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1.
Nat Genet ; 52(3): 306-319, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-32024998

RESUMO

About half of all cancers have somatic integrations of retrotransposons. Here, to characterize their role in oncogenesis, we analyzed the patterns and mechanisms of somatic retrotransposition in 2,954 cancer genomes from 38 histological cancer subtypes within the framework of the Pan-Cancer Analysis of Whole Genomes (PCAWG) project. We identified 19,166 somatically acquired retrotransposition events, which affected 35% of samples and spanned a range of event types. Long interspersed nuclear element (LINE-1; L1 hereafter) insertions emerged as the first most frequent type of somatic structural variation in esophageal adenocarcinoma, and the second most frequent in head-and-neck and colorectal cancers. Aberrant L1 integrations can delete megabase-scale regions of a chromosome, which sometimes leads to the removal of tumor-suppressor genes, and can induce complex translocations and large-scale duplications. Somatic retrotranspositions can also initiate breakage-fusion-bridge cycles, leading to high-level amplification of oncogenes. These observations illuminate a relevant role of L1 retrotransposition in remodeling the cancer genome, with potential implications for the development of human tumors.

2.
Philos Trans R Soc Lond B Biol Sci ; 375(1795): 20190332, 2020 Mar 30.
Artigo em Inglês | MEDLINE | ID: mdl-32075553

RESUMO

Transposable elements (TEs) are increasingly recognized as important contributors to mammalian regulatory systems. For instance, they have been shown to play a role in the human interferon response, but their involvement in other mechanisms of immune cell activation remains poorly understood. Here, we investigated the profile of accessible chromatin enhanced in stimulated human macrophages using ATAC-seq to assess the role of different TE subfamilies in regulating gene expression following an immune response. We found that both previously identified and new repeats belonging to the MER44, THE1, Tigger3 and MLT1 families provide 14 subfamilies that are enriched in differentially accessible chromatin and found near differentially expressed genes. These TEs also harbour binding motifs for several candidate transcription factors, including important immune regulators AP-1 and NF-κB, present in 96% of accessible MER44B and 83% of THE1C instances, respectively. To more directly assess their regulatory potential, we evaluated the presence of these TEs in regions putatively affecting gene expression, as defined by quantitative trait locus (QTL) analysis, and found that repeats are also contributing to accessible elements near QTLs. Together, these results suggest that a number of TE families have contributed to the regulation of gene expression in the context of the immune response to infection in humans. This article is part of a discussion meeting issue 'Crossroads between transposons and gene regulation'.

3.
Pac Symp Biocomput ; 25: 367-378, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31797611

RESUMO

Joint peak detection is a central problem when comparing samples in epigenomic data analysis, but current algorithms for this task are unsupervised and limited to at most 2 sample types. We propose PeakSegPipeline, a new genome-wide multi-sample peak calling pipeline for epigenomic data sets. It performs peak detection using a constrained maximum likelihood segmentation model with essentially only one free parameter that needs to be tuned: the number of peaks. To select the number of peaks, we propose to learn a penalty function based on user-provided labels that indicate genomic regions with or without peaks in specific samples. In comparisons with state-of-the-art peak detection algorithms, PeakSegPipeline achieves similar or better accuracy, and a more interpretable model with overlapping peaks that occur in exactly the same positions across all samples. Our novel approach is able to learn that predicted peak sizes vary by experiment type.

5.
Nat Genet ; 51(12): 1702-1713, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31768071

RESUMO

Childhood brain tumors have suspected prenatal origins. To identify vulnerable developmental states, we generated a single-cell transcriptome atlas of >65,000 cells from embryonal pons and forebrain, two major tumor locations. We derived signatures for 191 distinct cell populations and defined the regional cellular diversity and differentiation dynamics. Projection of bulk tumor transcriptomes onto this dataset shows that WNT medulloblastomas match the rhombic lip-derived mossy fiber neuronal lineage and embryonal tumors with multilayered rosettes fully recapitulate a neuronal lineage, while group 2a/b atypical teratoid/rhabdoid tumors may originate outside the neuroectoderm. Importantly, single-cell tumor profiles reveal highly defined cell hierarchies that mirror transcriptional programs of the corresponding normal lineages. Our findings identify impaired differentiation of specific neural progenitors as a common mechanism underlying these pediatric cancers and provide a rational framework for future modeling and therapeutic interventions.


