A farmer or hatchery manager who wants to manage the genetic aspects of his population must know how inbreeding can be used to improve productivity and profits. Inbreeding is one of the three major traditional breeding programmes that breeders have used for centuries to improve animals and plants. While it is not as important as selection or crossbreeding, inbreeding is used to produce genetically improved livestock, plants, and laboratory animals. Inbreeding might be the most important breeding technique used in the production of laboratory animals, because genetically uniform lines of rats, mice, etc. Inbreeding will never be as important in animal husbandry as it is in agronomy, because many plants can be self-fertilized; it is easy to create matings by artificial pollination; and many individuals can be raised cheaply in a small plot.
Double first cousin matings produce as much inbreeding as half-sib, grandparent-grandchild, and aunt-nephew or uncle-niece matings We also analysed reported illnesses in fathers Imbreads haveing sex mothers of UKB participants UKB fields 20, and 20, respectively as measure of health deprivation in haveong family. A schematic haveong chart of meiotic gynogenesis. The third step is the mating of the F 1 hybrids to produce a di-hybrid. B estimates the average number of lethal alleles per haploid genome or per zygote if doubled in the population under the assumption that recessive alleles are responsible for all of the deleterious effects of inbreeding [ 49 ], which recent Ibmreads suggests is Free anti tank gun models accurate [ 250 ]. Imbreads haveing sex distribution of the fraction of the genome identical by descent in finite random mating populations. All Football.
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The mutation accumulation theory of senescence predicts that age-related deterioration of fitness can be exaggerated when inbreeding causes homozygosity for deleterious alleles.
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Metrics details. Inbreeding increases homozygosity and exposes deleterious recessive alleles, generally decreasing the fitness of inbred individuals. Interestingly, males and females are usually affected differently by inbreeding, though the more vulnerable sex depends on the species and trait measured. We used the soil-dwelling nematode Caenorhabditis remanei to examine sex-specific inbreeding depression across nine lineages, five levels of inbreeding, and hundreds of thousands of progeny.
Female nematodes consistently suffered greater fitness losses than their male counterparts, especially at high levels of inbreeding. These results suggest that females experience stronger selection on genes contributing to reproductive traits. Inbreeding depression in males may be further reduced by sex chromosome hemizygosity, which affects the dominance of some mutations, as well as by the absence of sexual selection. Determining the relative contributions of sex-specific expression, genes on the sex chromosomes, and the environment they are filtered through—including opportunities for sexual selection—may explain the frequent though inconsistent records of sex differences in inbreeding depression, along with their implications for conservation and the evolution of mating systems.
Inbreeding depression, or the fitness decline resulting from mating among close relatives, has long been thought to underpin many important evolutionary processes [ 1 ]. Since inbreeding increases homozygosity, it exposes deleterious recessive alleles and eliminates any potential heterozygote advantage [ 2 ]. Inbreeding depression has been observed across many taxa [ 2 — 4 ] and has wide-ranging implications, particularly for the evolution of dispersal behavior, self-incompatibility, and other mating systems characters [ 2 , 5 ].
However, considerable variation exists in the strength of inbreeding depression, especially among populations and environments and between sexes [ 6 — 11 ]. This sex-specificity has a direct bearing on conservation strategies for small populations [ 12 , 13 ] and could contribute to the evolution of selfing and polyandry, which may be heavily influenced by inbreeding depression [ 14 , 15 ].
Despite these potential consequences, it is difficult to predict which sex will be more vulnerable to inbreeding. In theory, the same mutations may affect inbred males and females differently if they vary between the sexes in patterns of dominance or intensity of selection [ 16 ]. Generally, little is known about how dominance differs between sexes or across the genome [ 16 — 18 ], with the exception of genes on the sex chromosome.
In taxa with heteromorphic sex chromosomes, genes may be recessive for the sex with two copies e. XX females , but necessarily dominant for the sex with a single copy e. XY males , which could systematically influence inbreeding depression between the sexes. Selection on the same variant could also differ between sexes due to differences in expression, life history, sexual selection, or a number of other factors [ 19 — 21 ].
While differential gene expression and the relative rate of evolution of genes related to sex-specific traits has become a central feature of studies of molecular evolution [ 22 , 23 ], the relationship between these patterns and sex-specific inbreeding depression has remained largely unexplored.
In the most extreme case, loci that have evolved completely sex-limited expression will be influenced only by selection acting on that particular sex, as may be the case for maternal effects [ 24 — 26 ] and sexually selected ornaments or behaviors [ 27 , 28 ]. Many mutations are expressed in both sexes and have correlated effects in males and females [ 29 ], but may still have different fitness consequences that depend on behavior or the environment.
