Genetic diversity is defined as the total number of genetic characteristics in the genetic makeup of a species.

Biological variation at the DNA-level forms the basis for all biodiversity.

Genetic diversity can be defined in multiple ways.

The most common measures of genetic variation used in conservation genetic studies. These include percentage of polymorphic loci, alleles per locus/allelic richness, expected heterozygosity, dominant neutral markers, nucleotide diversity, haplotype diversity, non-neutral markers and neutrality tests, and quantitative additive gene variation.

Natural selection, genetic drift, and gene flow are the mechanisms that cause changes in allele frequencies over time. They do not act in isolation, so we must consider how the interplay among these mechanisms influences evolutionary trajectories in natural populations.

As explained in Andrews (2010):

"When one or more of these forces are acting in a population, the population violates the Hardy-Weinberg equilibrium assumptions, and evolution occurs. The Hardy-Weinberg Theorem thus provides a null model for the study of evolution, and the focus of population genetics is to understand the consequences of violating these assumptions.

• Natural selection occurs when individuals with certain genotypes are more likely than individuals with other genotypes to survive and reproduce, and thus to pass on their alleles to the next generation. As Charles Darwin (1859) argued in On the Origin of Species, if the following conditions are met, natural selection must occur:

1. There is variation among individuals within a population in some trait.

2. This variation is heritable (i.e., there is a genetic basis to the variation, such that offspring tend to resemble their parents in this trait).

3. Variation in this trait is associated with variation in fitness (the average net reproduction of individuals with a given genotype relative to that of individuals with other genotypes).

Directional selection leads to increase over time in the frequency of a favored allele.

Balancing selection, in contrast to directional selection, maintains genetic polymorphism in populations.

• Genetic drift results from the sampling error inherent in the transmission of gametes by individuals in a finite population. In a finite population, the adults in generation t will pass on a finite number of gametes to produce the offspring in generation t + 1. The allele frequencies in this gamete pool will generally deviate from the population frequencies in generation t because of sampling error (again, assuming there is no selection at the locus). Allele frequencies will thus change over time in this population due to chance events — that is, the population will undergo genetic drift. The smaller the population size (N), the more important the effect of genetic drift. In practice, when modeling the effects of drift, we must consider effective population size (N_e), which is essentially the number of breeding individuals, and may differ from the census size, N, under various scenarios, including unequal sex ratio, certain mating structures, and temporal fluctuations in population size.

At a locus with multiple neutral alleles (alleles that are identical in their effects on fitness), genetic drift leads to fixation of one of the alleles in a population and thus to the loss of other alleles, such that heterozygosity in the population decays to zero. At any given time, the probability that one of these neutral alleles will eventually be fixed equals that allele's frequency in the population. We can think about this issue in terms of multiple replicate populations, each of which represents a deme (subpopulation) within a metapopulation (collection of demes). Given 10 finite demes of equal N_e, each with a starting frequency of the A allele of 0.5, we would expect eventual fixation of A in 5 demes, and eventual loss of A in 5 demes. Our observations are likely to deviate from those expectations to some extent because we are considering a finite number of demes. Genetic drift thus removes genetic variation within demes but leads to differentiation among demes, completely through random changes in allele frequencies.

• Gene flow is the movement of genes into or out of a population. Such movement may be due to migration of individual organisms that reproduce in their new populations, or to the movement of gametes (e.g., as a consequence of pollen transfer among plants). In the absence of natural selection and genetic drift, gene flow leads to genetic homogeneity among demes within a metapopulation, such that, for a given locus, allele frequencies will reach equilibrium values equal to the average frequencies across the metapopulation. In contrast, restricted gene flow promotes population divergence via selection and drift, which, if persistent, can lead to speciation.

All real populations are finite, and thus subject to the effects of genetic drift. In an infinite population, we expect directional selection to eventually fix an advantageous allele, but this will not necessarily happen in a finite population, because the effects of drift can overcome the effects of selection if selection is weak and/or the population is small.

Loss of genetic variation due to drift is of particular concern in small, threatened populations, in which fixation of deleterious alleles can reduce population viability and raise the risk of extinction. Even if conservation efforts boost population growth, low heterozygosity is likely to persist, since bottlenecks (periods of reduced population size) have a more pronounced influence on effective population size (Ne) than periods of larger population size."