Assuntos
Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patologia , Encéfalo/embriologia , Regulação da Expressão Gênica no Desenvolvimento , Animais , Encéfalo/patologia , Linhagem Celular Tumoral , Humanos , Lactente , Meduloblastoma/genética , Meduloblastoma/patologia , Camundongos , Neoplasias Embrionárias de Células Germinativas/genética , Neoplasias Embrionárias de Células Germinativas/patologia , Fibras Nervosas/patologia , Fibras Nervosas/fisiologia , Prosencéfalo/citologia , Prosencéfalo/embriologia , Tumor Rabdoide/genética , Tumor Rabdoide/patologia , Análise de Célula Única
6.
Genes Immun ; 2019 Oct 08.
Artigo em Inglês | MEDLINE | ID: mdl-31591503

RESUMO

The transcription factor STAT5 is critical for peripheral NK-cell survival, proliferation, and cytotoxic function. STAT5 refers to two highly related proteins, STAT5A and STAT5B. In this study, we verified the importance of STAT5A isoform for NK cells. We characterized an incidental chemically induced W484G mutation in the Stat5a gene and found that this mutation was associated with a reduction of STAT5A protein expression. Closer examination of NK-cell subsets from Stat5a mutant mice showed marked reductions in NK-cell number and maturation. IL-15 treatment of Stat5a mutant NK cells exhibited defective induction of both STAT5 and mTOR signaling pathways and reduced expression of granzyme B and IFN-γ. Finally, we observed that Stat5a mutant mice revealed more tumor growth upon injection of RMA-S tumor cell line. Overall, our results demonstrate that the W484G mutation in the linker domain of STAT5A is sufficient to compromise STAT5A function in NK-cell homeostasis, responsiveness, and tumoricidal function.

7.
Nat Commun ; 10(1): 4856, 2019 10 24.
Artigo em Inglês | MEDLINE | ID: mdl-31649251

RESUMO

The functional effect of a gene edit by designer nucleases depends on the DNA repair outcome at the targeted locus. While non-homologous end joining (NHEJ) repair results in various mutations, microhomology-mediated end joining (MMEJ) creates precise deletions based on the alignment of flanking microhomologies (µHs). Recently, the sequence context surrounding nuclease-induced double strand breaks (DSBs) has been shown to predict repair outcomes, for which µH plays an important role. Here, we survey naturally occurring human deletion variants and identify that 11 million or 57% are flanked by µHs, covering 88% of protein-coding genes. These biologically relevant mutations are candidates for precise creation in a template-free manner by MMEJ repair. Using CRISPR-Cas9 in human induced pluripotent stem cells (hiPSCs), we efficiently create pathogenic deletion mutations for demonstrable disease models with both gain- and loss-of-function phenotypes. We anticipate this dataset and gene editing strategy to enable functional genetic studies and drug screening.


Assuntos
Reparo do DNA por Junção de Extremidades/genética , Edição de Genes/métodos , Células-Tronco Pluripotentes Induzidas/metabolismo , Deleção de Sequência/genética , Sequência de Bases , Sistemas CRISPR-Cas , Mutação com Ganho de Função , Humanos , Mutação com Perda de Função
8.
Environ Health Perspect ; 127(8): 87002, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31393794

