Mobile element variation contributes to population-specific genome diversification, gene regulation and disease risk

Mobile genetic elements (MEs) are heritable mutagens that recursively generate structural variants (SVs). ME variants (MEVs) are difficult to genotype and integrate in statistical genetics, obscuring their impact on genome diversification and traits. We developed a tool that accurately genotypes MEV...

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Published inNature genetics Vol. 55; no. 6; pp. 939 - 951
Main Authors Kojima, Shohei, Koyama, Satoshi, Ka, Mirei, Saito, Yuka, Parrish, Erica H., Endo, Mikiko, Takata, Sadaaki, Mizukoshi, Misaki, Hikino, Keiko, Takeda, Atsushi, Gelinas, Asami F., Heaton, Steven M., Koide, Rie, Kamada, Anselmo J., Noguchi, Michiya, Hamada, Michiaki, Kamatani, Yoichiro, Murakawa, Yasuhiro, Ishigaki, Kazuyoshi, Nakamura, Yukio, Ito, Kaoru, Terao, Chikashi, Momozawa, Yukihide, Parrish, Nicholas F.
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.06.2023
Nature Publishing Group
Subjects
45/43
631/208/200
631/208/205/2138
631/208/457
Agriculture
Animal Genetics and Genomics
Bias
Biomedical and Life Sciences
Biomedicine
Cancer Research
DNA methylation
Enhancers
Fasciitis
Gene expression
Gene Expression Regulation
Gene Function
Gene mapping
Gene regulation
Gene sequencing
Genetics
Genome-wide association studies
Genome-Wide Association Study
Genomes
Genotype & phenotype
Genotypes
Health risks
Human Genetics
Human populations
Humans
Insertion
Mutagens
Mutation
Phenotype
Polymorphism, Single Nucleotide
Populations
Post-transcription
Preferences
Quantitative Trait Loci
Risk
Statistical genetics
Whole genome sequencing
Online AccessGet full text

