Susceptibility to tuberculosis is associated with variants in the ASAP1 gene encoding a regulator of dendritic cell migration
Sergey Nejentsev and colleagues identify intronic variants in ASAP1 that associate with susceptibility to tuberculosis. They show that ASAP1 is downregulated in dendritic cells infected with Mycobacterium tuberculosis , impairing their migration and matrix degradation abilities. Human genetic factor...
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| Published in | Nature genetics Vol. 47; no. 5; pp. 523 - 527 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.05.2015
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1061-4036 1546-1718 |
| DOI | 10.1038/ng.3248 |
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| Abstract | Sergey Nejentsev and colleagues identify intronic variants in
ASAP1
that associate with susceptibility to tuberculosis. They show that
ASAP1
is downregulated in dendritic cells infected with
Mycobacterium tuberculosis
, impairing their migration and matrix degradation abilities.
Human genetic factors predispose to tuberculosis (TB). We studied 7.6 million genetic variants in 5,530 people with pulmonary TB and in 5,607 healthy controls. In the combined analysis of these subjects and the follow-up cohort (15,087 TB patients and controls altogether), we found an association between TB and variants located in introns of the
ASAP1
gene on chromosome 8q24 (
P
= 2.6 × 10
−11
for rs4733781;
P
= 1.0 × 10
−10
for rs10956514). Dendritic cells (DCs) showed high
ASAP1
expression that was reduced after
Mycobacterium tuberculosis
infection, and rs10956514 was associated with the level of reduction of
ASAP1
expression. The ASAP1 protein is involved in actin and membrane remodeling and has been associated with podosomes. The ASAP1-depleted DCs showed impaired matrix degradation and migration. Therefore, genetically determined excessive reduction of
ASAP1
expression in
M. tuberculosis
–infected DCs may lead to their impaired migration, suggesting a potential mechanism of predisposition to TB. |
|---|---|
| AbstractList | Human genetic factors predispose to tuberculosis (TB). We studied 7.6 million genetic variants in 5,530 people with pulmonary TB and in 5,607 healthy controls. In the combined analysis of these subjects and the follow-up cohort (15,087 TB patients and controls altogether), we found an association between TB and variants located in introns of the ASAP1 gene on chromosome 8q24 (P = 2.6 × 10(-11) for rs4733781; P = 1.0 × 10(-10) for rs10956514). Dendritic cells (DCs) showed high ASAP1 expression that was reduced after Mycobacterium tuberculosis infection, and rs10956514 was associated with the level of reduction of ASAP1 expression. The ASAP1 protein is involved in actin and membrane remodeling and has been associated with podosomes. The ASAP1-depleted DCs showed impaired matrix degradation and migration. Therefore, genetically determined excessive reduction of ASAP1 expression in M. tuberculosis-infected DCs may lead to their impaired migration, suggesting a potential mechanism of predisposition to TB. Human genetic factors predispose to tuberculosis (TB). We studied 7.6 million genetic variants in 5,530 people with pulmonary TB and in 5,607 healthy controls. In the combined analysis of these subjects and the follow-up cohort (15,087 TB patients and controls altogether), we found an association between TB and variants located in introns of the ASAP1 gene on chromosome 8q24 (P = 2.6 × 10^sup -11^ for rs4733781; P = 1.0 × 10^sup -10^ for rs10956514). Dendritic cells (DCs) showed high ASAP1 expression that was reduced after Mycobacterium tuberculosis infection, and rs10956514 was associated with the level of reduction of ASAP1 expression. The ASAP1 protein is involved in actin and membrane remodeling and has been associated with podosomes. The ASAP1-depleted DCs showed impaired matrix degradation and migration. Therefore, genetically determined excessive reduction of ASAP1 expression in M. tuberculosis-infected DCs may lead to their impaired migration, suggesting a potential mechanism of predisposition to TB. Human genetic factors predispose to tuberculosis (TB). We studied 7.6 million genetic variants in 5,530 people with pulmonary TB and in 5,607 healthy controls. In the combined analysis of these subjects and the follow-up cohort (15,087 TB patients and controls altogether), we found an association between TB and variants located in introns of the ASAP1 gene on chromosome 8q24 (P = 2.6 x [10.sup.-11] for rs4733781; P = 1.0 x [10.sup.-10] for rs10956514). Dendritic cells (DCs) showed high ASAP1 expression that was reduced after Mycobacterium tuberculosis infection, and rs10956514 was associated with the level of reduction of ASAP1 expression. The ASAP1 protein is involved in actin and membrane remodeling and has been associated with podosomes. The ASAP1 -depleted DCs showed impaired matrix degradation and migration. Therefore, genetically determined excessive reduction of ASAP1 expression in M. tuberculosis-infected DCs may lead to their impaired migration, suggesting a potential mechanism of predisposition to TB. Sergey Nejentsev and colleagues identify intronic variants in ASAP1 that associate with susceptibility to tuberculosis. They show that ASAP1 is downregulated in dendritic cells infected with Mycobacterium tuberculosis , impairing their migration and matrix degradation abilities. Human