Sex-biased dispersal, where individuals of one sex stay or return to their natal site (or group) to breed while individuals of the other sex are prone to disperse, is a wide-spread pattern in vertebrate organisms. In general, mammals exhibit male-biased dispersal whereas birds exhibit female-bias. Dispersal estimates are often difficult to obtain from direct field observations. Here we describe different methods for inferring sex-specific dispersal using population genetic tools and discuss the problems they can raise. We distinguish two types of methods: those based on bi-parental markers (eg comparison of male/female relatedness, F st and assignment probabilities) and those relying on the comparison between

The purpose of this study was to review published studies on the variability of age at menarche and age at menopause throughout the world, and to identify the main causes for age variation in the timing of these events. We first present a summary table including mean (or median) values of the age at menarche in 67 countries, and of the age at menopause in 26 countries. General linear models showed that mean age at menarche was strongly linked to the mean female life expectancy, suggesting that one or several variables responsible for inequalities in longevity similarly influenced the onset of menarche. A closer examination of the data revealed that among several variables reflecting living conditions, the factors best explaining the variation in age at menarche were adult illiteracy rate and vegetable calorie consumption. Because adult illiteracy rate has some correlation with the age at which children are involved in physical activities that can be detrimental in terms of energy expenditure, our results suggest that age at menarche reflects more a trend in energy balance than merely nutritional status. In addition, we found the main determinant of age at menopause to be the mean fertility. This study thus suggests that, on a large scale, age at menarche is mainly determined by extrinsic factors such as living conditions, while age at menopause seems to be mainly influenced by intrinsic factors such as the reproductive history of individuals. Finally, these findings suggest that human patterns cannot be addressed solely by traditional, small-scale investigations on single populations. Rather, complementary research on a larger scale, such as this study, may be more appropriate in defining some interesting applications to the practical problems of human ecology.

Leishmania species of the subgenus Viannia and especially Leishmania braziliensis are responsible for a large proportion of New World leishmaniasis cases. The reproductive mode of Leishmania species has often been assumed to be predominantly clonal, but remains unsettled. We have investigated the genetic polymorphism at 12 microsatellite loci on 124 human strains of Leishmania braziliensis from 2 countries, Peru and Bolivia. There is substantial genetic diversity, with an average of 12.4 ؎ 4.4 alleles per locus. There is linkage disequilibrium at a genome-wide scale, as well as a substantial heterozygote deficit (more than 50% the expected value from Hardy؊Weinberg equilibrium), which indicates high levels of inbreeding. These observations are inconsistent with a strictly clonal model of reproduction, which implies excess heterozygosity. Moreover, there is large genetic heterogeneity between populations within countries (Wahlund effect), which evinces a strong population structure at a microgeographic scale. Our findings are compatible with the existence of population foci at a microgeographic scale, where clonality alternates with sexuality of an endogamic nature, with possible occasional recombination events between individuals of different genotypes. These findings provide key clues on the ecology and transmission patterns of Leishmania parasites.clonality ͉ microsatellites ͉ population genetics ͉ endogamyl ͉ heterozygote defiency

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Evolutionary theory predicts that the lack of recombination and chromosomal re-assortment in strictly asexual organisms results in homologous chromosomes irreversibly accumulating mutations and thus evolving independently of each other, a phenomenon termed the Meselson effect. We apply a population genomics approach to examine this effect in an important human pathogen, Trypanosoma brucei gambiense. We determine that T.b. gambiense is evolving strictly asexually and is derived from a single progenitor, which emerged within the last 10,000 years. We demonstrate the Meselson effect for the first time at the genome-wide level in any organism and show large regions of loss of heterozygosity, which we hypothesise to be a short-term compensatory mechanism for counteracting deleterious mutations. Our study sheds new light on the genomic and evolutionary consequences of strict asexuality, which this pathogen uses as it exploits a new biological niche, the human population.DOI: http://dx.doi.org/10.7554/eLife.11473.001

There are a number of ways in which a host can respond in evolutionary time to reductions in survival and reproduction due to a virulent parasite. These include evolving physiological morphological, or behavioural mechanisms of resistance to infection (or to proliferation, once infection has occurred). But a more unexpected tactic is also possible. This is for hosts to reproduce (slightly) sooner when in the presence of a virulent parasite as compared to when the parasite is less virulent or absent. As such, hosts which reproduce younger may be at a selective advantage, since they can both evade parasitism in time and, even when parasitised, can reduce the likely impact of the parasite on survival and reproductive success. We employ a simple mathematical model to propose that parasites and pathogens can act as important agents in the evolution of the timing of reproduction and associated life-history characters (e.g. body size). Once established in a semelparous host population, evolutionary increases in parasite virulence should result in the evolution of shorter lived hosts; whereas the evolution of less virulent forms of the parasite should be accompanied by the evolution of longer lived hosts. We argue that in the presence of a sufficiently virulent parasite the evolution of longer pre-reproductive life-spans should require the previous or concomitant evolution of morphological, behavioural or physiological resistance to parasitic infection and proliferation.

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In this short review we report the basic notions needed for understanding the population genetics of clonal diploids. We focus on the consequences of clonality on the distribution of genetic diversity within individuals, between individuals and between populations. We then summarise how to detect clonality in mainly sexual populations, conversely, how to detect sexuality in mainly clonal populations and also how genetic differentiation between populations is affected by clonality in diploids. This information is then used for building recipes on how to analyse and interpret genetic polymorphism data in molecular epidemiology studies of clonal diploids. #