Small populations tend to lose genetic diversity more quickly than large populations due to stochastic sampling error (i.e., genetic drift). This is because some versions of a gene can be lost due to random chance, and this is more likely to occur when populations are small.

Genetic diversity is a key level of biodiversity. It carries the evolutionary potential that guarantees the capacity of populations, species and ecosystems to adapt to environmental changes and their short-, medium- and long-term viability (Lande & Shannon 1996). Fluctuations in allelic frequencies (microevolution) represent the first step in the evolution of populations and speciation. Furthermore, it has been shown that loss of genetic diversity within populations may be associated with inbreeding depression, which in turn may lead to reduced fertility (Amos et al. 2001), growth (Coltman et al. 1998) and survival (Coulson et al. 1998) of individuals, as well as increased susceptibility to disease and parasites (Acevedo-Whitehouse et al. 2003). Ultimately, the persistence of populations may be threatened and their risk of extinction increased (Frankham 2005). Genetic diversity may ultimately play a role from an ecological and functional perspective, promoting species richness and contributing to ecosystem functioning and resilience (Hughes & Stachowicz 2004; Crutsinger et al. 2006).

As explained in Blomqvist et al. (2010): "Fragmentation of natural habitats is associated with population declines of many species. The resulting small and isolated populations are threatened by extinction for several reasons. Such populations are more vulnerable to demographic and environmental stochasticity. They also face several genetic threats. First, due to restricted mating opportunities, inbreeding becomes more likely. Second, if populations remain small and isolated for many generations, they lose genetic variation necessary to respond to environmental challenges (random fixation or loss of alleles through genetic drift). Third, unfavourable mutations are expected to accumulate because selection operates less efficiently in small populations. Of these processes, inbreeding poses a more immediate threat, whereas genetic drift and mutation accumulation affect the population in the long term. Environmental, demographic and genetic factors can interact and reinforce each other in a downward spiral, an extinction vortex."

As explained in https://en.wikipedia.org/wiki/Inbreeding_avoidance:

"Inbreeding avoidance, or the inbreeding avoidance hypothesis, is a concept in evolutionary biology that refers to the prevention of the deleterious effects of inbreeding. The inbreeding avoidance hypothesis posits that certain mechanisms develop within a species, or within a given population of a species, as a result of assortative mating, natural and sexual selection in order to prevent breeding among related individuals in that species or population. Although inbreeding may impose certain evolutionary costs, inbreeding avoidance, which limits the number of potential mates for a given individual, can inflict opportunity costs. Therefore, a balance exists between inbreeding and inbreeding avoidance. This balance determines whether inbreeding mechanisms develop and the specific nature of said mechanisms.

Inbreeding can result in inbreeding depression, which is the reduction of fitness of a given population due to inbreeding. Inbreeding depression occurs via appearance of disadvantageous traits due to the pairing of deleterious recessive alleles in a mating pair's progeny. When two related individuals mate, the probability of deleterious recessive alleles pairing in the resulting offspring is higher as compared to when non-related individuals mate because of increased homozygosity. However, inbreeding also gives opportunity for genetic purging of deleterious alleles that otherwise would continue to exist in population, and can potentially increase in frequency over time. Another possible negative effect of inbreeding is weakened immune system due to less diverse immunity alleles.

A review of the genetics of inbreeding depression in wild animal and plant populations, as well as in humans, led to the conclusion that inbreeding depression and its opposite, heterosis (hybrid vigor), are predominantly caused by the presence of recessive deleterious alleles in populations. Inbreeding tends to lead to the harmful expression of deleterious recessive alleles (inbreeding depression). Cross-fertilization between unrelated individuals ordinarily leads to the masking of deleterious recessive alleles in progeny.

Many studies have demonstrated that homozygous individuals are often disadvantaged with respect to heterozygous individuals. (...) When heterozygotes possess a fitness advantage relative to a homozygote, a population with a large number of homozygotes will have a relatively reduced fitness, thus leading to inbreeding depression. Through these described mechanisms, the effects of inbreeding depression are often severe enough to cause the evolution of inbreeding avoidance mechanisms.

Inbreeding avoidance mechanisms have evolved in response to selection against inbred offspring. Inbreeding avoidance occurs in nature by at least four mechanisms: kin recognition, dispersal, extra-pair/extra-group copulations, and delayed maturation/reproductive suppression. These mechanisms are not mutually exclusive and more than one can occur in a population at a given time."