For example, paralyzing unc mutations have stronger reproductive consequences for male than hermaphroditic Caenorhabditis elegans [ 30 ]. The soil-dwelling nematode C. The evolution of mating systems and sexual selection within Caenorhabditis is relatively well-understood [ 36 — 38 ], and the C. Finally, while most previous work on sex-specific inbreeding depression has quantified fitness at one level of inbreeding, C.
Our study examined males and females from nine inbred lineages over a range of inbreeding coefficients, tallying over , offspring Fig.
The resulting patterns demonstrate that the genetic architecture underlying key fitness-related traits is largely sex-specific, and suggest that the pre- and post-mating costs of inbreeding depression may fall disproportionately on males and females. Summary of design of inbreeding and trait assays.
Red circles illustrate worms that were assayed each generation for three fitness-related traits. Only one of the ten total lineages is shown. The base population used for these inbreeding experiments was PX, a highly polymorphic strain derived from the intercrossing of 26 isofemale lines isolated from wood lice in a patch of forest detritus near Toronto, Ontario Koffler Scientific Reserve at Jokers Hill, King Township.
The 26 isolates were crossed in a controlled fashion to promote equal contributions from all strains, including from mitochondrial genomes and X chromosomes [ 41 ]. To measure the fitness effects of inbreeding depression over time, nine independent lineages of PX were maintained through virgin brother-sister matings for five generations, with fitness-related traits of the inbred offspring assayed each generation Fig.
Ten lineages were initiated from independent crosses between a randomly chosen male and virgin female from PX Fig. From the crosses that produced large enough brood sizes to assay, one brood was chosen at random to provide inbred worms to assay for fitness, as well as to continue inbreeding into the next generation with five new brother-sister pairs. The second lineage failed to survive past the first sibling cross, when all five replicates produced no offspring, and so was not included in the subsequent analyses.
This design allowed for multiple matings while minimizing the complex contributions of sexual conflict to lifetime reproductive success in C. Because C. Additionally, using an outbred partner for the inbred worm allowed us to determine its fecundity based only on its own level of inbreeding, without confounding effects of an inbred mate or inbred offspring. For each value of f , 20 male and 20 female offspring from a brother-sister mating were picked to a total of 40 individual plates.
When a female had ceased reproducing for two consecutive days, sperm were assumed to be depleted, and she was removed from the assay. A general linear model for offspring number was analyzed using JMP 9. For each sex and level of inbreeding, ten eggs were picked from 12 crosses and split among four plates of 30 eggs each to allow for an estimate of sampling error. After 4 days, once the surviving offspring reached adult stage, they were counted.
Because the survivorship data consist of alive-dead counts, they were analyzed using a logistic regression with the same causal model as the reproductive assays. As a measure of male mating ability, one male was picked onto a mm plate with seven adult virgin PX females for 1.
Both males and females were isolated to sex-specific plates the previous day, while at L4 final larval stage, to ensure virginity. After 1. As male C. Because this is a male-specific effect, only the effects of Inbreeding and Lineage were fit in the linear model. If deleterious mutations are largely independent of one another then they will act in a multiplicative manner, and the logarithm of mean fitness should decline in linear fashion as inbreeding increases [ 4 ].
Following this standard, inbreeding load B was calculated as the negative slope of the regression of the natural log of fitness or relevant trait on the inbreeding coefficient. Inbreeding depression the relative strength of selection against an inbred genotype was then calculated from B as:. B estimates the average number of lethal alleles per haploid genome or per zygote if doubled in the population under the assumption that recessive alleles are responsible for all of the deleterious effects of inbreeding [ 49 ], which recent evidence suggests is largely accurate [ 2 , 50 ].
Inbreeding decreases reproductive success for C. When reproductive patterns are broken down by day, it is evident that peak reproduction declines with increasing levels of inbreeding in females, but not in males Fig. Sex-specific effects of inbreeding on a total offspring number and b egg-to-adult survival. Females experience more severe inbreeding depression than males in both traits.
Error bars are one standard error. Age specific effects of inbreeding on reproductive output for females top and males bottom.
Day 1 indicates the first day of the cross. Six of the nine tested lineages suffered significant inbreeding depression when considered independently Fig. Of the three that did not, two lineages experienced no inbreeding depression for either sex Fig. Lineage-specific regressions of male and female inbreeding depression on offspring number. Each plot a - i represents the inbreeding trajectory for one of the nine lineages analyzed in the experiment, in the order in which they were founded.
Female values are represented by the dark circles and solid line; male values by the open squares and dashed line. On average, females lose fitness more quickly than males, although the actual responses are highly lineage-dependent.
