Low-density genotype panel for both parentage verification and discovery in a multi-breed sheep population

peer-reviewedThe generally low usage of artificial insemination and single-sire mating in sheep, compounded by mob lambing (and lambing outdoors), implies that parentage assignment in sheep is challenging. The objective here was to develop a low-density panel of single nucleotide polymorphisms (SNPs) for accurate parentage verification and discovery in sheep. Of particular interest was where SNP selection was limited to only a subset of chromosomes, thereby eliminating the ability to accurately impute genome-wide denser marker panels. Data used consisted of 10,933 candidate SNPs on 9,390 purebred sheep. These data consisted of 1,876 validated genotyped sire–offspring pairs and 2,784 validated genotyped dam–offspring pairs. The SNP panels developed consisted of 87 SNPs to 500 SNPs. Parentage verification and discovery were undertaken using 1) exclusion, based on the sharing of at least one allele between candidate parent–offspring pairs, and 2) a likelihood-based approach. Based on exclusion, allowing for one discordant offspring–parent genotype, a minimum of 350 SNPs was required when the goal was to unambiguously identify the true sire or dam from all possible candidates. Results suggest that, if selecting SNPs across the entire genome, a minimum of 250 carefully selected SNPs are required to ensure that the most likely selected parent (based on the likelihood approach) was, in fact, the true parent. If restricting the SNPs to just a subset of chromosomes, the recommendation is to use at least a 300-SNP panel from at least six chromosomes, with approximately an equal number of SNPs per chromosome

African animal genetic resources: Their characterisation, conservation and utilisation. Proceedings of the research planning workshop

Addresses different papers presented on the workshop organised by ILCA, as part of the research planning process on a project of characterisation, conservation and utilization of Africa's indigenous animal genetic resources. In taking on this challenging task, ILCA recognised that it could not succeed without substantial collaboration with NARS colleagues. However, it also recognised the need to work out standard characterisation methodology and to outline the implementation process. Workshop participants reached the consensus that this project was timely and that activities should be initiated to document Africa's animal genetic resources, with a view to developing strategies for their conservation and sustainable utilisation. While stressing the importance of breed characterisation, participants reiterated that those breeds identified as currently endangered should be conserved even if their value is not presently apparent. Considerable attention was given to development of experimental designs which would optimise collection of data on population dynamics, physical characteristics and phenotypic and genetic parameters of biological performance traits

Genetic parameters for animal mortality in pasture-based, seasonal-calving dairy and beef herds

peer-reviewedIn the absence of informative health and welfare phenotypes, breeding for reduced animal mortality could improve overall health and welfare, provided genetic variability in animal mortality exists. The objective of the present study was to estimate genetic (and other) variance components for animal mortality in pasture-based, seasonal-calving dairy and beef herds across multiple life stages as well as to quantify the genetic relationship in mortality among life stages. National mortality records were available for all cattle born in the Republic of Ireland. Cattle were grouped into three life stages based on age (0 to 30 days, 31 to 365 days, 366 to 1095 days) whereas females with ≥1 calving event were also grouped into five life stages, based on parity number (1, 2, 3, 4, and 5), considering both the initial 60 days of lactation and a cow's entire lactation period, separately. The mean mortality prevalence ranged from 0.70 to 5.79% in young animals and from 0.53 to 3.86% in cows. Variance components and genetic correlations were estimated using linear mixed models using 21,637 to 100,993 records. Where heritability estimates were different from zero, direct heritability estimates for mortality in young animals (≤1095 days) ranged from 0.006 to 0.040, whereas the genetic standard deviation ranged from 0.015 to 0.034. The contribution of a maternal genetic effect to mortality in young animals was evident up to 30 days of age in dairy herds, but this was only the case in preliminary analysis of stillbirths in beef herds. Based on the estimated genetic standard deviation in the present study, the incidence of mortality in young animals could be reduced through breeding by up to 3.4 percentage units per generation. For cows, direct heritability estimates for mortality, where different from zero, ranged from 0.003 to 0.049. The genetic standard deviation for mortality in cows ranged from 0.005 to 0.016 during the initial 60 days of lactation and ranged from 0.011 to 0.032 during the cow's entire lactation. Genetic correlations among the age groups as well as between the age groups and cow parities had high standard errors. Genetic correlations among the cow parities were moderate to strongly positive (ranging from 0.66 to 0.99) and mostly different from zero. Results from the present study can be used to inform genetic evaluations for mortality in young animals and in cows as well as the potential genetic gain achievable

A test of genetic models for the evolutionary maintenance of same-sex sexual behaviour

This study was supported by Natural Environment Research Council (NERC) fellowships to NWB (NE/G014906/1, NE/L011255/1) and a NERC grant to NWB and MGR (NE/I016937/1).The evolutionary maintenance of same-sex sexual behaviour (SSB) has received increasing attention because it is perceived to be an evolutionary paradox. The genetic basis of SSB is almost wholly unknown in non-human animals, though this is key to understanding its persistence. Recent theoretical work has yielded broadly applicable predictions centred on two genetic models for SSB: overdominance and sexual antagonism. Using Drosophila melanogaster, we assayed natural genetic variation for male SSB and empirically tested predictions about the mode of inheritance and fitness consequences of alleles influencing its expression. We screened 50 inbred lines derived from a wild population for male–male courtship and copulation behaviour, and examined crosses between the lines for evidence of overdominance and antagonistic fecundity selection. Consistent variation among lines revealed heritable genetic variation for SSB, but the nature of the genetic variation was complex. Phenotypic and fitness variation was consistent with expectations under overdominance, although predictions of the sexual antagonism model were also supported. We found an unexpected and strong paternal effect on the expression of SSB, suggesting possible Y-linkage of the trait. Our results inform evolutionary genetic mechanisms that might maintain low but persistently observed levels of male SSB in D. melanogaster, but highlight a need for broader taxonomic representation in studies of its evolutionary causes.PostprintPeer reviewe

