TY - CHAP
T1 - Protocol for Construction of Genome-Wide Epistatic SNP Networks Using WISH-R Package
AU - Kadarmideen, Haja N.
AU - Carmelo, Victor Adriano Okstoft
N1 - Funding Information: VAOC received partial Ph.D. stipends from the Technical University of Denmark. Authors thank all co-authors in two previously published papers related to this software WISH-R. Publisher Copyright: © 2021, Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2021
Y1 - 2021
N2 - Epistasis is the interaction between genes or genetic variants (such as Single Nucleotide Polymorphisms or SNPs) that influences a phenotype or a disease outcome. Statistically and biologically, significant evidence of epistatic loci for several traits and diseases is well known in human, animals, and plants. However, there is no straightforward way to compute a large number of pairwise epistasis among millions of variants along the whole genome, relate them to phenotypes or diseases, and visualize them. The WISH-R package (WISH-R) was developed to address this technology gap to calculate epistatic interactions using a linear or generalized linear model on a genome-wide level using genomic data and phenotype/disease data in a fully parallelized environment, and visualize genome-wide epistasis in many ways. This method protocol chapter provides an easy-to-follow systematic guide to install this R software in computers on Win OS, Mac OS, and Linux platforms and can be downloaded from https://github.com/QSG-Group/WISH with a user guide. The WISH-R package has several inbuilt functions to reduce genotype data dimensionality and hence computational demand. WISH-R software can be used to build scale-free weighted SNP interaction networks and relate them to quantitative traits or phenotypes and case–control diseases outcomes. The software leads to integrating biological knowledge to identify disease- or trait-relevant SNP or gene modules, hub genes, potential biomarkers, and pathways related to complex traits and diseases.
AB - Epistasis is the interaction between genes or genetic variants (such as Single Nucleotide Polymorphisms or SNPs) that influences a phenotype or a disease outcome. Statistically and biologically, significant evidence of epistatic loci for several traits and diseases is well known in human, animals, and plants. However, there is no straightforward way to compute a large number of pairwise epistasis among millions of variants along the whole genome, relate them to phenotypes or diseases, and visualize them. The WISH-R package (WISH-R) was developed to address this technology gap to calculate epistatic interactions using a linear or generalized linear model on a genome-wide level using genomic data and phenotype/disease data in a fully parallelized environment, and visualize genome-wide epistasis in many ways. This method protocol chapter provides an easy-to-follow systematic guide to install this R software in computers on Win OS, Mac OS, and Linux platforms and can be downloaded from https://github.com/QSG-Group/WISH with a user guide. The WISH-R package has several inbuilt functions to reduce genotype data dimensionality and hence computational demand. WISH-R software can be used to build scale-free weighted SNP interaction networks and relate them to quantitative traits or phenotypes and case–control diseases outcomes. The software leads to integrating biological knowledge to identify disease- or trait-relevant SNP or gene modules, hub genes, potential biomarkers, and pathways related to complex traits and diseases.
U2 - 10.1007/978-1-0716-0947-7_10
DO - 10.1007/978-1-0716-0947-7_10
M3 - Book chapter
C2 - 33733355
AN - SCOPUS:85102872925
SN - 978-1-0716-0946-0
T3 - Methods in Molecular Biology
SP - 155
EP - 168
BT - Methods in Molecular Biology
PB - Humana Press
ER -