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Article ; Online: Extensive Hidden Genomic Mosaicism Revealed in Normal Tissue.

Vattathil, Selina / Scheet, Paul

2016 Volume 98, Issue 3, Page(s) 571–578

Abstract: Genomic mosaicism arising from post-zygotic mutation has recently been demonstrated to occur in normal tissue of individuals ascertained with varied phenotypes, indicating that detectable mosaicism may be less an exception than a rule in the general ... ...

Abstract	Genomic mosaicism arising from post-zygotic mutation has recently been demonstrated to occur in normal tissue of individuals ascertained with varied phenotypes, indicating that detectable mosaicism may be less an exception than a rule in the general population. A challenge to comprehensive cataloging of mosaic mutations and their consequences is the presence of heterogeneous mixtures of cells, rendering low-frequency clones difficult to discern. Here we applied a computational method using estimated haplotypes to characterize mosaic megabase-scale structural mutations in 31,100 GWA study subjects. We provide in silico validation of 293 previously identified somatic mutations and identify an additional 794 novel mutations, most of which exist at lower aberrant cell fractions than have been demonstrated in previous surveys. These mutations occurred across the genome but in a nonrandom manner, and several chromosomes and loci showed unusual levels of mutation. Our analysis supports recent findings about the relationship between clonal mosaicism and old age. Finally, our results, in which we demonstrate a nearly 3-fold higher rate of clonal mosaicism, suggest that SNP-based population surveys of mosaic structural mutations should be conducted with haplotypes for optimal discovery.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Child, Preschool ; Chromosomes, Human/genetics ; Chromosomes, Human/metabolism ; Computational Biology/methods ; DNA Copy Number Variations ; Gene Frequency ; Genetic Association Studies ; Genetic Loci ; Genome, Human ; Genomics/methods ; Haplotypes ; Humans ; Infant ; Middle Aged ; Mosaicism ; Polymorphism, Single Nucleotide ; Young Adult
Language	English
Publishing date	2016-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2016.02.003
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Article ; Online: Small Amounts of Archaic Admixture Provide Big Insights into Human History.

Vattathil, Selina / Akey, Joshua M

Cell

2015 Volume 163, Issue 2, Page(s) 281–284

Abstract: Modern humans overlapped in time and space with other hominins, such as Neanderthals and Denisovans, and limited amounts of hybridization occurred. Here, we review recent work that has identified archaic hominin sequence that survives in modern human ... ...

Abstract	Modern humans overlapped in time and space with other hominins, such as Neanderthals and Denisovans, and limited amounts of hybridization occurred. Here, we review recent work that has identified archaic hominin sequence that survives in modern human genomes and what these genomic excavations reveal about human evolutionary history.
MeSH term(s)	Animals ; Biological Evolution ; Genetics, Medical ; Genome, Human ; Hominidae/genetics ; Humans ; Neanderthals/classification ; Neanderthals/genetics ; Selection, Genetic
Language	English
Publishing date	2015-10-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2015.09.042
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Article ; Online: Role of TET1-mediated epigenetic modulation in Alzheimer's disease.

Armstrong, Matthew J / Jin, Yulin / Vattathil, Selina M / Huang, Yanting / Schroeder, Jason P / Bennet, David A / Qin, Zhaohui S / Wingo, Thomas S / Jin, Peng

Neurobiology of disease

2023 Volume 185, Page(s) 106257

Abstract: Alzheimer's disease (AD) is a neurodegenerative disorder influenced by a complex interplay of environmental, epigenetic, and genetic factors. DNA methylation (5mC) and hydroxymethylation (5hmC) are DNA modifications that serve as tissue-specific and ... ...