Male mating ability in a non-competitive environment declines significantly with inbreeding Fig. Notably, two of nine lineages actually experience outbreeding depression in this trait, though its magnitude is not significantly different from zero. Average effect of inbreeding on male mating ability. Inbreeding depression appears to plateau after one generation of sibling mating. Our study found that C. Taken together, these results suggest that stronger selection in females is responsible for sex-specific inbreeding depression.
This may be due both to the reproductive traits chosen, which are particularly influenced by loci involved in maternal effects, and to the influence of the X chromosome. However, it is critical to note that sexual selection, which typically places stronger pressure on males, was minimized in these experiments. Females may experience stronger selection for loci involved in reproductive traits because of female-specific development and provisioning of eggs. The influence of maternal effects on offspring fitness is well-established [ 24 — 26 ] and has been invoked to explain female-specific inbreeding depression in a number of studies, particularly in birds [ 35 , 51 — 54 ].
In this study, we observed inbreeding depression for egg survivorship only in females Fig. It is then unsurprising that recessive mutations in genes affecting egg survivorship, which are made homozygous by inbreeding, have deleterious effects only in the sex in which they are expressed Fig.
Notably, based on the timing of the shift of transcriptional control from mother to zygote [ 56 ], this implies that most embryonic lethality from inbred females occurs early in development, prior to embryonic gastrulation. Inbreeding depression for offspring number is likewise stronger in females at high levels of inbreeding.
At earlier stages, fitness declines for males and females are statistically indistinguishable, suggesting that genes expressed in both sexes are involved in this trait Fig. This may be explained by differential target sizes for selection caused by some sex-specific expression, as for egg survivorship. Although C. Understanding sex-specific patterns of expression for focal traits will be central to predicting sex-specific responses to inbreeding and their population-level consequences.
In addition to exhibiting less inbreeding depression in offspring production and egg survivorship, male C. This finding may be unique to a laboratory environment that minimizes competition and sexual selection by providing ample access to females.
Stress and competition have repeatedly been shown to exacerbate inbreeding depression [ 6 , 8 , 16 ], particularly for male-male competition [ 57 ]. One key study found that inbred male mice have nearly normal fitness in laboratory conditions, but suffer severe inbreeding depression when housed in semi-natural enclosures requiring competition over resources, including mates [ 58 ].
Because selection is generally expected to be stronger on males due to sexual selection [ 27 ], but see also [ 59 ] , it is tempting to consider that reduced inbreeding depression in males could be a result of the purging of male-specific alleles through sexual selection.
However, sexual selection influences many genes beyond those directly involved in male morphology and behavior: overall health and vigor is correlated with male success, and most mutations impacting health are likely to also impact male mating [ 55 ]. Consequently, mutations which are deleterious for health in both sexes may be purged more efficiently by sexual selection on males, in which they are more deleterious, than by natural selection on both sexes.
This decrease in overall frequency, but maintenance of a larger selection coefficient in males, will actually reduce inbreeding depression to a greater degree for females than for males [ 16 , 54 , 55 ]. Thus, purging of deleterious alleles affecting male mating success in nature cannot explain the reduced inbreeding depression observed in males in this experiment.
Instead, the lack of sexual selection in the laboratory likely reduces the selection coefficient for many deleterious alleles in males, leading to a relaxation of inbreeding depression. Although the large declines in fitness observed in our experiment are consistent with empirical expectations for inbreeding depression [ 2 ], it is possible that some component of the laboratory environment could cause a systematic fitness decline in the tested lineages over time.
In this case, we would be unable to separate environmental effects from the effect of inbreeding.
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A Nature Research Journal. In most human societies, there are taboos and laws banning mating between first- and second-degree relatives, but actual prevalence and effects on health and fitness are poorly quantified. EI cases have phenotypic means between 0. Our study provides DNA-based quantification of the prevalence of EI in a European ancestry sample from the UK and measures its effects on health and fitness traits.
Mating between close relatives, that is inbreeding, is reported in many species to yield deleterious outcomes, such as reduced fertility 1 , 2 , 3 , 4 , stature 2 , 4 , 5 , 6 , 7 , 8 , 9 , 10 and lifespan 2. In humans, consanguineous mating leads to higher childhood mortality 3 , 11 , 12 and to adverse effects on traits such as lung function 4 , 10 , 13 and cognitive ability 4 , 8 , 10 , Because of its detrimental consequences, also referred to as inbreeding depression, a number of species have developed inbreeding avoidance mechanisms to limit its effects In humans, inbreeding avoidance mechanisms, include cultural and religious taboos on incest, and laws explicitly forbidding certain types of mating.
