scholarly journals GENETIC ARCHITECTURE OF INBREEDING DEPRESSION AND THE MAINTENANCE OF GAMETOPHYTIC SELF-INCOMPATIBILITY

Evolution ◽  
2014 ◽  
Vol 68 (11) ◽  
pp. 3317-3324 ◽  
Author(s):  
Camille Gervais ◽  
Diala Abu Awad ◽  
Denis Roze ◽  
Vincent Castric ◽  
Sylvain Billiard
2021 ◽  
Author(s):  
Marta B Bianchi ◽  
Thomas R Meagher ◽  
Peter E Gibbs

Abstract Background and Aims Genetically controlled self-incompatibility (SI) mechanisms constrain selfing and thus have contributed to the evolutionary diversity of flowering plants. In homomorphic gametophytic SI (GSI) and homomorphic sporophytic SI (SSI), genetic control is usually by a single multi-allelic locus S. Both GSI and SSI prevent self pollen tubes reaching the ovary and so are pre-zygotic in action. In contrast, in taxa with late-acting self-incompatibility (LSI), rejection is often post-zygotic, since self-pollen tubes grow to the ovary where fertilization may occur prior to floral abscission. Alternatively, lack of self fruit set could be due to early-acting inbreeding depression (EID). The aim of our study was to investigate mechanisms underlying lack of selfed fruit set in Handroanthus heptaphyllus in order to assess the likelihood of LSI versus EID. Methods We employed four full sib diallels to study the genetic control of LSI in Handroanthus heptaphyllus using a precociously flowering variant. We also used fluorescence microscopy to study the incidence of ovule penetration by pollen tubes in pistils that abscised following pollination or initiated fruits. Key Results All diallels showed reciprocally cross-incompatible full-sibs (RCI), reciprocally cross compatible full-sibs (RCC), and non-reciprocally compatible full-sibs (NRC) in almost equal proportions. There was no significant difference between the incidence of ovule penetrations in abscised pistils following self- and cross-incompatible pollinations, but those in successful cross pollinations were around twofold greater. Conclusions A genetic model postulating a single S locus with four s alleles, one of which, in the maternal parent, is dominant to the other three, will produce RCI, RCC and NRC situations each at 33 %, consistent with our diallel results. We favour this simple genetic control over an early-acting inbreeding depression (EID) explanation since none of our pollinations, successful or unsuccessful, resulted in partial embryo development, as would be expected under a whole genome EID effect.


Author(s):  
M.A. Stoffel ◽  
S.E. Johnston ◽  
J.G. Pilkington ◽  
J.M Pemberton

AbstractInbreeding depression is a phenomenon of long-standing importance, but we know surprisingly little about its genetic architecture, precise effects and life-history dynamics in wild populations. Here, we combined 417K imputed SNP genotypes for 5952 wild Soay sheep with detailed long-term life-history data to explore inbreeding depression on a key fitness component, annual survival. Inbreeding manifests in long runs of homozygosity (ROH) and these are abundant in Soay sheep, covering on average 24% of the autosomal genome and up to 50% in the most inbred individuals. The ROH landscape is shaped by recombination rate variation and differs widely across the genome, including islands where up to 87% of the population have an ROH and deserts where the ROH prevalence is as low as 4%. We next quantified individual inbreeding as the proportion of the autosomal genome in ROH (FROH) and estimated its effect on annual survival. The consequences of inbreeding are severe; a 10% increase in FROH was associated with a 68% [95% CI 55-78%] decrease in the odds of survival. However, the strength of inbreeding depression is dynamic across the lifespan. We estimate depression to peak in young adults, to decrease into older ages and to be weaker in lambs, where inbreeding effects are possibly buffered by maternal care. Finally, using a genome-wide association scan on ROH, we show that inbreeding causes depression predominantly through many loci with small effects, but we also find three regions in the genome with putatively strongly deleterious mutations. Our study reveals population and genome-wide patterns of homozygosity caused by inbreeding and sheds light on the strength, dynamics and genetic architecture of inbreeding depression in a wild mammal population.