Abstract	Alzheimer's disease (AD) is a neurodegenerative disorder influenced by a complex interplay of environmental, epigenetic, and genetic factors. DNA methylation (5mC) and hydroxymethylation (5hmC) are DNA modifications that serve as tissue-specific and temporal regulators of gene expression. TET family enzymes dynamically regulate these epigenetic modifications in response to environmental conditions, connecting environmental factors with gene expression. Previous epigenetic studies have identified 5mC and 5hmC changes associated with AD. In this study, we performed targeted resequencing of TET1 on a cohort of early-onset AD (EOAD) and control samples. Through gene-wise burden analysis, we observed significant enrichment of rare TET1 variants associated with AD (p = 0.04). We also profiled 5hmC in human postmortem brain tissues from AD and control groups. Our analysis identified differentially hydroxymethylated regions (DhMRs) in key genes responsible for regulating the methylome: TET3, DNMT3L, DNMT3A, and MECP2. To further investigate the role of Tet1 in AD pathogenesis, we used the 5xFAD mouse model with a Tet1 KO allele to examine how Tet1 loss influences AD pathogenesis. We observed significant changes in neuropathology, 5hmC, and RNA expression associated with Tet1 loss, while the behavioral alterations were not significant. The loss of Tet1 significantly increased amyloid plaque burden in the 5xFAD mouse (p = 0.044) and lead to a non-significant trend towards exacerbated AD-associated stress response in 5xFAD mice. At the molecular level, we found significant DhMRs enriched in genes involved in pathways responsible for neuronal projection organization, dendritic spine development and organization, and myelin assembly. RNA-Seq analysis revealed a significant increase in the expression of AD-associated genes such as Mpeg1, Ctsd, and Trem2. In conclusion, our results suggest that TET enzymes, particularly TET1, which regulate the methylome, may contribute to AD pathogenesis, as the loss of TET function increases AD-associated pathology.
MeSH term(s)	Humans ; Mice ; Animals ; Alzheimer Disease/metabolism ; 5-Methylcytosine ; Epigenesis, Genetic ; DNA Methylation ; Transcription Factors/metabolism ; Mixed Function Oxygenases/genetics ; Mixed Function Oxygenases/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Membrane Glycoproteins/metabolism ; Receptors, Immunologic/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism
Chemical Substances	5-Methylcytosine (6R795CQT4H) ; Transcription Factors ; TET1 protein, human (EC 1.-) ; Mixed Function Oxygenases (EC 1.-) ; Proto-Oncogene Proteins ; Trem2 protein, mouse ; Membrane Glycoproteins ; Receptors, Immunologic ; TET1 protein, mouse ; DNA-Binding Proteins
Language	English
Publishing date	2023-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2023.106257
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Article ; Online: Haplotype-based profiling of subtle allelic imbalance with SNP arrays.

Vattathil, Selina / Scheet, Paul

Genome research

2012 Volume 23, Issue 1, Page(s) 152–158

Abstract: Due to limitations of surgical dissection and tumor heterogeneity, tumor samples collected for cancer genomics studies are often heavily diluted with normal tissue or contain subpopulations of cells harboring important aberrations. Methods for profiling ... ...

Abstract	Due to limitations of surgical dissection and tumor heterogeneity, tumor samples collected for cancer genomics studies are often heavily diluted with normal tissue or contain subpopulations of cells harboring important aberrations. Methods for profiling tumor-associated allelic imbalance in such scenarios break down at aberrant cell proportions of 10%-15% and below. Here, we present an approach that offers a vast improvement for detection of subtle allelic imbalance, or low proportions of cells harboring aberrant allelic ratio among nonaberrant cells, in unpaired tumor samples using SNP microarrays. We leverage the expected pattern of allele-specific intensity ratios determined by an individual's germline haplotypes, information that has been ignored in existing approaches. We demonstrate our method on real and simulated data from the CRL-2324 breast cancer cell line genotyped on the Illumina 370K array. Assuming a 5 million SNP array, we can detect the presence of aberrant cells in proportions lower than 0.25% in the breast cancer sample, approaching the sensitivity of some minimal residual disease assays. Further, we apply a hidden Markov model to identify copy-neutral LOH (loss of heterozygosity) events as short as 11 Mb in mixtures of only 4% tumor using 370K data. We anticipate our approach will offer a new paradigm for genomic profiling of heterogeneous samples.
MeSH term(s)	Allelic Imbalance ; Breast Neoplasms/genetics ; Cell Line, Tumor ; DNA, Neoplasm ; Female ; Genome, Human ; Genotyping Techniques/methods ; Haplotypes ; Heterozygote ; Humans ; Markov Chains ; Models, Genetic ; Oligonucleotide Array Sequence Analysis/methods ; Polymorphism, Single Nucleotide ; Sensitivity and Specificity
Chemical Substances	DNA, Neoplasm
Language	English
Publishing date	2012-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1284872-4
ISSN	1549-5469 ; 1088-9051 ; 1054-9803
ISSN (online)	1549-5469
ISSN	1088-9051 ; 1054-9803
DOI	10.1101/gr.141374.112
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Article: Small Amounts of Archaic Admixture Provide Big Insights into Human History

Vattathil, Selina / JoshuaÂ M. Akey

Cell. 2015 Oct. 08, v. 163

2015

Abstract	Modern humans overlapped in time and space with other hominins, such as Neanderthals and Denisovans, and limited amounts of hybridization occurred. Here, we review recent work that has identified archaic hominin sequence that survives in modern human genomes and what these genomic excavations reveal about human evolutionary history.
Keywords	genome ; humans ; hybridization ; space and time
Language	English
Dates of publication	2015-1008
Size	p. 281-284.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2015.09.042
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Article ; Online: Sex differences in brain protein expression and disease.