RESUMO

BACKGROUND: The sperm DNA methylation landscape is unique and critical for offspring health. If gamete-derived DNA methylation escapes reprograming in early embryos, epigenetic defects in sperm may be transmitted to the next generation. Current techniques to assess sperm DNA methylation show bias toward CpG-dense regions and do not target areas of dynamic methylation, those predicted to be environmentally sensitive and tunable regulatory elements. OBJECTIVES: Our goal was to assess variation in human sperm DNA methylation and design a targeted capture panel to interrogate the human sperm methylome. METHODS: To characterize variation in sperm DNA methylation, we performed whole genome bisulfite sequencing (WGBS) on an equimolar pool of sperm DNA from a wide cross section of 30 men varying in age, fertility status, methylenetetrahydrofolate reductase (MTHFR) genotype, and exposures. With our targeted capture panel, in individual samples, we examined the effect of MTHFR genotype ([Formula: see text] 677CC, [Formula: see text] 677TT), as well as high-dose folic acid supplementation ([Formula: see text], per genotype, before and after supplementation). RESULTS: Through WGBS we discovered nearly 1 million CpGs possessing intermediate methylation levels (20-80%), termed dynamic sperm CpGs. These dynamic CpGs, along with 2 million commonly assessed CpGs, were used to customize a capture panel for targeted interrogation of the human sperm methylome and test its ability to detect effects of altered folate metabolism. As compared with MTHFR 677CC men, those with the 677TT genotype (50% decreased MTHFR activity) had both hyper- and hypomethylation in their sperm. High-dose folic acid supplement treatment exacerbated hypomethylation in MTHFR 677TT men compared with 677CC. In both cases, [Formula: see text] of altered methylation was found in dynamic sperm CpGs, uniquely measured by our assay. DISCUSSION: Our sperm panel allowed the discovery of differential methylation following conditions affecting folate metabolism in novel dynamic sperm CpGs. Improved ability to examine variation in sperm DNA methylation can facilitate comprehensive studies of environment-epigenome interactions. https://doi.org/10.1289/EHP4812.

9.
Gigascience ; 8(6)2019 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-31185495

RESUMO

BACKGROUND: With the decreasing cost of sequencing and the rapid developments in genomics technologies and protocols, the need for validated bioinformatics software that enables efficient large-scale data processing is growing. FINDINGS: Here we present GenPipes, a flexible Python-based framework that facilitates the development and deployment of multi-step workflows optimized for high-performance computing clusters and the cloud. GenPipes already implements 12 validated and scalable pipelines for various genomics applications, including RNA sequencing, chromatin immunoprecipitation sequencing, DNA sequencing, methylation sequencing, Hi-C, capture Hi-C, metagenomics, and Pacific Biosciences long-read assembly. The software is available under a GPLv3 open source license and is continuously updated to follow recent advances in genomics and bioinformatics. The framework has already been configured on several servers, and a Docker image is also available to facilitate additional installations. CONCLUSIONS: GenPipes offers genomics researchers a simple method to analyze different types of data, customizable to their needs and resources, as well as the flexibility to create their own workflows.


Assuntos
Genômica/métodos , Software , Metilação de DNA , Epigenômica/métodos , Humanos , Metagenômica/métodos , Análise de Sequência de DNA/métodos , Análise de Sequência de RNA/métodos
10.
Bioinformatics ; 35(22): 4767-4769, 2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31161210

RESUMO

SUMMARY: The Illumina Infinium EPIC BeadChip is a new high-throughput array for DNA methylation analysis, extending the earlier 450k array by over 400 000 new sites. Previously, a method named eFORGE was developed to provide insights into cell type-specific and cell-composition effects for 450k data. Here, we present a significantly updated and improved version of eFORGE that can analyze both EPIC and 450k array data. New features include analysis of chromatin states, transcription factor motifs and DNase I footprints, providing tools for epigenome-wide association study interpretation and epigenome editing. AVAILABILITY AND IMPLEMENTATION: eFORGE v2.0 is implemented as a web tool available from https://eforge.altiusinstitute.org and https://eforge-tf.altiusinstitute.org/. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

12.
Bioinformatics ; 35(4): 674-676, 2019 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-30052804

RESUMO

SUMMARY: In recent years, major initiatives such as the International Human Epigenome Consortium have generated thousands of high-quality genome-wide datasets for a large variety of assays and cell types. This data can be used as a reference to assess whether the signal from a user-provided dataset corresponds to its expected experiment, as well as to help reveal unexpected biological associations. We have developed the epiGenomic Efficient Correlator (epiGeEC) tool to enable genome-wide comparisons of very large numbers of datasets. A public Galaxy implementation of epiGeEC allows comparison of user datasets with thousands of public datasets in a few minutes. AVAILABILITY AND IMPLEMENTATION: The source code is available at https://bitbucket.org/labjacquespe/epigeec and the Galaxy implementation at http://epigeec.genap.ca. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.