genetic factors predispose to tuberculosis (TB). We studied 7.6 million genetic variants in 5,530 people with pulmonary TB and in 5,607 healthy controls. In the combined analysis of these subjects and the follow-up cohort (15,087 TB patients and controls altogether), we found an association between TB and variants located in introns of the ASAP1 gene on chromosome 8q24 ( P = 2.6 × 10 −11 for rs4733781; P = 1.0 × 10 −10 for rs10956514). Dendritic cells (DCs) showed high ASAP1 expression that was reduced after Mycobacterium tuberculosis infection, and rs10956514 was associated with the level of reduction of ASAP1 expression. The ASAP1 protein is involved in actin and membrane remodeling and has been associated with podosomes. The ASAP1-depleted DCs showed impaired matrix degradation and migration. Therefore, genetically determined excessive reduction of ASAP1 expression in M. tuberculosis –infected DCs may lead to their impaired migration, suggesting a potential mechanism of predisposition to TB. Human genetic factors predispose to tuberculosis (TB). We studied 7.6 million genetic variants in 5,530 pulmonary TB patients and 5,607 healthy controls. In the combined analysis of these subjects and the follow-up cohort (15,087 TB patients and controls altogether), we found association between TB and variants located in introns of the ASAP1 gene on chromosome 8q24 ( P = 2.6 × 10 −11 for rs4733781; P = 1.0 × 10 −10 for rs10956514). Dendritic cells (DCs) showed high level of ASAP1 expression, which was reduced after M. tuberculosis infection, and rs10956514 was associated with the level of reduction of ASAP1 expression. The ASAP1 protein is involved in actin and membrane remodeling and has been associated with podosomes. The ASAP1-depleted DCs showed impaired matrix degradation and migration. Therefore, genetically determined excessive reduction of ASAP1 expression in M. tuberculosis -infected DCs may lead to their impaired migration, suggesting a potential novel mechanism that predisposes to TB. |
| Audience | Academic |
| Author | Zenner, Helen L Ignatyeva, Olga Maes, Mailis Meyer, Christian G Nürnberg, Peter Thye, Thorsten Barrett, Jeffrey C Luo, Yang Nejentsev, Sergey Stebbings, Emma Plagnol, Vincent Kopanitsa, Liliya Alisaac, Ali Drobniewski, Francis Curtis, James Baessmann, Ingelore Wu, Changxin Lo, Kitty Balabanova, Yanina Cuchet-Lourenço, Delphine Liu, Jimmy Z Nikolayevskyy, Vladyslav Horstmann, Rolf D |
| AuthorAffiliation | 1 Department of Medicine, University of Cambridge, Cambridge, UK 2 Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK 5 Robert Koch Institute, Berlin, Germany 10 Department of Molecular Medicine, Bernhard Nocht Institute for Topical Medicine, Hamburg, Germany 12 Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germany 8 Queen Mary, University of London, London, UK 3 University College London Genetics Institute, University College London, London, UK 7 Imperial College London, London, UK 11 Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany 4 Samara Oblast Tuberculosis Dispensary, Samara, Russia 6 Public Health England National Mycobacterium Reference Laboratory, London, UK 9 Cologne Center for Genomics, University of Cologne, Cologne, Germany |
| AuthorAffiliation_xml | – name: 5 Robert Koch Institute, Berlin, Germany – name: 11 Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany – name: 6 Public Health England National Mycobacterium Reference Laboratory, London, UK – name: 1 Department of Medicine, University of Cambridge, Cambridge, UK – name: 9 Cologne Center for Genomics, University of Cologne, Cologne, Germany – name: 2 Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK – name: 8 Queen Mary, University of London, London, UK – name: 10 Department of Molecular Medicine, Bernhard Nocht Institute for Topical Medicine, Hamburg, Germany – name: 4 Samara Oblast Tuberculosis Dispensary, Samara, Russia – name: 7 Imperial College London, London, UK – name: 3 University College London Genetics Institute, University College London, London, UK – name: 12 Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germany |
| Author_xml | – sequence: 1 givenname: James surname: Curtis fullname: Curtis, James organization: Department of Medicine, University of Cambridge – sequence: 2 givenname: Yang surname: Luo fullname: Luo, Yang organization: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus – sequence: 3 givenname: Helen L surname: Zenner fullname: Zenner, Helen L organization: Department of Medicine, University of Cambridge – sequence: 4 givenname: Delphine surname: Cuchet-Lourenço fullname: Cuchet-Lourenço, Delphine organization: Department of Medicine, University of Cambridge – sequence: 5 givenname: Changxin surname: Wu fullname: Wu, Changxin organization: Department of Medicine, University of Cambridge – sequence: 6 givenname: Kitty surname: Lo fullname: Lo, Kitty organization: University College London Genetics Institute, University College London – sequence: 7 givenname: Mailis surname: Maes fullname: Maes, Mailis organization: Department of Medicine, University of Cambridge – sequence: 8 givenname: Ali surname: Alisaac fullname: Alisaac, Ali organization: Department of Medicine, University of Cambridge – sequence: 9 givenname: Emma surname: Stebbings fullname: Stebbings, Emma organization: Department of Medicine, University of Cambridge – sequence: 10 givenname: Jimmy Z surname: Liu fullname: Liu, Jimmy Z