Search arXivSearch

arXiv · q-bio/0611063

Asexual and sexual replication in sporulating organisms

Abstract

This paper develops models describing asexual and sexual replication in sporulating organisms. Replication via sporulation is the replication strategy for all multicellular life, and may even be observed in unicellular life (such as with budding yeast). We consider diploid populations replicating via one of two possible sporulation mechanisms: (1) Asexual sporulation, whereby adult organisms produce single-celled diploid spores that grow into adults themselves. (2) Sexual sporulation, whereby adult organisms produce single-celled diploid spores that divide into haploid gametes. The haploid gametes enter a haploid "pool", where they may recombine with other haploids to form a diploid spore that then grows into an adult. We consider a haploid fusion rate given by second-order reaction kinetics. We work with a simplified model where the diploid genome consists of only two chromosomes, each of which may be rendered defective with a single point mutation of the wild-type. We find that the asexual strategy is favored when the rate of spore production is high compared to the characteristic growth rate from a spore to a reproducing adult. Conversely, the sexual strategy is favored when the rate of spore production is low compared to the characteristic growth rate from a spore to a reproducing adult. As the characteristic growth time increases, or as the population density increases, the critical ratio of spore production rate to organism growth rate at which the asexual strategy overtakes the sexual one is pushed to higher values. Therefore, the results of this model suggest that, for complex multicellular organisms, sexual replication is favored at high population densities, and low growth and sporulation rates.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Bohyun Lee, Emmanuel Tannenbaum. 2006-11-19. Asexual and sexual replication in sporulating organisms. https://doi.org/10.1103/physreve.76.021909

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related papers

Graph construction in QUBO-based recursive phylogenetic tree reconstruction

Molecular sequence data are used to reconstruct evolutionary relationships among taxa, but reconstruction accuracy depends not only on the tree-building method but also on how pairwise sequence relationships are represented. We evaluated sequence-to-affinity representations in a recursive normalized-cut (Ncut) framework whose graph-partitioning subproblems were formulated as quadratic unconstrained binary optimization (QUBO) models and solved using Simulated Bifurcation. Using simulated amino-acid and nucleotide datasets spanning multiple tree-generation settings and evolutionary divergence, we compared normalized bit-score affinities with representations derived from transformed sequence similarities and evolutionary distances, examined post-swap refinement, and used neighbor joining (NJ) as a distance-based comparator. Affinity representation substantially affected internal split recovery, particularly for nucleotide data. JC69-based local affinities maintained comparatively high accuracy as divergence increased, whereas normalized bit-score and BLAST-derived kernel representations declined more markedly. Post-swap refinement generally improved recovery, but not consistently across individual reconstructions. NJ achieved higher mean split recovery than corresponding recursive Ncut reconstructions for WAG and JC69 distances across all evaluated conditions, whereas recursive Ncut outperformed NJ for BLAST-derived logarithmic distances under some conditions. These results show that graph construction is an important determinant of recursive Ncut-based phylogenetic reconstruction. A representation that performs well within Ncut does not necessarily provide the most accurate use of the underlying pairwise distances. Pairwise representation, affinity transformation, optimization, and recursive tree construction should therefore be evaluated jointly.

q-bio.PE

A conceptual predator-prey model with super-long transients

Drawing on the understanding of the logistic map, we propose a simple predator-prey model where predators and prey adapt to each other, leading to the co-evolution of the system. The special dynamics observed in periodic windows contribute to the coexistence of multiple time scales, adding to the complexity of the system. Typical dynamics in ecosystems, such as the persistence and coexistence of population cycles and chaotic behaviors, the emergence of super-long transients, regime shifts, and the quantifying of resilience, are encapsulated within this single model. The simplicity of our model allows for detailed analysis, reinforcing its potential as a conceptual tool for understanding ecosystems deeply.

q-bio.PE

Mutation Order and Selection Shape Intratumor Heterogeneity in Tumor Evolution

Cancer progression often requires multiple driver mutations, but the same drivers may be acquired in different orders. How these pathways jointly shape tumor clonal structure remains unclear. We develop a multitype branching-process model in which malignant transformation requires two driver mutations, distinguishing malignant cells by mutation order and the independent transformation event that founded their clone. Under a successive exponential approximation, we establish point-process limits for pathway-specific clone sizes and derive a closed-form expression for the limiting expected Simpson's index of the combined malignant population. When both mutation orders yield malignant cells with the same net growth rate, the index decomposes into effective pathway weights, determined by mutation rates and birth-death dynamics at preceding stages, and within-pathway concentration terms, determined by intermediate-to-malignant growth-rate ratios. A driver's effect on heterogeneity thus depends critically on when it is acquired. A strong driver acquired early expands the intermediate lineage and increases the supply of independent malignant founders, whereas the same driver acquired last strengthens the growth and age advantage of early-founded malignant clones. Under additive fitness effects, these opposing mechanisms can produce a non-monotone relationship between selective advantage and clonal concentration. Threshold-like non-additive fitness effects can generate highly concentrated malignant populations, while order-dependent terminal fitness causes the faster-growing pathway to dominate asymptotically. These results show how mutation order, mutational accessibility, selection, and epistasis jointly determine lineage-level intratumor heterogeneity.

q-bio.PE