A single genetic locus controls both expression of DPEP1/CHMP1A and kidney disease development via ferroptosis

Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify two kidney disease genes Dipeptidase 1 ( DPEP1 ) and Charged Multivesicular Body Protein 1 A ( CHMP1A ) via the triangulation of kidney functi...

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Published inNature communications Vol. 12; no. 1; pp. 5078 - 17
Main Authors Guan, Yuting, Liang, Xiujie, Ma, Ziyuan, Hu, Hailong, Liu, Hongbo, Miao, Zhen, Linkermann, Andreas, Hellwege, Jacklyn N., Voight, Benjamin F., Susztak, Katalin
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 23.08.2021
Nature Publishing Group
Nature Portfolio
Subjects
38/1
38/88
38/91
631/208
631/208/191
64/60
692/4022/1585
82/29
82/51
96/106
96/109
Animal models
Animals
Blood Urea Nitrogen
Chromatin
Chromatin - metabolism
Cisplatin
CRISPR
Dipeptidase
Dipeptidases - deficiency
Dipeptidases - genetics
Dipeptidases - metabolism
DNA methylation
DNA Methylation - genetics
Editing
Ferroptosis
Ferroptosis - genetics
Folic Acid
Gene Editing
Gene expression
Gene Expression Regulation
Gene mapping
Genes
Genetic Loci
Genetic Predisposition to Disease
Genome editing
Genome-wide association studies
Genome-Wide Association Study
Genomes
Genomics
Haploinsufficiency - genetics
Humanities and Social Sciences
Humans
Iron - metabolism
Kidney - pathology
Kidney diseases
Kidney Diseases - chemically induced
Kidney Diseases - genetics
Kidneys
Mice
multidisciplinary
Necroptosis - genetics
Organ Specificity
Physical Chromosome Mapping
Pyroptosis - genetics
Quantitative Trait Loci
RNA, Messenger - genetics
RNA, Messenger - metabolism
Science
Science (multidisciplinary)
Triangulation
Vesicular Transport Proteins - deficiency
Vesicular Transport Proteins - genetics
Vesicular Transport Proteins - metabolism
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/s41467-021-25377-x