organization: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus – sequence: 11 givenname: Liliya surname: Kopanitsa fullname: Kopanitsa, Liliya organization: Department of Medicine, University of Cambridge – sequence: 12 givenname: Olga surname: Ignatyeva fullname: Ignatyeva, Olga organization: Samara Oblast Tuberculosis Dispensary – sequence: 13 givenname: Yanina surname: Balabanova fullname: Balabanova, Yanina organization: Robert Koch Institute, Imperial College London, Queen Mary University of London – sequence: 14 givenname: Vladyslav orcidid: 0000-0002-9502-0332 surname: Nikolayevskyy fullname: Nikolayevskyy, Vladyslav organization: Imperial College London, Queen Mary University of London, Public Health England National Mycobacterium Reference Laboratory – sequence: 15 givenname: Ingelore surname: Baessmann fullname: Baessmann, Ingelore organization: Cologne Center for Genomics, University of Cologne – sequence: 16 givenname: Thorsten surname: Thye fullname: Thye, Thorsten organization: Department of Molecular Medicine, Bernhard Nocht Institute for Topical Medicine – sequence: 17 givenname: Christian G surname: Meyer fullname: Meyer, Christian G organization: Department of Molecular Medicine, Bernhard Nocht Institute for Topical Medicine – sequence: 18 givenname: Peter surname: Nürnberg fullname: Nürnberg, Peter organization: Cologne Center for Genomics, University of Cologne, Center for Molecular Medicine Cologne, University of Cologne, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne – sequence: 19 givenname: Rolf D surname: Horstmann fullname: Horstmann, Rolf D organization: Department of Molecular Medicine, Bernhard Nocht Institute for Topical Medicine – sequence: 20 givenname: Francis surname: Drobniewski fullname: Drobniewski, Francis organization: Imperial College London, Queen Mary University of London, Public Health England National Mycobacterium Reference Laboratory – sequence: 21 givenname: Vincent orcidid: 0000-0002-5597-9215 surname: Plagnol fullname: Plagnol, Vincent organization: University College London Genetics Institute, University College London – sequence: 22 givenname: Jeffrey C orcidid: 0000-0002-1152-370X surname: Barrett fullname: Barrett, Jeffrey C organization: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus – sequence: 23 givenname: Sergey surname: Nejentsev fullname: Nejentsev, Sergey email: sn262@cam.ac.uk organization: Department of Medicine, University of Cambridge |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25774636$$D View this record in MEDLINE/PubMed |
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| Copyright | Springer Nature America, Inc. 2015 COPYRIGHT 2015 Nature Publishing Group Copyright Nature Publishing Group May 2015 |
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| Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 Author contribution SN conceived and supervised the study, participated in sample collection and data analysis and wrote the first draft of the manuscript. JC prepared DNA samples and participated in their genotyping and analysis. YL performed statistical analysis of the GWAS data. JZL participated in the GWAS data analysis. HLZ and DCL studied dendritic cells and performed matrix degradation and cell migration experiments. CW studied ASAP1 mRNA expression in leukocytes. KL performed eQTL analysis in dendritic cells. MM and AA prepared cells for functional experiments. OI, YB, VN, RDH and FD participated in study design, protocol development and sample collection. ES and LK participated in DNA sample extraction. IB and PN participated in genotyping. TT and CGM participated in genotyping and analysis of the Ghanaian data. VP and JCB participated in and supervised statistical analyses. All authors contributed to the writing of the manuscript. |
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| Snippet | Sergey Nejentsev and colleagues identify intronic variants in
ASAP1
that associate with susceptibility to tuberculosis. They show that
ASAP1
is downregulated... Human genetic factors predispose to tuberculosis (TB). We studied 7.6 million genetic variants in 5,530 people with pulmonary TB and in 5,607 healthy controls.... Human genetic factors predispose to tuberculosis (TB). We studied 7.6 million genetic variants in 5,530 pulmonary TB patients and 5,607 healthy controls. In... |
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| SubjectTerms | 14/1 14/34 14/63 45/43 631/208/205 692/699/255/1856 Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Adult Agriculture Animal Genetics and Genomics Biomedical research Biomedicine Cancer Research Case-Control Studies Cell Movement Cells, Cultured Data analysis Datasets Dendritic Cells - physiology Deoxyribonucleic acid Disease Disease susceptibility DNA Female Gene Expression Gene Function Genetic aspects Genetic factors Genetic Predisposition to Disease Genetic testing Genetic variance Genetic variation Genome-Wide Association Study Genomes Health aspects Human Genetics Humans Identification and classification Infections Inflammatory bowel disease Introns letter Logistics Male Middle Aged Polymorphism, Single Nucleotide Protein Transport Proteins Risk factors Studies Tuberculosis Tuberculosis, Pulmonary - genetics |
| Title | Susceptibility to tuberculosis is associated with variants in the ASAP1 gene encoding a regulator of dendritic cell migration |
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