SNP-based heritability of simulated traits from pooled dataset with correlated maternal-fetal genetic effects and parent-of-origin effects (POEs).

of simulated traits from pooled dataset with correlated maternal-fetal genetic effects and POEs, estimated through conventional GCTA, M-GCTA and H-GCTA approach using GREML (α = -1.0) model. For simplicity, we assumed that all causal variants exhibit POEs. POEs were incorporated by reducing the effect of m1 as compared to p1 by multiplying effects of m1 with (1 – I) where I is the imprinting factor such as 0.25, 0.50, 0.75 and 1.0. m1 shows either no imprinting, i.e., I = 0.0 () or partial imprinting, i.e., I = 0.25-0.75 () or complete imprinting, i.e., I = 1.0 (). For GCTA, M is the GRM generated from maternal genotypes (m), and F is the GRM generated from fetal genotypes (f). For M-GCTA, M’ represents the genetic relationship matrix of mothers; G represents genetic relationship matrix of children and D represents mother-child covariance matrix. For H-GCTA, M1 is the GRM generated from maternal transmitted alleles (m1), M2 is the GRM generated from maternal non-transmitted alleles (m2), and P1 is the GRM generated from paternal transmitted alleles (p1). A total of 100 replicates of each phenotype were simulated using empirical genotypes of Pooled dataset. P-values were calculated using z test statistics (two sided). (DOCX)

Publication Details

Journal
Figshare
Published
2025-03-10
DOI
https://doi.org/10.1371/journal.pgen.1011575.s023
Primary Topic
Genetic Associations and Epidemiology
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article
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article

SNP-based heritability of simulated traits from pooled dataset with correlated maternal-fetal genetic effects and parent-of-origin effects (POEs).

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Genetic Associations and Epidemiology
article

SNP-based heritability of simulated traits from pooled dataset with correlated maternal-fetal genetic effects and parent-of-origin effects (POEs).

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Abstract

of simulated traits from pooled dataset with correlated maternal-fetal genetic effects and POEs, estimated through conventional GCTA, M-GCTA and H-GCTA approach using GREML (α = -1.0) model. For simplicity, we assumed that all causal variants exhibit POEs. POEs were incorporated by reducing the effect of m1 as compared to p1 by multiplying effects of m1 with (1 – I) where I is the imprinting factor such as 0.25, 0.50, 0.75 and 1.0. m1 shows either no imprinting, i.e., I = 0.0 () or partial imprinting, i.e., I = 0.25-0.75 () or complete imprinting, i.e., I = 1.0 (). For GCTA, M is the GRM generated from maternal genotypes (m), and F is the GRM generated from fetal genotypes (f). For M-GCTA, M’ represents the genetic relationship matrix of mothers; G represents genetic relationship matrix of children and D represents mother-child covariance matrix. For H-GCTA, M1 is the GRM generated from maternal transmitted alleles (m1), M2 is the GRM generated from maternal non-transmitted alleles (m2), and P1 is the GRM generated from paternal transmitted alleles (p1). A total of 100 replicates of each phenotype were simulated using empirical genotypes of Pooled dataset. P-values were calculated using z test statistics (two sided). (DOCX)

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Genetic Associations and Epidemiology
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