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Abstract Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify two kidney disease genes Dipeptidase 1 ( DPEP1 ) and Charged Multivesicular Body Protein 1 A ( CHMP1A ) via the triangulation of kidney function GWAS, human kidney expression, and methylation quantitative trait loci. Using single-cell chromatin accessibility and genome editing, we fine map the region that controls the expression of both genes. Mouse genetic models demonstrate the causal roles of both genes in kidney disease. Cellular studies indicate that both Dpep1 and Chmp1a are important regulators of a single pathway, ferroptosis and lead to kidney disease development via altering cellular iron trafficking. Identifying causal variants and genes is an essential step in interpreting GWAS loci. Here, the authors investigate a kidney disease GWAS locus with functional genomics data, CRISPR editing and mouse experiments to identify DPEP1 and CHMP1A as putative kidney disease genes via ferroptosis.
AbstractList Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify two kidney disease genes Dipeptidase 1 ( DPEP1 ) and Charged Multivesicular Body Protein 1 A ( CHMP1A ) via the triangulation of kidney function GWAS, human kidney expression, and methylation quantitative trait loci. Using single-cell chromatin accessibility and genome editing, we fine map the region that controls the expression of both genes. Mouse genetic models demonstrate the causal roles of both genes in kidney disease. Cellular studies indicate that both Dpep1 and Chmp1a are important regulators of a single pathway, ferroptosis and lead to kidney disease development via altering cellular iron trafficking. Identifying causal variants and genes is an essential step in interpreting GWAS loci. Here, the authors investigate a kidney disease GWAS locus with functional genomics data, CRISPR editing and mouse experiments to identify DPEP1 and CHMP1A as putative kidney disease genes via ferroptosis.
Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify two kidney disease genes Dipeptidase 1 (DPEP1) and Charged Multivesicular Body Protein 1 A (CHMP1A) via the triangulation of kidney function GWAS, human kidney expression, and methylation quantitative trait loci. Using single-cell chromatin accessibility and genome editing, we fine map the region that controls the expression of both genes. Mouse genetic models demonstrate the causal roles of both genes in kidney disease. Cellular studies indicate that both Dpep1 and Chmp1a are important regulators of a single pathway, ferroptosis and lead to kidney disease development via altering cellular iron trafficking.Identifying causal variants and genes is an essential step in interpreting GWAS loci. Here, the authors investigate a kidney disease GWAS locus with functional genomics data, CRISPR editing and mouse experiments to identify DPEP1 and CHMP1A as putative kidney disease genes via ferroptosis.
Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify two kidney disease genes Dipeptidase 1 (DPEP1) and Charged Multivesicular Body Protein 1 A (CHMP1A) via the triangulation of kidney function GWAS, human kidney expression, and methylation quantitative trait loci. Using single-cell chromatin accessibility and genome editing, we fine map the region that controls the expression of both genes. Mouse genetic models demonstrate the causal roles of both genes in kidney disease. Cellular studies indicate that both Dpep1 and Chmp1a are important regulators of a single pathway, ferroptosis and lead to kidney disease development via altering cellular iron trafficking.
Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify two kidney disease genes Dipeptidase 1 (DPEP1) and Charged Multivesicular Body Protein 1 A (CHMP1A) via the triangulation of kidney function GWAS, human kidney expression, and methylation quantitative trait loci. Using single-cell chromatin accessibility and genome editing, we fine map the region that controls the expression of both genes. Mouse genetic models demonstrate the causal roles of both genes in kidney disease. Cellular studies indicate that both Dpep1 and Chmp1a are important regulators of a single pathway, ferroptosis and lead to kidney disease development via altering cellular iron trafficking.Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify two kidney disease genes Dipeptidase 1 (DPEP1) and Charged Multivesicular Body Protein 1 A (CHMP1A) via the triangulation of kidney function GWAS, human kidney expression, and methylation quantitative trait loci. Using single-cell chromatin accessibility and genome editing, we fine map the region that controls the expression of both genes. Mouse genetic models demonstrate the causal roles of both genes in kidney disease. Cellular studies indicate that both Dpep1 and Chmp1a are important regulators of a single pathway, ferroptosis and lead to kidney disease development via altering cellular iron trafficking.
Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify two kidney disease genes Dipeptidase 1 ( DPEP1 ) and Charged Multivesicular Body Protein 1 A ( CHMP1A ) via the triangulation of kidney function GWAS, human kidney expression, and methylation quantitative trait loci. Using single-cell chromatin accessibility and genome editing, we fine map the region that controls the expression of both genes. Mouse genetic models demonstrate the causal roles of both genes in kidney disease. Cellular studies indicate that both Dpep1 and Chmp1a are important regulators of a single pathway, ferroptosis and lead to kidney disease development via altering cellular iron trafficking.
Identifying causal variants and genes is an essential step in interpreting GWAS loci. Here, the authors investigate a kidney disease GWAS locus with functional genomics data, CRISPR editing and mouse experiments to identify DPEP1 and CHMP1A as putative kidney disease genes via ferroptosis.
ArticleNumber 5078
Author Voight, Benjamin F.
Ma, Ziyuan
Miao, Zhen
Susztak, Katalin
Liang, Xiujie
Hu, Hailong
Linkermann, Andreas
Hellwege, Jacklyn N.
Liu, Hongbo
Guan, Yuting
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34426578$$D View this record in MEDLINE/PubMed
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Snippet Genome-wide association studies (GWAS) have identified loci for kidney disease, but the causal variants, genes, and pathways remain unknown. Here we identify...
Identifying causal variants and genes is an essential step in interpreting GWAS loci. Here, the authors investigate a kidney disease GWAS locus with functional...
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SubjectTerms 38/1
38/88
38/91
631/208
631/208/191
64/60
692/4022/1585
82/29
82/51
96/106
96/109
Animal models
Animals
Blood Urea Nitrogen
Chromatin
Chromatin - metabolism
Cisplatin
CRISPR
Dipeptidase
Dipeptidases - deficiency
Dipeptidases - genetics
Dipeptidases - metabolism
DNA methylation
DNA Methylation - genetics
Editing
Ferroptosis
Ferroptosis - genetics
Folic Acid
Gene Editing
Gene expression
Gene Expression Regulation
Gene mapping
Genes
Genetic Loci
Genetic Predisposition to Disease
Genome editing
Genome-wide association studies
Genome-Wide Association Study
Genomes
Genomics
Haploinsufficiency - genetics
Humanities and Social Sciences
Humans
Iron - metabolism
Kidney - pathology
Kidney diseases
Kidney Diseases - chemically induced
Kidney Diseases - genetics
Kidneys
Mice
multidisciplinary
Necroptosis - genetics
Organ Specificity
Physical Chromosome Mapping
Pyroptosis - genetics
Quantitative Trait Loci
RNA, Messenger - genetics
RNA, Messenger - metabolism
Science
Science (multidisciplinary)
Triangulation
Vesicular Transport Proteins - deficiency
Vesicular Transport Proteins - genetics
Vesicular Transport Proteins - metabolism
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Title A single genetic locus controls both expression of DPEP1/CHMP1A and kidney disease development via ferroptosis
URI https://link.springer.com/article/10.1038/s41467-021-25377-x
https://www.ncbi.nlm.nih.gov/pubmed/34426578
https://www.proquest.com/docview/2576118207
https://www.proquest.com/docview/2564135810
https://pubmed.ncbi.nlm.nih.gov/PMC8382756
https://doaj.org/article/94c00b491872474289c332bf354c853a
Volume 12
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