Assuntos
Epigenômica , Software , Animais , Biologia Computacional , Conjuntos de Dados como Assunto , Genoma , Humanos , Camundongos
13.
Biometrics ; 75(1): 210-221, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30168593

RESUMO

DNA methylation studies have enabled researchers to understand methylation patterns and their regulatory roles in biological processes and disease. However, only a limited number of statistical approaches have been developed to provide formal quantitative analysis. Specifically, a few available methods do identify differentially methylated CpG (DMC) sites or regions (DMR), but they suffer from limitations that arise mostly due to challenges inherent in bisulfite sequencing data. These challenges include: (1) that read-depths vary considerably among genomic positions and are often low; (2) both methylation and autocorrelation patterns change as regions change; and (3) CpG sites are distributed unevenly. Furthermore, there are several methodological limitations: almost none of these tools is capable of comparing multiple groups and/or working with missing values, and only a few allow continuous or multiple covariates. The last of these is of great interest among researchers, as the goal is often to find which regions of the genome are associated with several exposures and traits. To tackle these issues, we have developed an efficient DMC identification method based on Hidden Markov Models (HMMs) called "DMCHMM" which is a three-step approach (model selection, prediction, testing) aiming to address the aforementioned drawbacks. Our proposed method is different from other HMM methods since it profiles methylation of each sample separately, hence exploiting inter-CpG autocorrelation within samples, and it is more flexible than previous approaches by allowing multiple hidden states. Using simulations, we show that DMCHMM has the best performance among several competing methods. An analysis of cell-separated blood methylation profiles is also provided.


Assuntos
Ilhas de CpG/genética , Metilação de DNA , Cadeias de Markov , Sulfitos , Algoritmos , Animais , Sítios de Ligação , Células Sanguíneas/metabolismo , Simulação por Computador/economia , Simulação por Computador/estatística & dados numéricos , Humanos , Análise de Sequência de DNA/métodos
14.
Circ Res ; 124(4): 553-563, 2019 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-30582441

RESUMO

RATIONALE: Familial recurrence studies provide strong evidence for a genetic component to the predisposition to sporadic, nonsyndromic Tetralogy of Fallot (TOF), the most common cyanotic congenital heart disease phenotype. Rare genetic variants have been identified as important contributors to the risk of congenital heart disease, but relatively small numbers of TOF cases have been studied to date. OBJECTIVE: We used whole exome sequencing to assess the prevalence of unique, deleterious variants in the largest cohort of nonsyndromic TOF patients reported to date. METHODS AND RESULTS: Eight hundred twenty-nine TOF patients underwent whole exome sequencing. The presence of unique, deleterious variants was determined; defined by their absence in the Genome Aggregation Database and a scaled combined annotation-dependent depletion score of ≥20. The clustering of variants in 2 genes, NOTCH1 and FLT4, surpassed thresholds for genome-wide significance (assigned as P<5×10-8) after correction for multiple comparisons. NOTCH1 was most frequently found to harbor unique, deleterious variants. Thirty-one changes were observed in 37 probands (4.5%; 95% CI, 3.2%-6.1%) and included 7 loss-of-function variants 22 missense variants and 2 in-frame indels. Sanger sequencing of the unaffected parents of 7 cases identified 5 de novo variants. Three NOTCH1 variants (p.G200R, p.C607Y, and p.N1875S) were subjected to functional evaluation, and 2 showed a reduction in Jagged1-induced NOTCH signaling. FLT4 variants were found in 2.4% (95% CI, 1.6%-3.8%) of TOF patients, with 21 patients harboring 22 unique, deleterious variants. The variants identified were distinct to those that cause the congenital lymphoedema syndrome Milroy disease. In addition to NOTCH1, FLT4 and the well-established TOF gene, TBX1, we identified potential association with variants in several other candidates, including RYR1, ZFPM1, CAMTA2, DLX6, and PCM1. CONCLUSIONS: The NOTCH1 locus is the most frequent site of genetic variants predisposing to nonsyndromic TOF, followed by FLT4. Together, variants in these genes are found in almost 7% of TOF patients.


