Natural Mutagenesis of Human Genomes by Endogenous Retrotransposons
Two abundant classes of mobile elements, namely Alu and L1 elements, continue to generate new retrotransposon insertions in human genomes. Estimates suggest that these elements have generated millions of new germline insertions in individual human genomes worldwide. Unfortunately, current technologi...
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| Published in | Cell Vol. 141; no. 7; pp. 1253 - 1261 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
25.06.2010
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0092-8674 1097-4172 1097-4172 |
| DOI | 10.1016/j.cell.2010.05.020 |
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| Abstract | Two abundant classes of mobile elements, namely Alu and L1 elements, continue to generate new retrotransposon insertions in human genomes. Estimates suggest that these elements have generated millions of new germline insertions in individual human genomes worldwide. Unfortunately, current technologies are not capable of detecting most of these young insertions, and the true extent of germline mutagenesis by endogenous human retrotransposons has been difficult to examine. Here, we describe technologies for detecting these young retrotransposon insertions and demonstrate that such insertions indeed are abundant in human populations. We also found that new somatic L1 insertions occur at high frequencies in human lung cancer genomes. Genome-wide analysis suggests that altered DNA methylation may be responsible for the high levels of L1 mobilization observed in these tumors. Our data indicate that transposon-mediated mutagenesis is extensive in human genomes and is likely to have a major impact on human biology and diseases.
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► “Transposon-seq” methods were developed to find mobile element insertions in humans ► New germline retrotransposon insertions were identified in personal human genomes ► Tumor-specific somatic L1 insertions were uncovered in human lung cancer genomes ► Transposon mutagenesis is likely to have a major impact on human traits and diseases |
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| AbstractList | Two abundant classes of mobile elements, namely Alu and L1 elements, continue to generate new retrotransposon insertions in human genomes. Estimates suggest that these elements have generated millions of new germline insertions in individual human genomes worldwide. Unfortunately, current technologies are not capable of detecting most of these young insertions, and the true extent of germline mutagenesis by endogenous human retrotransposons has been difficult to examine. Here, we describe technologies for detecting these young retrotransposon insertions and demonstrate that such insertions indeed are abundant in human populations. We also found that new somatic L1 insertions occur at high frequencies in human lung cancer genomes. Genome-wide analysis suggests that altered DNA methylation may be responsible for the high levels of L1 mobilization observed in these tumors. Our data indicate that transposon-mediated mutagenesis is extensive in human genomes and is likely to have a major impact on human biology and diseases.Two abundant classes of mobile elements, namely Alu and L1 elements, continue to generate new retrotransposon insertions in human genomes. Estimates suggest that these elements have generated millions of new germline insertions in individual human genomes worldwide. Unfortunately, current technologies are not capable of detecting most of these young insertions, and the true extent of germline mutagenesis by endogenous human retrotransposons has been difficult to examine. Here, we describe technologies for detecting these young retrotransposon insertions and demonstrate that such insertions indeed are abundant in human populations. We also found that new somatic L1 insertions occur at high frequencies in human lung cancer genomes. Genome-wide analysis suggests that altered DNA methylation may be responsible for the high levels of L1 mobilization observed in these tumors. Our data indicate that transposon-mediated mutagenesis is extensive in human genomes and is likely to have a major impact on human biology and diseases. Two abundant classes of mobile elements, namely Alu and L1 elements, continue to generate new retrotransposon insertions in human genomes. Estimates suggest that these elements have generated millions of new germline insertions in individual human genomes worldwide. Unfortunately, current technologies are not capable of detecting most of these young insertions, and the true extent of germline mutagenesis by endogenous human retrotransposons has been difficult to examine. Here, we describe technologies for detecting these young retrotransposon insertions and demonstrate that such insertions indeed are abundant in human populations. We also found that new somatic L1 insertions occur at high frequencies in human lung cancer genomes. Genome-wide analysis suggests that altered DNA methylation may be responsible for the high levels of L1 mobilization observed in these tumors. Our data indicate that transposon-mediated mutagenesis is extensive in human genomes and is likely to have a major impact on human biology and diseases. Two abundant classes of mobile elements, namely Alu and L1 elements, continue to generate new retrotransposon insertions in human genomes. Estimates suggest that these elements have generated millions of new germline insertions in individual human genomes worldwide. Unfortunately, current technologies are not capable of detecting most of these young insertions, and the true extent of germline mutagenesis by endogenous human retrotransposons has been difficult to examine. Here, we describe technologies for