2018 ◽  
Author(s):  
Aaron J. Sams ◽  
Adam R. Boyko

Abstract/SummaryInbreeding and consanguinity leave distinct genomic traces, most notably long genomic tracts that are identical by descent and completely homozygous. These runs of homozygosity (ROH) can contribute to inbreeding depression if they contain deleterious variants that are fully or partially recessive. Several lines of evidence have been used to show that long (> 5 megabase (Mb)) ROH are disproportionately likely to harbor deleterious variation, but the extent to which long versus short tracts contribute to autozygosity at loci known to be deleterious and recessive has not been studied.In domestic dogs, nearly 200 mutations are known to cause recessive diseases, most of which can be efficiently assayed using SNP arrays. By examining genome-wide data from over 200,000 markers, including 150 recessive disease variants, we built high-resolution ROH density maps for nearly 2,500 dogs, recording ROH down to 500 kilobases. We observed over 500 homozygous deleterious recessive genotypes in the panel, 90% of which overlapped with ROH inferred by GERMLINE. Although most of these genotypes were contained in ROH over 5 Mb in length, 14% were contained in short (0.5 - 2.5 Mb) tracts, a significant enrichment compared to the genetic background, suggesting that even short tracts are useful for computing inbreeding metrics like the coefficient of inbreeding estimated from ROH (FROH).In our dataset, FROH differed significantly both within and among dog breeds. All breeds harbored some regions of reduced genetic diversity due to drift or selective sweeps, but the degree of inbreeding and the proportion of inbreeding caused by short versus long tracts differed between breeds, reflecting their different population histories. Although only available for a few species, large genome-wide datasets including recessive disease variants hold particular promise not only for disentangling the genetic architecture of inbreeding depression, but also evaluating and improving upon current approaches for detecting ROH.


2018 ◽  
Author(s):  
Thomas Brom ◽  
Vincent Castric ◽  
Sylvain Billiard

AbstractMany hermaphroditic flowering plants species possess a genetic self-incompatibility (SI) system that prevents self-fertilization and is typically controlled by a single multiallelic locus, the S-locus. The conditions under which SI can be stably maintained in single isolated populations are well known and depend chiefly on the level of inbreeding depression and the number of SI alleles segregating at the S-locus. However, while both the number of SI alleles and the level of inbreeding depression are potentially affected by population subdivision, the conditions for the maintenance of SI in subdivided populations remain to be studied. In this paper, we combine analytical predictions and two different individual-based simulation models to show that population subdivision can severely compromise the maintenance of SI. Under the conditions we explored, this effect is mainly driven by the decrease of the local diversity of SI alleles rather than by a change in the dynamics of inbreeding depression. We discuss the implications of our results for the interpretation of empirical data on the loss of SI in natural populations.Data accessibility statementNo data to be archived


Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 893-907
Author(s):  
Sara R Lipow ◽  
Robert Wyatt

Abstract Most individuals of Asclepias exaltata are self-sterile, but all plants lack prezygotic barriers to self-fertilization. To determine whether postzygotic rejection of self-fertilized ovules is due to late-acting self-incompatibility or to extreme, early acting inbreeding depression, we performed three diallel crosses among self-sterile plants related as full-sibs. The full-sibs segregated into four compatibility classes, suggesting that late acting self-incompatibility is controlled by a single gene (S-locus). Crosses between plants sharing one or both alleles at the S-locus are incompatible. An additional diallel cross was done among full-sib progeny from a cross of a self-sterile and a self-fertile plant. These progeny grouped into two compatibility classes, and plants within classes displayed varying levels of self-fertility. This suggests that the occasional self-fertility documented in natural pollinations is caused by pseudo-self-fertility alleles that alter the functioning of the S-locus.


2017 ◽  
Vol 114 (32) ◽  
pp. 8602-8607 ◽  
Author(s):  
Loic Yengo ◽  
Zhihong Zhu ◽  
Naomi R. Wray ◽  
Bruce S. Weir ◽  
Jian Yang ◽  
...  

Quantifying the effects of inbreeding is critical to characterizing the genetic architecture of complex traits. This study highlights through theory and simulations the strengths and shortcomings of three SNP-based inbreeding measures commonly used to estimate inbreeding depression (ID). We demonstrate that heterogeneity in linkage disequilibrium (LD) between causal variants and SNPs biases ID estimates, and we develop an approach to correct this bias using LD and minor allele frequency stratified inference (LDMS). We quantified ID in 25 traits measured in ∼140,000 participants of the UK Biobank, using LDMS, and confirmed previously published ID for 4 traits. We find unique evidence of ID for handgrip strength, waist/hip ratio, and visual and auditory acuity (ID between −2.3 and −5.2 phenotypic SDs for complete inbreeding; P<0.001). Our results illustrate that a careful choice of the measure of inbreeding combined with LDMS stratification improves both detection and quantification of ID using SNP data.


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