What does the geography of parthenogenesis teach us about sex?

Theory predicts that sexual reproduction is difficult to maintain if asexuality is an option, yet sex is very common. To understand why, it is important to pay attention to repeatably occurring conditions that favour transitions to, or persistence of, asexuality. Geographic parthenogenesis is a term that has been applied to describe a large variety of patterns where sexual and related asexual forms differ in their geographic distribution. Often asexuality is stated to occur in a habitat that is in some sense marginal, but the interpretation differs across studies: parthenogens might predominate near the margin of the sexuals’ distribution but might also extend far beyond the sexual range, they may be disproportionately found in newly colonizable areas (e.g., areas previously glaciated), or in habitats where abiotic selection pressures are relatively stronger than biotic ones (e.g. cold, dry). Here we review the various patterns proposed in the literature, the hypotheses put forward to explain them, and the assumptions they rely on. Surprisingly few mathematical models consider geographic parthenogenesis as their focal question, but all models for the evolution of sex could be evaluated in this framework if the (often ecological) causal factors vary predictably with geography. We also recommend broadening the taxa studied beyond the traditional favourites

Mitochondrial complementation: a possible neglected factor behind early eukaryotic sex

Sex is ancestral in eukaryotes. Meiotic sex differs from bacterial ways of exchanging genetic material by involving the fusion of two cells. We examine the hypothesis that fusion evolved in early eukaryotes because it was directly beneficial, rather than a passive side effect of meiotic sex. We assume that the uptake of (proto)mitochondria into eukaryotes preceded the evolution of cell fusion and that Muller's ratchet operating within symbiont lineages led to the accumulation of lineage‐specific sets of mutations in asexual host cells. We examine whether cell fusion, and the consequent biparental inheritance of symbionts, helps to mitigate the effects of this mutational meltdown of mitochondria. In our model, host cell fitness improves when two independently evolved mitochondrial strains co‐inhabit a single cytoplasm, mirroring mitochondrial complementation found in modern eukaryotes. If fusion incurs no cost, we find that an allele coding for fusion can invade a population of nonfusers. If fusion is costly, there are two thresholds. The first describes a maximal fusing rate (probability of fusion per round of cell division) that is able to fix. An allele that codes for a rate above this threshold can reach a polymorphic equilibrium with nonfusers, as long as the rate is below the second threshold, above which the fusion allele is counter‐selected. Whenever it evolves, fusion increases the population‐wide level of heteroplasmy, which allows mitochondrial complementation and increases population fitness. We conclude that beneficial interactions between mitochondria are a potential factor that selected for cell fusion in early eukaryotes

Data from: Mitochondrial complementation: a possible neglected factor behind early eukaryotic sex

Sex is ancestral in eukaryotes. Meiotic sex differs from bacterial ways of exchanging genetic material by involving the fusion of two cells. We examine the hypothesis that fusion evolved in early eukaryotes because it was directly beneficial, rather than a passive side-effect of meiotic sex. We assume that the uptake of (proto)mitochondria into eukaryotes preceded the evolution of cell fusion, and that Muller’s ratchet operating within symbiont lineages led to the accumulation of lineage-specific sets of mutations in asexual host cells. We examine if cell fusion, and the consequent biparental inheritance of symbionts, helps to mitigate the effects of this mutational meltdown of mitochondria. In our model, host cell fitness improves when two independently-evolved mitochondrial strains co-inhabit a single cytoplasm, mirroring mitochondrial complementation found in modern eukaryotes. If fusion incurs no cost, we find that an allele coding for fusion can invade a population of non-fusers. If fusion is costly, there are two thresholds. The first describes a maximal fusing rate (probability of fusion per round of cell division) that is able to fix. An allele that codes for a rate above this threshold can reach a polymorphic equilibrium with non-fusers, as long as the rate is below the second threshold, above which the fusion allele is counterselected. Whenever it evolves, fusion increases the population-wide level of heteroplasmy, which allows mitochondrial complementation and increases population fitness. We conclude that beneficial interactions between mitochondria are a potential factor that selected for cell fusion in early eukaryotes

R scripts + data

All the R scripts used to create the model, analyse it, and plot the figures presented in the paper and its supplementary material are contained in this .zip folder. The data used to plot the figures of the main text is also available. Everything also available on https://github.com/Redsiana/Escape-from-mitochondri

Deep learning‐based segmentation in prostate radiation therapy using Monte Carlo simulated cone‐beam CT

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