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Abstract Mobile genetic elements (MEs) are heritable mutagens that recursively generate structural variants (SVs). ME variants (MEVs) are difficult to genotype and integrate in statistical genetics, obscuring their impact on genome diversification and traits. We developed a tool that accurately genotypes MEVs using short-read whole-genome sequencing (WGS) and applied it to global human populations. We find unexpected population-specific MEV differences, including an Alu insertion distribution distinguishing Japanese from other populations. Integrating MEVs with expression quantitative trait loci (eQTL) maps shows that MEV classes regulate tissue-specific gene expression by shared mechanisms, including creating or attenuating enhancers and recruiting post-transcriptional regulators, supporting class-wide interpretability. MEVs more often associate with gene expression changes than SNVs, thus plausibly impacting traits. Performing genome-wide association study (GWAS) with MEVs pinpoints potential causes of disease risk, including a LINE-1 insertion associated with keloid and fasciitis. This work implicates MEVs as drivers of human divergence and disease risk. MEGAnE is a new tool to detect and genotype mobile element variants (MEVs) from short-read whole-genome sequencing datasets. Genetic analyses implicate MEVs as population-specific drivers of gene expression variation and disease risk.
AbstractList Mobile genetic elements (MEs) are heritable mutagens that recursively generate structural variants (SVs). ME variants (MEVs) are difficult to genotype and integrate in statistical genetics, obscuring their impact on genome diversification and traits. We developed a tool that accurately genotypes MEVs using short-read whole-genome sequencing (WGS) and applied it to global human populations. We find unexpected population-specific MEV differences, including an Alu insertion distribution distinguishing Japanese from other populations. Integrating MEVs with expression quantitative trait loci (eQTL) maps shows that MEV classes regulate tissue-specific gene expression by shared mechanisms, including creating or attenuating enhancers and recruiting post-transcriptional regulators, supporting class-wide interpretability. MEVs more often associate with gene expression changes than SNVs, thus plausibly impacting traits. Performing genome-wide association study (GWAS) with MEVs pinpoints potential causes of disease risk, including a LINE-1 insertion associated with keloid and fasciitis. This work implicates MEVs as drivers of human divergence and disease risk.Mobile genetic elements (MEs) are heritable mutagens that recursively generate structural variants (SVs). ME variants (MEVs) are difficult to genotype and integrate in statistical genetics, obscuring their impact on genome diversification and traits. We developed a tool that accurately genotypes MEVs using short-read whole-genome sequencing (WGS) and applied it to global human populations. We find unexpected population-specific MEV differences, including an Alu insertion distribution distinguishing Japanese from other populations. Integrating MEVs with expression quantitative trait loci (eQTL) maps shows that MEV classes regulate tissue-specific gene expression by shared mechanisms, including creating or attenuating enhancers and recruiting post-transcriptional regulators, supporting class-wide interpretability. MEVs more often associate with gene expression changes than SNVs, thus plausibly impacting traits. Performing genome-wide association study (GWAS) with MEVs pinpoints potential causes of disease risk, including a LINE-1 insertion associated with keloid and fasciitis. This work implicates MEVs as drivers of human divergence and disease risk.
Mobile genetic elements (MEs) are heritable mutagens that recursively generate structural variants (SVs). ME variants (MEVs) are difficult to genotype and integrate in statistical genetics, obscuring their impact on genome diversification and traits. We developed a tool that accurately genotypes MEVs using short-read whole-genome sequencing (WGS) and applied it to global human populations. We find unexpected population-specific MEV differences, including an Alu insertion distribution distinguishing Japanese from other populations. Integrating MEVs with expression quantitative trait loci (eQTL) maps shows that MEV classes regulate tissue-specific gene expression by shared mechanisms, including creating or attenuating enhancers and recruiting post-transcriptional regulators, supporting class-wide interpretability. MEVs more often associate with gene expression changes than SNVs, thus plausibly impacting traits. Performing genome-wide association study (GWAS) with MEVs pinpoints potential causes of disease risk, including a LINE-1 insertion associated with keloid and fasciitis. This work implicates MEVs as drivers of human divergence and disease risk.
Mobile genetic elements (MEs) are heritable mutagens that recursively generate structural variants (SVs). ME variants (MEVs) are difficult to genotype and integrate in statistical genetics, obscuring their impact on genome diversification and traits. We developed a tool that accurately genotypes MEVs using short-read whole-genome sequencing (WGS) and applied it to global human populations. We find unexpected population-specific MEV differences, including an Alu insertion distribution distinguishing Japanese from other populations. Integrating MEVs with expression quantitative trait loci (eQTL) maps shows that MEV classes regulate tissue-specific gene expression by shared mechanisms, including creating or attenuating enhancers and recruiting post-transcriptional regulators, supporting class-wide interpretability. MEVs more often associate with gene expression changes than SNVs, thus plausibly impacting traits. Performing genome-wide association study (GWAS) with MEVs pinpoints potential causes of disease risk, including a LINE-1 insertion associated with keloid and fasciitis. This work implicates MEVs as drivers of human divergence and disease risk. MEGAnE is a new tool to detect and genotype mobile element variants (MEVs) from short-read whole-genome sequencing datasets. Genetic analyses implicate MEVs as population-specific drivers of gene expression variation and disease risk.
Author Takeda, Atsushi
Noguchi, Michiya
Heaton, Steven M.
Takata, Sadaaki
Koide, Rie
Parrish, Nicholas F.
Ishigaki, Kazuyoshi
Terao, Chikashi
Ka, Mirei
Hikino, Keiko
Kamatani, Yoichiro
Hamada, Michiaki
Mizukoshi, Misaki
Gelinas, Asami F.
Murakawa, Yasuhiro
Saito, Yuka
Parrish, Erica H.
Ito, Kaoru
Koyama, Satoshi
Kamada, Anselmo J.
Endo, Mikiko
Nakamura, Yukio
Momozawa, Yukihide
Kojima, Shohei
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/37169872$$D View this record in MEDLINE/PubMed
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Yamanashi, Yuji
Koretsune, Yukihiro
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Snippet Mobile genetic elements (MEs) are heritable mutagens that recursively generate structural variants (SVs). ME variants (MEVs) are difficult to genotype and...
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SubjectTerms 45/43
631/208/200
631/208/205/2138
631/208/457
Agriculture
Animal Genetics and Genomics
Bias
Biomedical and Life Sciences
Biomedicine
Cancer Research
DNA methylation
Enhancers
Fasciitis
Gene expression
Gene Expression Regulation
Gene Function
Gene mapping
Gene regulation
Gene sequencing
Genetics
Genome-wide association studies
Genome-Wide Association Study
Genomes
Genotype & phenotype
Genotypes
Health risks
Human Genetics
Human populations
Humans
Insertion
Mutagens
Mutation
Phenotype
Polymorphism, Single Nucleotide
Populations
Post-transcription
Preferences
Quantitative Trait Loci
Risk
Statistical genetics
Whole genome sequencing
Title Mobile element variation contributes to population-specific genome diversification, gene regulation and disease risk
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