For instance, the Sexual Offences Act in the UK specifically forbids mating between first-degree parent—offspring or fullsibs FS , i. Cultural, legal, religious and health-related constraints strongly weigh on the ability to observe, and therefore study the causes and consequences of inbreeding between first- and second-degree relatives, hereafter referred to as extreme inbreeding EI.
A number of previous studies have attempted to quantify the prevalence and incidence of EI 15 , 16 , 17 , 18 , 19 , We also characterise the distribution of runs of homozygosity ROHs in EI cases and assess its consistency with theoretical predictions. Finally, we characterise the phenotypic consequences of EI on a number of health-related traits measured in UKB participants.
We previously identified 22 , individuals of European ancestry among the , UKB participants who have been genotyped. Ancestry was called in our previous study using projected principal components analysis based on known ancestry and whole-genome sequence data from participants of the Genomes Project 23 Methods. Given that 12 participants had retracted consent, we only analysed , UKB participants in the present study.
We then estimated for each study participant the percentage of their autosome comprising ROHs as a measure of inbreeding. Such inbreeding measure, hereafter denoted F ROH , is a well-established predictor of pedigree inbreeding 24 , The use of both F ROH as a measure of inbreeding and of this threshold are recommended by the ACMG for detecting suspected consanguinity between parents. We thus identified unrelated participants 65 males and 60 females whose genomes are consistent with their parents being first- or second-degree relatives.
We also estimated the prevalence of EI using allele-frequency based inbreeding measures or using ROHs detected on both autosome and X-chromosomes of female participants. That survey reports a total of 11, cases of police-recorded incest offences over this time period URLs.
The latter estimate is of the same order of magnitude as our estimated prevalence of EI in the UKB although these two estimates are based on different time periods births — in the UKB vs. Fry et al. Such an ascertainment on traits which are negatively correlated with inbreeding e. As a consequence, our estimate of prevalence of EI is likely conservative, although the magnitude of the underestimation is difficult to predict as it depends on many other unknown factors which might differ between UKB participants and the general population.
We next estimated the proportion of EI cases born from mating between first-degree relatives mating type 1; MT1 vs. It is worth noting that complex inbreeding loops between second degree-relatives may also lead to extreme values of F ROH. However, mating between first-degree relatives remains a more parsimonious explanation of the empirical observations, in particular in a population of European ancestry where such complex inbreeding loops are uncommon.
Predictive performances of FROH to discriminate different types of inbreeding: mating type 1 MT1: parent-offspring or fullsibs mating , mating type 2 MT2: halfsibs, avuncular, grandparent-grandchild or double-first cousins mating or mating type 3 MT3: first-cousins mating.
Predictive statistics assessed are the area under the receiver characteristics operating curve AUC , the sensitivity to detect MT1 over MT2 true positive rate and specificity to distinguish MT1 from MT2 true negative rate.
We further attempted to quantify the proportion of MT1 born from PO vs. Given that the theoretical expectation of F ROH is 0. We also considered an alternative approach that aims at directly estimating the proportion of EI cases born from PO vs.
We first stratified these 26 female EI cases into two groups Group 1 and Group 2 depending on whether the likelihood of their autosomal segments lengths is larger under PO mating or under FS mating. Altogether, we found that between We recall here that the coefficient of relationship between first-cousins is 0.
Also, MT3 is legal in most countries and thus more common in the population. We represent in Fig. Each length was subtracted 1. Each row, with possibly multiple segments, represents a unique participant.
Segments are groups by autosomal chromosomes from chromosome 1 bottom of each panel to chromosome 22 top of each panel ROHs are grouped in 6 length categories: between 1. Previous theoretical studies have often considered the length of genomic segments homozygous by descent HBD to follow an exponential distribution 31 , These studies generally relied on specific assumptions regarding recombination map functions, like Haldane or Kosambi map functions, which yield tractable algebraical simplifications.
However, empirical evidence supporting these assumptions remains limited. Moreover, some of these simplifying assumptions like that of independence between the lengths and the numbers of HBD segments have also been criticised Here, we used an empirical approach to estimate the length distribution of ROHs segments detected in EI cases using a mixture of exponential distributions. Given that only ROHs larger than 1. Mixtures of exponential distributions represent a flexible family of probability distributions, from which the exponential distribution is a special case.
Our simulations are based on observed recombination maps from the Genomes Project 23 , and therefore do not make additional assumptions regarding recombination rates Methods. We found for all simulated mating types that BIC selects two mixture components, which suggests that the single exponential distribution is likely too simple to characterise the length distribution of HBD segments.