detecting these young retrotransposon insertions and demonstrate that such insertions indeed are abundant in human populations. We also found that new somatic L1 insertions occur at high frequencies in human lung cancer genomes. Genome-wide analysis suggests that altered DNA methylation may be responsible for the high levels of L1 mobilization observed in these tumors. Our data indicate that transposon-mediated mutagenesis is extensive in human genomes and is likely to have a major impact on human biology and diseases. [Display omitted] ► “Transposon-seq” methods were developed to find mobile element insertions in humans ► New germline retrotransposon insertions were identified in personal human genomes ► Tumor-specific somatic L1 insertions were uncovered in human lung cancer genomes ► Transposon mutagenesis is likely to have a major impact on human traits and diseases Two abundant classes of mobile elements, namely Alu and L1 elements, continue to generate new retrotransposon insertions in human genomes. Estimates suggest that these elements have generated millions of new germline insertions in individual human genomes worldwide. Unfortunately, current technologies are not capable of detecting most of these young insertions, and the true extent of germline mutagenesis by endogenous human retrotransposons has been difficult to examine. Here, we describe new technologies for detecting these young retrotransposon insertions and demonstrate that such insertions indeed are abundant in human populations. We also found that new somatic L1 insertions occur at high frequencies in human lung cancer genomes. Genome-wide analysis suggests that altered DNA methylation may be responsible for the high levels of L1 mobilization observed in these tumors. Our data indicate that transposon-mediated mutagenesis is extensive in human genomes, and is likely to have a major impact on human biology and diseases. |
| Author | Pittard, W. Stephen Mills, Ryan E. Iskow, Rebecca C. Torene, Spencer Neuwald, Andrew F. Devine, Scott E. McCabe, Michael T. Van Meir, Erwin G. Vertino, Paula M. |
| AuthorAffiliation | 9 Bimcore, Emory University, Atlanta, GA 30322 10 Institute for Genome SciencesBiology, University of Maryland School of Medicine, Baltimore, MD 20201 12 Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 20201 7 Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA 30322 2 Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322 8 Winship Cancer Institute, Emory University, Atlanta, GA 30322 4 Department of Radiation Oncology, Emory University School of Medicine, Atlanta, GA 30322 11 Department of Biochemistry and Molecular, University of Maryland School of Medicine, Baltimore, MD 20201 1 Genetics and Molecular Biology Graduate Program, Emory University, Atlanta, GA 30322 6 Department of Neurosurgery, Emory University School of Medicine, Atlanta, GA 30322 13 Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 20201 |
| AuthorAffiliation_xml | – name: 6 Department of Neurosurgery, Emory University School of Medicine, Atlanta, GA 30322 – name: 1 Genetics and Molecular Biology Graduate Program, Emory University, Atlanta, GA 30322 – name: 2 Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322 – name: 4 Department of Radiation Oncology, Emory University School of Medicine, Atlanta, GA 30322 – name: 9 Bimcore, Emory University, Atlanta, GA 30322 – name: 11 Department of Biochemistry and Molecular, University of Maryland School of Medicine, Baltimore, MD 20201 – name: 13 Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 20201 – name: 10 Institute for Genome SciencesBiology, University of Maryland School of Medicine, Baltimore, MD 20201 – name: 12 Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 20201 – name: 7 Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA 30322 – name: 8 Winship Cancer Institute, Emory University, Atlanta, GA 30322 |
| Author_xml | – sequence: 1 givenname: Rebecca C. surname: Iskow fullname: Iskow, Rebecca C. organization: Genetics and Molecular Biology Graduate Program, Emory University, Atlanta, GA 30322, USA – sequence: 2 givenname: Michael T. surname: McCabe fullname: McCabe, Michael T. organization: Department of Radiation Oncology, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 3 givenname: Ryan E. surname: Mills fullname: Mills, Ryan E. organization: Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 4 givenname: Spencer surname: Torene fullname: Torene, Spencer organization: Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 5 givenname: W. Stephen surname: Pittard fullname: Pittard, W. Stephen organization: Bimcore, Emory University, Atlanta, GA 30322, USA – sequence: 6 givenname: Andrew F. surname: Neuwald fullname: Neuwald, Andrew F. organization: Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 20201, USA – sequence: 7 givenname: Erwin G. surname: Van Meir fullname: Van Meir, Erwin G. organization: Department of Neurosurgery, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 8 givenname: Paula M. surname: Vertino fullname: Vertino, Paula M. organization: Genetics and Molecular Biology Graduate Program, Emory University, Atlanta, GA 30322, USA – sequence: 9 givenname: Scott E. surname: Devine fullname: Devine, Scott E. email: sdevine@som.umaryland.edu organization: Genetics and Molecular Biology Graduate Program, Emory University, Atlanta, GA 30322, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20603005$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Alu Elements Brain Neoplasms - genetics DNA EVO_ECOL Genome, Human Humans HUMDISEASE Long Interspersed Nucleotide Elements Lung Neoplasms - genetics Methylation Mutagenesis Sequence Analysis, DNA - methods |
| Title | Natural Mutagenesis of Human Genomes by Endogenous Retrotransposons |
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