In nearly all eukaryotes, at least some individuals inherit mitochondrial and chloroplast genes from only one parent. There is no single mechanism of uniparental inheritance: organelle gene inheritance is blocked by a variety of mechanisms and at different stages of reproduction in different species. Frequent changes in the pattern of organelle gene inheritance during evolution suggest that it is subject to varying selective pressures. Organelle genes often fail to recombine even when inherited biparentally; consequently, their inheritance is asexual. Sexual reproduction is apparently less important for genes in organelles than for nuclear genes, probably because there are fewer of them. As a result organelle sex can be lost because of selection for special reproductive features such as oogamy or because uniparental inheritance reduces the spread of cytoplasmic parasites and selfish organelle DNA.

When an advantageous mutation is fixed in a population by selection, a closely linked selectively neutral or mildly detrimental mutation may "hitchhike" to fixation along with it. It has been suggested that hitchhiking might increase the rate of molecular evolution. Computer simulations and a mathematical argument show that complete linkage to either advantageous or deleterious mutations does not affect the substitution of selectively neutral mutations. However, the simulations show that linkage to selected background mutations decreases the rate of fixation of advantageous mutations and increases the rate of fixation of detrimental mutations. This is true whether the linked background mutations are advantageous or detrimental, and it verifies and extends previous observations that linkage tends to reduce the effects of selection on evolution. These results can be interpreted in terms of the Hil-Robertson effect: a locus linked to another locus under selection experiences a reduction in effective population size. The interpretation of differences in evolutionary rates between different genomes or different regions of a genome may be confounded by the effects of strong linkage and selection.Recombination is expected to reduce the overall rate of molecular evolution while enhancing the rate of adaptive evolution. It (4) argued that the evolution of the inactive animal Y chromosome involved the accelerated fixation of mildly detrimental mutations linked to advantageous mutations. These suggestions were evidently based on the intuition that the fixation probability of a neutral or detrimental mutation, which is normally quite low, might be increased by linkage to an advantageous mutation. When linkage is complete, the unit of selection is a whole chromosome. Then a chromosome carrying a neutral or mildly detrimental mutation together with a strongly advantageous mutation will have a positive selection coefficient and a high probability offixation. By the same reasoning, detrimental mutations should slow the rate of substitution of linked neutral and weakly advantageous mutations (hitchhiking with a driver going backward). In contrast, Schaeffer and Aquadro (5) and Cann et al. (6) felt that it is unlikely that linkage would affect the fixation probability of a neutral mutation, but the latter proposed that the accumulation of detrimental mutations might be increased in the absence of recombination.There has been no rigorous theoretical treatment of any of these cases. In contrast, there is extensive literature on the evolutionary advantage of recombination, in which it has been shown that the accumulation or fixation of advantageous mutations is decreased by linkage to other advantageous mutations, and the accumulation or fixation of detrimental mutations is increased by linkage to other detrimental mutations (7-16). Thus, it is clear that at least some combinations of linked sites do not evolve independently. It is important to know what effects selection at one site will have on the rate of evolution of ...

BackgroundIt is widely agreed that species are fundamental units of biology, but there is little agreement on a definition of species or on an operational criterion for delimiting species that is applicable to all organisms.Methodology/Principal FindingsWe focus on asexual eukaryotes as the simplest case for investigating species and speciation. We describe a model of speciation in asexual organisms based on basic principles of population and evolutionary genetics. The resulting species are independently evolving populations as described by the evolutionary species concept or the general lineage species concept. Based on this model, we describe a procedure for using gene sequences from small samples of individuals to assign them to the same or different species. Using this method of species delimitation, we demonstrate the existence of species as independent evolutionary units in seven groups of invertebrates, fungi, and protists that reproduce asexually most or all of the time.Conclusions/SignificanceThis wide evolutionary sampling establishes the general existence of species and speciation in asexual organisms. The method is well suited for measuring species diversity when phenotypic data are insufficient to distinguish species, or are not available, as in DNA barcoding and environmental sequencing. We argue that it is also widely applicable to sexual organisms.

Abstract. Sexual reproduction has long been proposed as a major factor explaining the existence of species and species diversity. Yet, the importance of sex for diversification remains obscure because of a lack of critical theory, difficulties of applying universal concepts of species and speciation, and above all the scarcity of empirical tests. Here, we use genealogical theory to compare the relative tendency of strictly sexual and asexual organisms to diversify into discrete genotypic and morphological clusters. We conclude that asexuals are expected to display discrete clusters similar to those found in sexual organisms. Whether sexuals or asexuals display stronger clustering depends on a number of factors, but in at least some scenarios asexuals should display a stronger pattern. Confounding factors aside, the only explanation we identify for stronger patterns of diversification in sexuals than asexuals is if the faster rates of adaptive change conferred by sexual reproduction promote greater clustering. Quantitative comparisons of diversification in related sexual and asexual taxa are needed to resolve this issue. The answer should shed light not only on the importance of the different stages leading to diversification, but also on the adaptive consequences of sex, still largely unexplored from a macroevolutionary perspective.

More than 100 females of the obligately asexual bdelloid rotifers were isolated from nature and their mitochondrial cox1 genes (encoding cytochrome oxidase subunit 1) were sequenced. Phylogenetic analysis of the sequences showed that most of the isolates fall into 21 clades that show two characteristics of species: they are reciprocally monophyletic and have sequence diversities similar to that of species in other organisms. These clades have been evolving independently in spite of being effectively sympatric, indicating that they are adapted to different ecological niches. In support of this, at least some of the clades differ in morphology, food utilization, and temperature tolerance. We conclude that the bdelloid rotifers have undergone substantial speciation in the absence of sexual reproduction. We also used these sequences to test the prediction that asexual organisms should be subject to relaxed natural selection and hence will accumulate detrimental mutations. In contrast to this prediction, several estimates of the ratio K a /K s for the cox1 gene showed that this gene is subject to strong selection in the bdelloid rotifers.

Phenotypic loss is an important evolutionary force in nature but the mechanism(s) responsible for loss remains unclear. We used both simulation and multiple-regression approaches to analyze data on the loss of sporulation, a complex bacterial developmental process, during experimental evolution of Bacillus subtilis. Neutral processes of mutational degradation alone were sufficient to explain loss-of-sporulation ability in four of five populations, while evidence that selection facilitated mutational loss was found for only one population. These results are discussed in the context of the evolution of sporulation in particular and phenotypic loss in general.

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Giardia lamblia is medically important as a cause of diarrhea and malabsorption throughout the world and is thought to be one of the earliest-branching eukaryotes on a phylogenetic tree. Nevertheless, the mechanisms of inheritance are largely unknown. The trophozoites of Giardia and other diplomonads are interesting in their possession of two nuclei that are identical or similar in several respects. They replicate at nearly the same time, have similar quantities of DNA, and are both transcriptionally active. We used fluorescence in situ hybridization to demonstrate that genes from each of the five chromosomes are found in both nuclei, confirming that each nucleus has at least one complete copy of the genome. This raises a second question. The alleles of a gene in different nuclei are expected to accumulate different mutations, but surprisingly, the degree of heterozygosity in a clone is very low. One possible mechanism for eliminating sequence differences between nuclei is that each daughter cell receives two copies of the same nucleus at cell division. We used trophozoites with a plasmid transfected into a single nucleus to demonstrate that the two nuclei are partitioned equationally at cytokinesis. The mechanism(s) by which homozygosity is maintained will require further investigation.