All plant and animal species arise by speciation - the evolutionary splitting of one species into two reproductively incompatible species. But until recently our understanding of the molecular genetic details of speciation was slow in coming and largely limited to Drosophila species. Here, I review progress in determining the molecular identities and evolutionary histories of several new 'speciation genes' that cause hybrid dysfunction between species of yeast, flies, mice and plants. The new work suggests that, surprisingly, the first steps in the evolution of hybrid dysfunction are not necessarily adaptive.
Meiotic drivers are genetic variants that selfishly manipulate the production of gametes to increase their own rate of transmission, often to the detriment of the rest of the genome and the individual that carries them. This genomic conflict potentially occurs whenever a diploid organism produces a haploid stage, and can have profound evolutionary impacts on gametogenesis, fertility, individual behaviour, mating system, population survival, and reproductive isolation. Multiple research teams are developing artificial drive systems for pest control, utilising the transmission advantage of drive to alter or exterminate target species. Here, we review current knowledge of how natural drive systems function, how drivers spread through natural populations, and the factors that limit their invasion. Trends Box Both naturally occurring and synthetic "meiotic drivers" violate Mendel's law of equal segregation and can rapidly spread through populations even when they reduce the fitness of individuals carrying them. Synthetic drivers are being developed to spread desirable genes in natural populations of target species. How ecology influences the population dynamics of meiotic drivers is important for predicting the success of synthetic drive elements. An enduring puzzle concerns why some meiotic drivers persist at stable, intermediate frequencies rather than sweeping to fixation. Drivers can have a wide range of consequences from extinction to changes in mating system. preferentially associating with and moving toward the egg pole at Meiosis I) will be 75 transmitted to more than half of the maturing eggs. Although this bias does not necessarily 76 reduce the production of eggs (as only one egg matures per meiosis), the fitness of other 77 alleles at the same locus, that do not bias transmission, and alleles linked to them, is 78 reduced. Such meiotic drivers could reduce the fitness of individuals that carry them, if the 79 driving variant is genetically linked to deleterious mutations or has deleterious pleiotropic 80 effects. 81Male meiotic drive takes multiple forms -some at least partially meiotic, some entirely 82 post-meiotic -but all involve a driving element that prevents maturation or function of 83 sperm that do not contain it. Because haploid sperm within a single ejaculate compete to 84 fertilize the same pool of eggs, disabling non-carrier sperm results in transmission of the 85 driving element to more than half of the functional gametes and resulting offspring ([5], Box 86 1). However, disabling non-carrier sperm often reduces fertility [6]. 87Spore drive in fungi, in which the products of meiosis are packaged together in an ascus, 88 operates via similar mechanisms. Spores with one haploid genotype will kill or disable 89 spores of the alternative haplotype ([7], Box 1). If spores disperse long distances sibling 90 spores are unlikely to compete and killing them will not increase the killer's fitness. 91However, spore killing can be beneficial if there is local resource competition. 92Excit...
Postzygotic reproductive isolation is characterized by two striking empirical patterns. The first is Haldane's rule—the preferential inviability or sterility of species hybrids of the heterogametic (XY) sex. The second is the so-called large X effect—substitution of one species's X chromosome for another's has a disproportionately large effect on hybrid fitness compared to similar substitution of an autosome. Although the first rule has been well-established, the second rule remains controversial. Here, we dissect the genetic causes of these two rules using a genome-wide introgression analysis of Drosophila mauritiana chromosome segments in an otherwise D. sechellia genetic background. We find that recessive hybrid incompatibilities outnumber dominant ones and that hybrid male steriles outnumber all other types of incompatibility, consistent with the dominance and faster-male theories of Haldane's rule, respectively. We also find that, although X-linked and autosomal introgressions are of similar size, most X-linked introgressions cause hybrid male sterility (60%) whereas few autosomal introgressions do (18%). Our results thus confirm the large X effect and identify its proximate cause: incompatibilities causing hybrid male sterility have a higher density on the X chromosome than on the autosomes. We evaluate several hypotheses for the evolutionary cause of this excess of X-linked hybrid male sterility.
Two empirical rules suggest that sex chromosomes play a special role in speciation. The first is Haldane's rule-the preferential sterility and inviability of species hybrids of the heterogametic (XY) sex. The second is the disproportionately large effect of the X chromosome in genetic analyses of hybrid sterility. Whereas the causes of Haldane's rule are well established, the causes of the 'large X-effect' have remained controversial. New genetic analyses in Drosophila confirm that the X is a hotspot for hybrid male sterility factors, providing a proximate explanation for the large X-effect. Several other new findings-on faster X evolution, X chromosome meiotic drive, and the regulation of the X chromosome in the male-germline-provide plausible evolutionary explanations for the large X-effect. The two rules of speciation revisitedSpeciation-the process by which new biological species arise-corresponds to the evolution of reproductive barriers that limit the potential for genetic exchange between populations [1,2]. For geographically isolated populations, reproductive barriers evolve as incidental byproducts of genetic divergence. Eventually, 'good species' come to be completely isolated by one or more reproductive barriers that take the form of, e.g., incompatible courtship signals that prevent mating (prezygotic isolation) or incompatible gene interactions that cause the sterility or lethality of species hybrids (postzygotic isolation; Box 1). The past decade has seen good progress in the molecular characterization of the 'speciation genes' involved in reproductive barriers. In particular, the recent identification of genes causing intrinsic postzygotic isolation has begun to provide important information about the functions of these genes within species and on the population genetic forces that shape their evolutionary history [3,4]. I will not review the details of particular speciation genes here as they have been amply discussed elsewhere [3,4]. Instead, this review will focus on new developments that concern an older but still controversial problem-the special role of sex chromosomes in the evolution of postzygotic reproductive isolation between animal species.The idea that sex chromosomes play a special role in speciation is based on two empirical rules that characterize speciation in animals: Haldane's rule and the so-called 'large X-effect' [5,6]. Haldane's rule refers to the preferential sterility or inviability of species hybrids of the heterogametic (XY) sex: in crosses between many recently diverged species, XY hybrids are often sterile or inviable whereas their XX siblings are not [7]. In cases of unisexual hybrid sterility or inviability, Haldane's rule holds in 95% (n = 131) and 100% (n = 26) of species crosses in Drosophila and mammals, respectively, in which males are the XY sex, and in 97% (n = 87) and 96% (n = 114) of species crosses in birds and butterflies, respectively, in which dvnp@mail.rochester.edu, phone: (585) 275-8946, FAX: (585) 275-6066. Publisher's Disclaimer: This is a P...
I present patterns characterizing the evolution of intrinsic postzygotic isolation in Lepidoptera by analyzing data from the literature on genetic distance, strength of hybrid sterility and inviability, biogeography, and natural hybridization. Using genetic distance as a proxy for time, I investigate the time-course of the evolution of postzygotic isolation and the waiting times to particular hybrid fitness problems. The results show that postzygotic isolation increases gradually as species diverge, but that hybrid sterility evolves faster than hybrid inviability. The overwhelming preponderance of female-specific hybrid problems in Lepidoptera shows that Haldane's rule (the preferential sterility or inviability of the heterogametic sex) is well obeyed. Together the rates and patterns characterizing the accumulation of postzygotic isolation allow several tests of the composite theory of Haldane's rule. Interestingly, comparing these data with those from Drosophila reveals that Haldane's rule for sterility evolves as fast (if not faster) in Lepidoptera. Finally, I show that a substantial fraction of sympatric species hybridizes in nature and that the majority of these suffer some level of hybrid sterility or inviability.
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