Assuntos
Exoma , Taxa de Mutação , Tetralogia de Fallot/genética , Autoantígenos/genética , Proteínas de Ligação ao Cálcio/genética , Proteínas de Ciclo Celular/genética , Proteínas de Homeodomínio/genética , Humanos , Mutação com Perda de Função , Mutação de Sentido Incorreto , Proteínas Nucleares/genética , Receptor Notch1/genética , Transativadores/genética , Fatores de Transcrição/genética , Receptor 3 de Fatores de Crescimento do Endotélio Vascular/genética
15.
PLoS One ; 13(11): e0207250, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30440012

RESUMO

Very long intergenic non-coding RNAs (vlincRNAs) are a novel class of long transcripts (~50 kb to 1 Mb) with cell type- or cancer-specific expression. We report the discovery and characterization of 256 vlincRNAs from a cohort of 64 primary childhood pre-B and pre-T acute lymphoblastic leukemia (cALL) samples, of which 61% are novel and specifically expressed in cALL. Validation was performed in 35 pre-B and pre-T cALL primary samples. We show that their expression is cALL immunophenotype and molecular subtype-specific and correlated with epigenetic modifications on their promoters, much like protein-coding genes. While the biological functions of these vlincRNAs are still unknown, our results suggest they could play a role in cALL etiology or progression.


Assuntos
Leucemia-Linfoma Linfoblástico de Células Precursoras B/metabolismo , Leucemia-Linfoma Linfoblástico de Células T Precursoras/metabolismo , RNA Longo não Codificante/metabolismo , Adolescente , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Criança , Pré-Escolar , Estudos de Coortes , Ilhas de CpG , Metilação de DNA , Epigênese Genética , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Lactente , Masculino , Leucemia-Linfoma Linfoblástico de Células Precursoras B/genética , Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética , RNA Longo não Codificante/genética , Transcriptoma
16.
Genome Biol ; 19(1): 199, 2018 11 19.
Artigo em Inglês | MEDLINE | ID: mdl-30454069

RESUMO

Transposable elements (TEs) are major components of eukaryotic genomes. However, the extent of their impact on genome evolution, function, and disease remain a matter of intense interrogation. The rise of genomics and large-scale functional assays has shed new light on the multi-faceted activities of TEs and implies that they should no longer be marginalized. Here, we introduce the fundamental properties of TEs and their complex interactions with their cellular environment, which are crucial to understanding their impact and manifold consequences for organismal biology. While we draw examples primarily from mammalian systems, the core concepts outlined here are relevant to a broad range of organisms.


Assuntos
Elementos de DNA Transponíveis , Animais , Rearranjo Gênico , Humanos , Mutação , Polimorfismo Genético
17.
Nat Rev Genet ; 19(11): 688-704, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-30232369

RESUMO

A substantial proportion of the genome of many species is derived from transposable elements (TEs). Moreover, through various self-copying mechanisms, TEs continue to proliferate in the genomes of most species. TEs have contributed numerous regulatory, transcript and protein innovations and have also been linked to disease. However, notwithstanding their demonstrated impact, many genomic studies still exclude them because their repetitive nature results in various analytical complexities. Fortunately, a growing array of methods and software tools are being developed to cater for them. This Review presents a summary of computational resources for TEs and highlights some of the challenges and remaining gaps to perform comprehensive genomic analyses that do not simply 'mask' repeats.


