Dissection of identical‐by‐descent segments during the formation of foundation parents derived from Suwan germplasm of maize

2020 ◽  
Vol 139 (5) ◽  
pp. 862-869
Author(s):  
Xiangyang Guo ◽  
Xun Wu ◽  
Wenqiang Wu ◽  
Angui Wang ◽  
Pengfei Liu ◽  
...  
Keyword(s):  
Identical By Descent

The use of linkage disequilibrium to map quantitative trait loci

2005 ◽  
Vol 45 (8) ◽  
pp. 837 ◽  
Author(s):  
M. E. Goddard ◽  
T. H. E. Meuwissen
Keyword(s):  
Linkage Disequilibrium ◽  
Quantitative Trait Loci ◽  
Statistical Model ◽  
Quantitative Trait ◽  
Linear Models ◽  
Chromosome Segment ◽  
Identical By Descent ◽  
Trait Loci ◽  
Linkage Disequilibrium Information ◽  
Chromosome Segments

This paper reviews the causes of linkage disequilibrium and its use in mapping quantitative trait loci. The many causes of linkage disequilibrium can be understood as due to similarity in the coalescence tree of different loci. Consideration of the way this comes about allows us to divide linkage disequilibrium into 2 types: linkage disequilibrium between any 2 loci, even if they are unlinked, caused by variation in the relatedness of pairs of animals; and linkage disequilibrium due to the inheritance of chromosome segments that are identical by descent from a common ancestor. The extent of linkage disequilibrium due to the latter cause can be logically measured by the chromosome segment homozygosity which is the probability that chromosome segments taken at random from the population are identical by descent. This latter cause of linkage disequilibrium allows us to map quantitative trait loci to chromosome regions. The former cause of linkage disequilibrium can cause artefactual quantitative trait loci at any position in the genome. These artefacts can be avoided by fitting the relatedness of animals in the statistical model used to map quantitative trait loci. In the future it may be convenient to estimate this degree of relatedness between individuals from markers covering the whole genome. The statistical model for mapping quantitative trait loci also requires us to estimate the probability that 2 animals share quantitative trait loci alleles at a particular position because they have inherited a chromosome segment containing the quantitative trait loci identical by descent. Current methods to do this all involve approximations. Methods based on concepts of coalescence and chromosome segment homozygosity are useful, but improvements are needed for practical analysis of large datasets. Once these probabilities are estimated they can be used in flexible linear models that conveniently combine linkage and linkage disequilibrium information.

scholarly journals Blocks of chromosomes identical by descent in a population: Models and predictions

PLoS ONE ◽  
2017 ◽  
Vol 12 (11) ◽  
pp. e0187416 ◽  
Author(s):  
Mathieu Tiret ◽  
Frédéric Hospital
Keyword(s):  
Population Models ◽  
Identical By Descent

scholarly journals Haplotype assembly in polyploid genomes and identical by descent shared tracts

2013 ◽  
Vol 29 (13) ◽  
pp. i352-i360 ◽  
Author(s):  
Derek Aguiar ◽  
Sorin Istrail
Keyword(s):  
Haplotype Assembly ◽  
Identical By Descent

scholarly journals Identical by descent L1CAM mutation in two apparently unrelated families with intellectual disability without L1 syndrome

2015 ◽  
Vol 58 (6-7) ◽  
pp. 364-368 ◽  
Author(s):  
Marie Shaw ◽  
Tzu Ying Yap ◽  
Lyndal Henden ◽  
Melanie Bahlo ◽  
Alison Gardner ◽  
...  
Keyword(s):  
Intellectual Disability ◽  
Identical By Descent ◽  
L1 Syndrome

scholarly journals A chromosome 10 variant with a 12 Mb inversion [inv(10)(q11.22q21.1)] identical by descent and frequent in the Swedish population

2009 ◽  
Vol 149A (3) ◽  
pp. 380-386 ◽  
Author(s):  
Miriam Entesarian ◽  
Birgit Carlsson ◽  
Mahmoud Reza Mansouri ◽  
Eva-Lena Stattin ◽  
Eva Holmberg ◽  
...  
Keyword(s):  
Chromosome 10 ◽  
Swedish Population ◽  
Identical By Descent

scholarly journals Control of Simian Immunodeficiency Virus SIVmac239 Is Not Predicted by Inheritance of Mamu-B*17-Containing Haplotypes

2006 ◽  
Vol 81 (1) ◽  
pp. 406-410 ◽  
Author(s):  
Jason A. Wojcechowskyj ◽  
Levi J. Yant ◽  
Roger W. Wiseman ◽  
Shelby L. O'Connor ◽  
David H. O'Connor
Keyword(s):  
Human Immunodeficiency Virus ◽  
Disease Progression ◽  
Simian Immunodeficiency Virus ◽  
Virus Disease ◽  
Rhesus Macaques ◽  
Host Genetics ◽  
Mhc Genes ◽  
Histocompatibility Complex ◽  
Identical By Descent ◽  
Immunodeficiency Virus