In the current context of the biodiversity crisis and global changes, there is therefore an urgent need to fill the gaps in our knowledge on the causes and consequences of the structure and dynamics of genetic diversity.

My research aims at better understanding :

(i) how genetic diversity is structured at different spatial scales (social group to continent)?

(ii) what are the different natural and anthropogenic processes that govern the structure and dynamics of genetic diversity at different spatial and temporal scales (including the respective roles of demographic history, social structure and landscape characteristics)?

(iii) how individual heterozygosity affects behaviours and fitness-related traits (heterozygosity-fitness correlation)?

(iv) do animals avoid mating with close relatives and what kind of inbreeding avoidance mechanisms have evolved in response to selection against inbred offspring?

(v) what are the consequences of low population genetic diversity on population dynamics?

Large-scale genetic structure and phylogeography

Echidna project

Despite their wide spatial distribution in Australia and Papua New Guinea and their great diversity of habitats, all short-nosed echidnas (Tachyglossus aculeatus) are assigned to a single species, itself divided into 5 subspecies defined by their geographical location, morphology and coloration. However, there are significant variations in physiology and life history traits between subspecies. The question is therefore whether these differences reflect a plasticity of response to environmental conditions or significant genetic differences. During my one-year postdoctoral fellowship at the University of Canterbury and then at Otago University (New Zealand) in 2007-2008 in Neil Gemmell's group, I developed for the first time polymorphic molecular markers in an echidna species, combining 3 approaches: (i) genomic library, (ii) cross-amplification of conserved microsatellites in mammals and (iii) 454 genomic sequencing (Vanpé et al. 2009 Aust J Zool). I then used these markers to study genetic structure and phylogeography of short-nosed echidnas across Australia. The results revealed a strong genetic structuring between the Kangaroo Island (KI) and Tasmanian (TAS) subspecies and the 2 continental subspecies, but little structuring within the Australian continent, the separation of Tasmania and KI having taken place about 10,000 years ago (results presented at the Rennes Environmental Genomics Symposium in 2013; Vanpé et al. In preparation). Genetic diversity is also lower at KI and TAS than on the continent, probably related to a founder effect followed by a long isolation. I am currently collaborating on a study to use data from the recent genome sequencing of the short-nosed echidna genome to study genetic diversity, phylogeography and phenotypic plasticity in this species (collaboration with Steve Donnellan, University of Adelaide, Australia).

Genetic diversity from landscape to social group scale

Lemur project

My postdoctoral fellowship at the Instituto Gulbenkian de Ciência (IGC, Portugal) for 2 years (2010-2012) in Lounès Chikhi's group aimed at studying the diversity and genetic structure of 2 species of lemurs from Madagascar at different spatial scales (from the social group to the whole range of the species through the forest fragment) and temporal scales (respective effects of recent anthropogenic factors vs. older climatic events). Populations can in fact be subdivided into several hierarchical levels. Most landscapes are made up of disconnected habitat patches occupied by local populations linked by dispersal events. In mammals, these populations are often subdivided into social groups. However, this level of organization is often ignored in population genetics. We studied the distribution of genetic and genotypic diversity within a fragmented population of Tattersall's Sifaka (Propithecus tattersalli) (Parreira et al. 2020 Heredity). We combined data analysis and simulation approach in order to understand to what extent social structure contributes to explain the observed distribution of genetic diversity. We focused on measuring the inbreeding coefficient (FIS) at different levels of subdivision: social groups, sampling sites, forest plots. We found lower than expected inbreeding levels under the assumption of random mating (FIS < 0) at all hierarchical levels considered. Our simulations, which assumed that the population was subdivided into social groups, but without any geographical constraint, well confirm the empirical results, indicating that social subdivision decreases inbreeding and allows maintaining high levels of genotypic (individual) diversity in a highly fragmented population. These results have important implications for species conservation.

Genetic diversity at the population and individual scales

Brown bear project

The Pyrenean brown bear population with its small size, isolation and the reduced number of founder individuals is probably the most endangered population in Europe. In 1995, this population had reached the critical threshold of 5 individuals confined to the Western Pyrenees.