Assuntos
Biologia Computacional , Elementos de DNA Transponíveis , Evolução Molecular , Genômica , Software , Biologia Computacional/instrumentação , Biologia Computacional/métodos , Genômica/instrumentação , Genômica/métodos
18.
Nucleic Acids Res ; 46(14): 7236-7249, 2018 08 21.
Artigo em Inglês | MEDLINE | ID: mdl-30137632

RESUMO

Copy number variants (CNVs) are known to affect a large portion of the human genome and have been implicated in many diseases. Although whole-genome sequencing (WGS) can help identify CNVs, most analytical methods suffer from limited sensitivity and specificity, especially in regions of low mappability. To address this, we use PopSV, a CNV caller that relies on multiple samples to control for technical variation. We demonstrate that our calls are stable across different types of repeat-rich regions and validate the accuracy of our predictions using orthogonal approaches. Applying PopSV to 640 human genomes, we find that low-mappability regions are approximately 5 times more likely to harbor germline CNVs, in stark contrast to the nearly uniform distribution observed for somatic CNVs in 95 cancer genomes. In addition to known enrichments in segmental duplication and near centromeres and telomeres, we also report that CNVs are enriched in specific types of satellite and in some of the most recent families of transposable elements. Finally, using this comprehensive approach, we identify 3455 regions with recurrent CNVs that were missing from existing catalogs. In particular, we identify 347 genes with a novel exonic CNV in low-mappability regions, including 29 genes previously associated with disease.


Assuntos
Centrômero/genética , Mapeamento Cromossômico/métodos , Variações do Número de Cópias de DNA , Genoma Humano/genética , Sequências Repetitivas de Ácido Nucleico/genética , Telômero/genética , Genômica/métodos , Humanos , Neoplasias/genética , Neoplasias/patologia , Polimorfismo de Nucleotídeo Único , Reprodutibilidade dos Testes , Sequenciamento Completo do Genoma/métodos
19.
Nat Commun ; 9(1): 2547, 2018 06 29.
Artigo em Inglês | MEDLINE | ID: mdl-29959321

RESUMO

Emerging evidence has illustrated the importance of epigenomic reprogramming in cancer, with altered post-translational modifications of histones contributing to pathogenesis. However, the contributions of histone modifiers to breast cancer progression are unclear, and how these processes vary between molecular subtypes has yet to be adequately addressed. Here we report that genetic or pharmacological targeting of the epigenetic modifier Ezh2 dramatically hinders metastatic behaviour in both a mouse model of breast cancer and patient-derived xenografts reflective of the Luminal B subtype. We further define a subtype-specific molecular mechanism whereby EZH2 maintains H3K27me3-mediated repression of the FOXC1 gene, thereby inactivating a FOXC1-driven, anti-invasive transcriptional program. We demonstrate that higher FOXC1 is predictive of favourable outcome specifically in Luminal B breast cancer patients and establish the use of EZH2 methyltransferase inhibitors as a viable strategy to block metastasis in Luminal B breast cancer, where options for targeted therapy are limited.


Assuntos
Neoplasias da Mama/tratamento farmacológico , Proteína Potenciadora do Homólogo 2 de Zeste/genética , Fatores de Transcrição Forkhead/genética , Regulação Neoplásica da Expressão Gênica , Histonas/genética , Indóis/farmacologia , Neoplasias Pulmonares/tratamento farmacológico , Piridonas/farmacologia , Animais , Antineoplásicos/farmacologia , Neoplasias da Mama/genética , Neoplasias da Mama/mortalidade , Neoplasias da Mama/patologia , Linhagem Celular Tumoral , Doxiciclina/farmacologia , Proteína Potenciadora do Homólogo 2 de Zeste/antagonistas & inibidores , Proteína Potenciadora do Homólogo 2 de Zeste/deficiência , Inibidores Enzimáticos/farmacologia , Feminino , Fatores de Transcrição Forkhead/agonistas , Fatores de Transcrição Forkhead/metabolismo , Histonas/metabolismo , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/mortalidade , Neoplasias Pulmonares/secundário , Camundongos , Camundongos Knockout , Terapia de Alvo Molecular , Processamento de Proteína Pós-Traducional , Transdução de Sinais , Transcrição Genética , Ensaios Antitumorais Modelo de Xenoenxerto
20.
Trends Genet ; 34(8): 571-572, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29853203

RESUMO

A new study sequenced and assembled two rodent genomes to better understand the evolutionary forces shaping mammalian genomes. Their results suggest multiple roles for genomic repeats.


Assuntos
Evolução Biológica , Genoma , Animais , Camundongos
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