ABSTRACT It is well established that host genetics, especially major histocompatibility complex (MHC) genes, are important determinants of human immunodeficiency virus disease progression. Studies with simian immunodeficiency virus (SIV)-infected Indian rhesus macaques have associated Mamu-B*17 with control of virus replication. Using microsatellite haplotyping of the 5-Mb MHC region, we compared disease progression among SIVmac239-infected Indian rhesus macaques that possess Mamu-B*17-containing MHC haplotypes that are identical by descent. We discovered that SIV-infected animals possessing identical Mamu-B*17-containing haplotypes had widely divergent disease courses. Our results demonstrate that the inheritance of a particular Mamu-B*17-containing haplotype is not sufficient to predict SIV disease outcome.

scholarly journals Crossover interference and sex-specific genetic maps shape identical by descent sharing in close relatives

PLoS Genetics ◽  
2019 ◽  
Vol 15 (12) ◽  
pp. e1007979 ◽  
Author(s):  
Madison Caballero ◽  
Daniel N. Seidman ◽  
Ying Qiao ◽  
Jens Sannerud ◽  
Thomas D. Dyer ◽  
...  
Keyword(s):  
Genetic Maps ◽  
Crossover Interference ◽  
Identical By Descent ◽  
Close Relatives

Joint effect of 21 marker loci and effect of realized inbreeding on growth in pigs

1996 ◽  
Vol 62 (3) ◽  
pp. 541-546 ◽  
Author(s):  
K. Christensen ◽  
M. Fredholm ◽  
A. K. Winterø ◽  
J. N. Jørgensen ◽  
S. Andersen
Keyword(s):  
Growth Traits ◽  
Average Daily Gain ◽  
Joint Effect ◽  
Linear Increase ◽  
Inbreeding Coefficient ◽  
Lean Meat ◽  
Identical By Descent ◽  
Genetic Potential ◽  
Marker Loci ◽  
Daily Gain

AbstractFour litters produced by father-daughter matings (back crosses) resulting in 35 animals with a theoretical inbreeding coefficient of 25% were typed with 21 independent informative markers. The differences between the two founder animals were estimated, based on the marker information, and it was found that the founder boar had higher genetic potential for proportion of lean meat and lower genetic potential for groivth than the founder sow. The proportion of the genome of each offspring which was identical by descent was investigated. On the basis of these markers the realized inbreeding was found to vary between 7 and 47%. The linear decrease in weight at days 1, 26 and 136, average daily gain and proportion of lean meat regressed on the realized inbreeding were estimated to 0·6 kg, 2·4 kg, 18 kg, 95 g/day and 15 g/kg, respectively. For weight at day 88 a corresponding linear increase of 11 kg was observed. The joint effect of founder differences and realized inbreeding were as expected negative and statistically significant for all growth traits.

False Disease Region Identification From Identity-By-Descent Haplotype Sharing in the Presence of Phenocopies

2006 ◽  
Vol 9 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Stuart Macgregor ◽  
Sara A. Knott ◽  
Peter M. Visscher
Keyword(s):  
Confidence Interval ◽  
Complex Disease ◽  
Linkage Peak ◽  
Disease Locus ◽  
Linkage Phase ◽  
Disease Mutation ◽  
Identical By Descent ◽  
Related Individuals ◽  
Disease Region ◽  
Chromosome Segments

AbstractLinkage analysis (either parametric or nonparametric) is commonly applied to identify chromosomal regions using related individuals affected by disease. In complex disease the incomplete relationship between phenotype and genotype can be modeled using a phenocopy parameter, the probability that an individual is affected given they do not carry the disease mutation of interest, and a nonpenetrance parameter, the probability that an individual is not affected given they do carry the disease mutation of interest. If the linkage phase between multiple markers and a putative disease locus is known, then haplotypes carrying the mutation can, in principle, be identified by comparing the chromosome segments that are shared identical-by-descent (IBD) across affected individuals. We consider here the effect of a nonzero phenocopy rate on the linkage peak and hence upon the identification of disease haplotypes that are shared IBD between affected individuals. We show, by theory and computer simulation, that in diseases for which there is a nonzero phenocopy rate, the chromosomal regions identified may not include the true disease locus. We utilize a LOD-1 confidence interval for a widely used nonparametric linkage statistic. We find that in small/moderate samples this confidence interval may be inappropriate. We give specific examples where the phenocopy rates are nonnegligible in some complex diseases. The success of further work to identify the causal mutations underlying the linkage peaks in these diseases will depend on researchers allowing for the presence of phenocopies by examining appropriately wide regions around the initial positive linkage finding.

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