous elements usually result in the extinction of one type. Here, we study a stochastic model that allows for the stable coexistence of autonomous and nonautonomous retrotransposons. We determine the conditions for this coexistence and derive an analytical expression for the stationary distribution of their copy numbers, showing that nonautonomous elements regulate stochastic fluctuations and the number of autonomous elements in stationarity. We find that the stationary variances of each element can be expressed as a function of the average copy numbers and their covariance, enabling data comparison and model validation. These results suggest that continued transposition activity of transposable elements, regulated by nonautonomous elements, is a possible evolutionary outcome that could for example explain the long co-evolutionary history of autonomous LINE1 and nonautonomous Alu element transposition in the human ancestry.

evolutionary biology↗