Effect of parentage misidentification on estimates of genetic parameters for milk yield in the Mediterranean Italian buffalo population

The objective of this study was to evaluate the effect of parentage misidentification on estimation of genetic parameters for the Italian buffalo population for milk yield from 45,194 lactation records of 23,104 Italian buffalo cows. Animals were grouped into 10 data sets in which sires and dams were DNA identified, or reported from the pedigree, or unknown. A derivativefree restricted maximum likelihood method was used to estimate components of variance with a repeatability model. The model contained age at calving nested within parity and days from calving to conception as linear covariates, herd-year-seasons as fixed effects, and additive genetic, permanent environmental, and temporary environmental effects as random effects. Estimates of heritability (±SE) ranged from 0.00 ± 0.099 (sires and dams as reported in the pedigree) to 0.39 ± 0.094 (sires DNA identified and dams as reported in the pedigree). When identification of sires was as reported in the pedigree, estimates of heritability were close to zero. These small estimates indicate that a large proportion of reported paternity is incorrect. When sires are unknown and dams are DNA identified, the proportion of variance due to sires seems to be captured in the estimate of permanent environmental variance as a fraction of phenotypic variance. Therefore, as heritability decreased, permanent environmental variance increased about the same amount. Data sets with dams identified from pedigree and sires DNA identified showed the largest estimate of heritability (0.39), which was essentially the same as when dams were DNA identified (0.38). This result supports that most dams are correctly reported from the pedigree. Genetic progress should be much greater with bulls DNA identified because of greater heritability, but without artificial insemination and progeny testing, progress would be slow and would depend mostly on selection of sires based on dam estimated breeding values. Implementation of artificial insemination programs and DNA testing to identify sires are the keys for increasing genetic progress in the Italian buffalo population

Parentage verification and identity test of Ghezel sheep using microsatillate markers

The Ghezel sheep is a fat tail high weight Iranian breed which is raised in the North-west of Iran. To design an efficient improvement program and genetic evaluation system for this indigenous breed, accurate estimates of the population genetic parameters is per-required and all pedigrees and relationships should be correctly recorded. Otherwise, it can produce biased evaluations when pedigrees contain errors and procedures utilize information from relatives. The pedigree and genotype data of Ghezel sheep were examined for errors. Parentage control has been performed by amplification of microsatellites. Mean heterozygosities, mean polymorphism index content (PIC) and mean number of alleles per loci were 0.50, 0.43 and 3.71, respectively. Mendelian errors were found following the pedigree corrections. Alleles at the following seven microsatellite loci were identified: BM4307, CSSM004, BM415, RM029, INRA49, BM3205 and OarFCB5. The pedigree was considered incorrect in 6 (12%) out of all the evaluated progeny, as their genotype did not match their parents. The present findings attest to the usefulness of the investigated microsatellites for parentage control in Ghezel sheep.Key words: Ghezel sheep, microsatellites, genotyping errors, progeny test

Quantitative trait loci affecting lactose and total solids on chromosome 6 in Brazilian Gir dairy cattle.

Fourteen Brazilian Gir sire families with 657 daughters were analyzed for quantitative trait loci (QTL) on chromosome 6 affecting lactose and total solids. Cows and sires were genotyped with 27 microsatellites with a mean spacing between markers of 4.9 cM. We used a 1% chromosome-wide threshold for QTL qualification. A QTL for lactose yield was found close to marker MNB66 in three families. A QTL for total solid yield was identified close to marker BMS2508 in three families. A QTL for lactose percentage, close to marker DIK1182, was identified in two families. A QTL for total solid percentage, close to marker MNB208, was identified in four families. These QTLs could be used for selection of animals in dairy production systems

Heritability of malaria in Africa

Background While many individual genes have been identified that confer protection against malaria, the overall impact of host genetics on malarial risk remains unknown. Methods and Findings We have used pedigree-based genetic variance component analysis to determine the relative contributions of genetic and other factors to the variability in incidence of malaria and other infectious diseases in two cohorts of children living on the coast of Kenya. In the first, we monitored the incidence of mild clinical malaria and other febrile diseases through active surveillance of 640 children 10 y old or younger, living in 77 different households for an average of 2.7 y. In the second, we recorded hospital admissions with malaria and other infectious diseases in a birth cohort of 2,914 children for an average of 4.1 y. Mean annual incidence rates for mild and hospital-admitted malaria were 1.6 and 0.054 episodes per person per year, respectively. Twenty-four percent and 25% of the total variation in these outcomes was explained by additively acting host genes, and household explained a further 29% and 14%, respectively. The haemoglobin S gene explained only 2% of the total variation. For nonmalarial infections, additive genetics explained 39% and 13% of the variability in fevers and hospital-admitted infections, while household explained a further 9% and 30%, respectively. Conclusion Genetic and unidentified household factors each accounted for around one quarter of the total variability in malaria incidence in our study population. The genetic effect was well beyond that explained by the anticipated effects of the haemoglobinopathies alone, suggesting the existence of many protective genes, each individually resulting in small population effects. While studying these genes may well provide insights into pathogenesis and resistance in human malaria, identifying and tackling the household effects must be the more efficient route to reducing the burden of disease in malaria-endemic areas