Faced with this situation, translocations of brown bears from Slovenia were carried out in 1996 (2 females), 1997 (1 male), 2006 (4 females and 1 male), 2016 (1 male) in the central Pyrenees, and finally in 2018 (2 females) in the western core, which had no females since 2004. Despite the increase in the population, the assessment of its conservation status carried out over the period 2013-2018 under the Habitat-Fauna-Flora Directive remains "unfavourable poor". This assessment focuses on the evolution of the range and numbers of the brown bear population over the period under consideration. While the viability analyses carried out on this population (Chapron 2009, Quenette el al 2011) reveal the demographic risks associated with the reduced population size, these analyses do not take into account the genetic risks associated with the inbreeding observed in this population.

An assessment of the genetic conservation status of the Pyrenean ursine population is therefore necessary, including an estimate of the effective population size Ne. Ne is recognised as a key parameter for assessing the conservation status and threats to the viability of populations, particularly in the context of reintroduction programmes. Indeed, it allows the assessment of the adverse genetic effects of small or reduced population size. When Ne decreases, the degree of inbreeding increases, genetic diversity decreases due to genetic drift and mating between relatives, the probability of binding deleterious alleles increases, and selection becomes less efficient (Ralls et al. 1988; Hedrick 2001). All these processes in turn lead to a short-term loss of adaptive value through inbreeding depression, as well as a long-term loss of evolutionary potential, increasing the risk of extinction (Leberg 2005; Wang 2005; Palstra & Ruzzante 2008; Hare et al. 2011).

A first analysis carried out in 2016 (Beaumelle 2016) revealed a decrease in genetic diversity over time and an effective population size equal to 3.6 (based on the linkage disequilibrium method) for a population size estimated that year at 39 individuals in the central Pyrenees. But it would be interesting to re-estimate the current effective population size and genetic diversity in order to assess the impact of recent translocations (Swenson et al 2011). In addition, it is recommended to use several methods to estimate the effective population size (Waples 2010), as many effective size estimators are biased and comparisons using computer simulations have shown considerable differences in precision between estimators (Tallmon et al. 2004).

The aim of this project was therefore to evaluate the genetic diversity as well as the current effective size of the Pyrenean brown bear population by comparing the results obtained using different estimation methods.

These analyses were based on the non-invasive genetic monitoring of the Pyrenean brown bear population carried out from 1996 to 2020. Each year, hair and faeces samples were collected in the field as part of the bear population monitoring operations organized by the OFB (formerly ONCFS) with the assistance of the Réseau Ours Brun (ROB). These samples were genotyped using 13 microsatellite markers (Duchamp & Quenette 2006; De Barba et al 2016) by LECA-CNRS (Miquel et al. 2006; De Barba et al. 2017) between 1996 and 2016, then by the ANTAGENE laboratory between 2017 and 2020, with an average of 165 samples analysed per year since 2006. Almost all individuals present in the population from 1996 to 2020 could thus be genetically identified.

The genetic variability of the population was measured using different parameters classically used in conservation genetics: average number of alleles per locus, expected and observed heterozygosity, inbreeding coefficient, etc. (Skrbinsek 2012a; Karamanlidis et al. 2014).

Several methods were also used and compared to estimate the effective population size (Leberg 2005; Wang 2005; Kamath et al. 2015; Skrbinsek et al. 2012b; Gonzalez et al. 2016).

Individual heterozygosity was estimated as well as the degrre of consanguinity of the population and the degree of relatedness between individuals within the population.

From 2006 to 2020, 84 brown ears were genetically identified on the basis of a panel of 13 microsatellite markers in the Pyrenees. Despite an increasing Ne since 2006, linked to the increasing number of individuals (especially breeders) and the death of the dominant male in 2017, Ne remains extremely low with 6.6 individuals (95% CI = 4.1-8.6), and is much lower than the estimated population size in 2020 due to the high variance in the reproductive success of males. Expected heterozygosity is significantly lower in 2020 than in 2006, despite an increasing trend since 2016, while allelic richness shows no significant trend. 67.8% of the population gene pool is generated by a single male and a single female, both introduced. Increasing trends in the average inbreeding and relatedness coefficients since 2006 (0.132 ± 0.110 and 0.184 ± 0.074, respectively, in 2020) indicate a high risk of inbreeding depression. Therefore, it is essential to prioritise conservation actions that attempt to increase Ne. Continued genetic monitoring in the coming years is needed to confirm the expected evolutionary prospects and identify sound conservation strategies.