Of note, mixtures of two exponential distributions also yield a better fit than gamma distributions that have previously also been proposed 1. We found consistently that the length distribution of simulated ROHs is also well characterised by a mixture of two exponential distributions. Overall, our findings suggest that the length distribution of HBD segments and ROHs can be well approximated with a mixture of two exponential distributions. Another observation in our simulations was that that the mean number of ROHs detected in an individual was larger than the number of true HBD segments simulated.
This somewhat counterintuitive observation is explained by the fact that HBD were defined as segments identical-by-descent from parents to offspring , while ROHs were re-estimated from the genotypes of simulated offspring. We found that simulated offspring of matings between unrelated parents had on average 4.
If we subtract that number i. More specifically, for each simulated inbred mating we find, after this correction, We first analysed ten control traits with prior evidence of inbreeding depression 4 , 8 , 10 , We performed linear regressions of these traits on the EI status adjusted for age at recruitment, recruitment centre treated as a categorical factor , sex, year of birth treated as a continuous variable , genotyping batch treated as a factor , socioeconomic status measured by the Townsend deprivation index and population structure measured by ten genetic principal components estimated from HM3 SNPs.
As expected, we found that EI cases had a reduced mean in these ten traits as compared to EI controls. More specifically, we found phenotypic means in EI cases to be between 0. We also specifically estimated the inbreeding load often denoted B , which represents the number of loci with deleterious alleles that would cause one death on average if made homozygous 3.
As previously recommended 34 , we estimated B using Poisson regression of the number of children engendered onto F ROH. Poisson regression was performed using a logarithmic link function as also previously recommended 34 and adjusted for the same covariates listed above. For this analysis, we used the entire distribution of F ROH , i.
The effect of inbreeding on fertility of the resulting inbred offspring, that we have quantified here, has been previously detected in humans However, the latter study did not provide an estimate of inbreeding load that can be directly compared with ours. Nonetheless, we found that our estimate is consistent with estimates of inbreeding load on survival of offspring from inbred mating in humans 3 , 36 and other species 34 , 37 , although these are different traits.
We then assessed whether the observed reduction in these ten traits was consistent with inbreeding depression quantified within EI controls.
Under the assumption that inbreeding depression results only from directional dominance effects of deleterious alleles or heterozygote advantage overdominance , phenotypes are expected to decline linearly with increased inbreeding. However, if epistasis contributes to inbreeding depression 38 , 39 or if causal variants for inbreeding depression are rarer 1 , a nonlinear relationship could be observed in particular for large inbreeding coefficients.
To test this hypothesis we first estimated inbreeding depression in , EI controls unrelated with each other and unrelated with the EI cases. For each of the 10 control traits, we then compared the phenotypic mean in the EI cases, with a linear prediction based on the estimate of inbreeding depression in EI controls. For this analysis inbreeding depression was also estimated using an alternative inbreeding measure F UNI , which we previously showed to be more powerful for detecting inbreeding depression 4.
This also suggests that causal variants contributing to inbreeding depression in those traits are likely well-tagged i. However, we acknowledge that the estimate of inbreeding depression from the EI cases present in the UKB might be too low if, as seems plausible, they are a relatively healthy sample from the population of all EI cases in the UK Traits were adjusted for age at recruitment, sex, recruitment centre, year of birth, genotyping batch, socioeconomic status measured by the Townsend deprivation index and population structure measured by 10 genetic principal components estimated from HM3 SNPs.
Resulting estimates were used to linearly predict the reduction in EI cases. Vertical bars around predictions corresponds to We next analysed the number of diseases diagnosed in an individual as an overall measure of health Methods. We used overdispersed Poisson regression to estimate the relative risk RR of being diagnosed with at least one disease in EI cases as compared to EI controls. To minimise potential biases due to partial or differential disease reporting between UKB participants, we re-estimated RR in individuals with at least one disease diagnosed.
We also provide additional evidence that offspring resulting from EI have increased risk for developing any type of disease. We tested the association between EI and the Townsend depression index, which quantifies the level of socioeconomic deprivation in areas where UKB participants live. We found significant evidence that EI is enriched in more socioeconomically deprived area odds ratio: 1. We further investigated the social contexts in which EI arose.
For that we compared different characteristics of the parents of EI cases with that of the parents of EI controls. We found that Given the significance of this difference we therefore focused all subsequent comparisons in nonadopted participants EI cases vs. Previous studies 40 have suggested that low EA of parents could be a cause of inbreeding in the population. Note that mean genetic predictor of EA is an estimate of the parental average for this trait.