Heterozygosity-fitness correlation

Roe deer project

Understanding how natural selection acts in contemporary populations is a major goal for evolutionary biologists. Although this task can be undertaken at the phenotypic level using quantitative genetics and selection gradient analysis, the gene level is mainly studied through molecular techniques. However the link between molecular and phenotypic variation is often complex. This link can be dissected based on correlated inheritance patterns of molecular markers and traits in controlled crosses (QTL analysis). Another, less-demanding method is to study the statistical association between molecular genotypes and traits under selection in natural populations. In particular, one kind of such associations, the correlation between individual multilocus heterozygosity (MLH) at allozyme or microsatellite loci and fitness-related traits, also called heterozygosity-fitness correlation (hereafter, HFC), has been studied and discussed for more than three decades. All these studies share a common, fundamental aim, that is, to study natural selection in wild populations, but with different points of view. Some of them ultimately intend to identify selection on one or a few polymorphic genes, whereas others are interested in much more general sources of variation in fitness, such as inbreeding.

As explained in Szulkin et al. (2010): "Historically, debates on HFC were concerned with the selective neutrality of allozymes. The focus of the debates has changed with the advent of noncoding DNA markers. The repeated observation of HFC with such markers (Coltman and Slate 2003; Chapman et al. 2009) calls for a general explanation that would not imply any direct effect of the marker loci on phenotypes. This explanation also has to account for the fact that HFC is not a strong and consistent phenomenon, but rather a weak and unstable signal that shows up from time to time in various organisms in a context-dependent fashion (Britten 1996; Chapman et al. 2009). We argue that such an explanation has existed from the beginning (Ohta 1971, 1973), namely, that heterozygosity at neutral markers is correlated to heterozygosity at both linked and unlinked selected loci through genetic associations. However, the latter only arise in particular contexts, involving a form of inbreeding sensu lato, such as small population size, nonrandom mating, population admixture, or bottlenecks."

Traditionally, three processes have been suggested as drivers of the relationship between fitness-related traits and individual multilocus heterozygosity at microsatellite markers—the so-called heterozygosity–fitness correlation (HFC) (David 1998; Hansson and Westerberg 2002):

(1) direct effects resulting from selection at the genotyped loci themselves, which thus have a direct effect on fitness;

(2) general effects resulting from inbreeding depression that occur when the heterozygosity of the genotyped markers is correlated with overall heterozygosity in the genome;

(3) local effects that occur when the genotyped markers are in linkage disequilibrium with nearby loci under selection.

Within the framework of HFC, I investigated the effect of individual heterozygosity at both neutral (microsatellite loci) and selected markers (immune gene loci) on roe deer dispersal.

Although theoretical studies have predicted a link between individual multilocus heterozygosity and dispersal, few empirical studies have investigated the effect of individual heterozygosity on dispersal propensity or distance. We investigated this link using measures of heterozygosity at 12 putatively neutral microsatellite markers and natal dispersal behaviour in three contrasting populations of European roe deer, a species displaying pre-saturation condition-dependent natal dispersal. We found no effect of individual heterozygosity on either dispersal propensity or dispersal distance (Vanpé et al. 2015 Oecologia). Average heterozygosity was similar across the three studied populations, but dispersal propensity and distance differed markedly among them. In Aurignac, dispersal propensity and distance were positively related to individual body mass, whereas there was no detectable effect of body mass on dispersal behaviour in Chizé and Trois Fontaines. We suggest that we should expect both dispersal propensity and distance to be greater when heterozygosity is lower only in those species where dispersal behaviour is driven by density-dependent competition for resources.

We also assessed whether individual heterozygosity at five immune gene loci (one from the Major histocompatibility complex :and four from encoding Toll-like receptors) influences roe deer natal dispersal. We found that dispersal propensity was affected by immune gene diversity, suggesting potential pathogen-mediated selection through over-dominance. However, the direction of this effect differed between high and low quality individuals, suggesting that dispersal propensity is driven by two different mechanisms. In support of the condition-dependent dispersal hypothesis, dispersal propensity increased with increasing body mass and, among high quality individuals only (standardized body mass 18 kg), with increasing immune gene diversity (Vanpé et al. 2016 Oikos). However, among poor quality individuals, we observed the opposite pattern such that dispersal propensity was higher for individuals with lower immune gene diversity. We suggest that these poor quality individuals expressed an emergency dispersal tactic in an attempt to escape a heavily infested environment associated with poor fitness prospects. Our results have potentially important consequences in terms of population genetics and demography, as well as host–pathogen evolution.

Inbreeding avoidance

Roe deer project

Because of anisogamy and differential parental investment between the sexes, males have the capacity to fertilize a number of females, whereas females usually need only one male to father a particular litter (Bateman, 1948). Hence, to maximize fitness, males are expected to mate with as many females as possible, whereas females are not expected to solicit multiple mating. Yet, females often do mate multiply within a single reproductive cycle (Arnqvist & Nilsson, 2000), either with the same male (repeated matings), or with different males (polyandry), potentially resulting in multiple paternity (i.e. paternity shared by several males within a single litter or brood; Birdsall & Nash 1973; Gavin & Bollinger 1985; Zane et al. 1999). Despite the crucial importance of multiple mating in sexual selection and in the maintenance of genetic variation (Sugg & Chesser, 1994), the reasons why females frequently mate with several males are still subject to controversy (Fedorka & Mousseau, 2002).

Optimization theory predicts that multiple mating by females should evolve when the direct costs (e.g. increased susceptibility to predation, physical injury, disease, energetic loss; Daly, 1978; Thornhill & Alcock, 1983; Hurst et al., 1995; Blanckenhorn et al., 2002) are offset by benefits (Reynolds, 1996; Newcomer et al., 1999). In some species, costs can be offset by direct benefits provided by males such as nuptial gifts, access to territories, protection against predators, and paternal care of offspring (Arnqvist & Nilsson, 2000; Wiklund et al., 2001). Alternatively, females may mate several times to avoid male harassment (Galimberti et al., 2000) and ensure fertility (Orsetti & Rutowski, 2003). However, in large mammalian herbivores, where males contribute no material resources other than sperm and females do not gain obvious direct mating benefits, females are assumed to obtain some genetic (indirect) benefits from multiple mating.

Potential genetic benefits may involve: (1) gaining ‘good genes’, either via sperm competition or female choice of sperm (Kempenaers et al., 1992; Otter & Ratcliffe, 1996; Simmons, 2001), which may result in the production of offspring of higher genetic quality (Zeh & Zeh, 2001); (2) genetic incompatibility avoidance (Zeh & Zeh, 1996), exploiting post-copulatory mechanisms in order to minimize the risk and/or cost of fertilization by genetically incompatible sperm; (3) increasing offspring genetic diversity (Madsen et al., 1992; Byrne & Roberts, 2000) by producing offspring sired by different males, potentially reducing sibling competition or serving as a hedge against environmental uncertainty (‘genetic bet-hedging’; Zeh & Zeh, 2001); and finally, (4) inbreeding avoidance (Brooked et al., 1990; Stockley et al., 1993). Although high levels of multiple mating can be compatible with all these hypotheses, only the offspring diversity hypothesis predicts high rates of multiple paternities.

Under the inbreeding avoidance hypothesis, we expected that:

• • • a lower degree of relatedness between parents should result in more highly heterozygous offspring and, as a result, higher offspring survival (DiBattista et al., 2008);

    • offspring from multiple paternity litters should survive better than offspring from single paternity litters.

I tested these hypotheses in a Swedish population of European roe deer (Bogesund). I calculated three microsatellite measures of genetic diversity (individual heterozygosity) aimed at reflecting levels of individual inbreeding [standardized multilocus heterozygosity (std H), internal relatedness (IR) and homozygosity by locus (HL); Coltman et al., 1999; Pemberton et al., 1999; Amos et al., 2001; Aparicio et al., 2006 for all fawns. I also estimated the relatedness between parents of each multiple litter, as well as mean relatedness among candidate mothers and fathers for each cohort.

In the studied population, 13.5% of polytocous litters were sired by more than one male. I also found that a half-sib relationship was more likely than a full-sib relationship for 20.5% of all litters. In support of the inbreeding avoidance hypothesis, I finally found that parents who were strongly related produced offspring with lower individual heterozygosity that survived less well during their first summer than fawns with unrelated parents. However, I did not find any evidence for an influence of genetic factors on fawn survival (slight positive trend for std H and slight negative trends for HL and IR). Finally, females that produced litters sired by different males did not have offspring of higher genetic diversity than females that produced litters sired by only one male.