Wingo, Aliza P / Liu, Yue / Gerasimov, Ekaterina S / Vattathil, Selina M / Liu, Jiaqi / Cutler, David J / Epstein, Michael P / Blokland, Gabriëlla A M / Thambisetty, Madhav / Troncoso, Juan C / Duong, Duc M / Bennett, David A / Levey, Allan I / Seyfried, Nicholas T / Wingo, Thomas S

Nature medicine

2023 Volume 29, Issue 9, Page(s) 2224–2232

Abstract: Most complex human traits differ by sex, but we have limited insight into the underlying mechanisms. Here, we investigated the influence of biological sex on protein expression and its genetic regulation in 1,277 human brain proteomes. We found that 13.2% ...

Abstract	Most complex human traits differ by sex, but we have limited insight into the underlying mechanisms. Here, we investigated the influence of biological sex on protein expression and its genetic regulation in 1,277 human brain proteomes. We found that 13.2% (1,354) of brain proteins had sex-differentiated abundance and 1.5% (150) of proteins had sex-biased protein quantitative trait loci (sb-pQTLs). Among genes with sex-biased expression, we found 67% concordance between sex-differentiated protein and transcript levels; however, sex effects on the genetic regulation of expression were more evident at the protein level. Considering 24 psychiatric, neurologic and brain morphologic traits, we found that an average of 25% of their putatively causal genes had sex-differentiated protein abundance and 12 putatively causal proteins had sb-pQTLs. Furthermore, integrating sex-specific pQTLs with sex-stratified genome-wide association studies of six psychiatric and neurologic conditions, we uncovered another 23 proteins contributing to these traits in one sex but not the other. Together, these findings begin to provide insights into mechanisms underlying sex differences in brain protein expression and disease.
MeSH term(s)	Female ; Male ; Humans ; Sex Characteristics ; Genome-Wide Association Study ; Brain ; Multifactorial Inheritance ; Phenotype
Language	English
Publishing date	2023-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-023-02509-y
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Article ; Online: Shared mechanisms across the major psychiatric and neurodegenerative diseases.

Wingo, Thomas S / Liu, Yue / Gerasimov, Ekaterina S / Vattathil, Selina M / Wynne, Meghan E / Liu, Jiaqi / Lori, Adriana / Faundez, Victor / Bennett, David A / Seyfried, Nicholas T / Levey, Allan I / Wingo, Aliza P

Nature communications

2022 Volume 13, Issue 1, Page(s) 4314

Abstract: Several common psychiatric and neurodegenerative diseases share epidemiologic risk; however, whether they share pathophysiology is unclear and is the focus of our investigation. Using 25 GWAS results and LD score regression, we find eight significant ... ...

Abstract	Several common psychiatric and neurodegenerative diseases share epidemiologic risk; however, whether they share pathophysiology is unclear and is the focus of our investigation. Using 25 GWAS results and LD score regression, we find eight significant genetic correlations between psychiatric and neurodegenerative diseases. We integrate the GWAS results with human brain transcriptomes (n = 888) and proteomes (n = 722) to identify cis- and trans- transcripts and proteins that are consistent with a pleiotropic or causal role in each disease, referred to as causal proteins for brevity. Within each disease group, we find many distinct and shared causal proteins. Remarkably, 30% (13 of 42) of the neurodegenerative disease causal proteins are shared with psychiatric disorders. Furthermore, we find 2.6-fold more protein-protein interactions among the psychiatric and neurodegenerative causal proteins than expected by chance. Together, our findings suggest these psychiatric and neurodegenerative diseases have shared genetic and molecular pathophysiology, which has important ramifications for early treatment and therapeutic development.
MeSH term(s)	Brain ; Genetic Predisposition to Disease ; Genome-Wide Association Study/methods ; Humans ; Mental Disorders/genetics ; Neurodegenerative Diseases/genetics ; Polymorphism, Single Nucleotide
Language	English
Publishing date	2022-07-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-31873-5
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Article ; Online: LDL cholesterol is associated with higher AD neuropathology burden independent of APOE.

Wingo, Aliza P / Vattathil, Selina M / Liu, Jiaqi / Fan, Wen / Cutler, David J / Levey, Allan I / Schneider, Julie A / Bennett, David A / Wingo, Thomas S

Journal of neurology, neurosurgery, and psychiatry

2022

Abstract: Objective: APOE: Methods: Individuals in the Religious Orders Study/Memory and Ageing Project cohorts with longitudinal measures of blood lipids and detailed autopsies were studied. We modelled the relationship between blood lipids and 12 age-related ...

Abstract	Objective: APOE Methods: Individuals in the Religious Orders Study/Memory and Ageing Project cohorts with longitudinal measures of blood lipids and detailed autopsies were studied. We modelled the relationship between blood lipids and 12 age-related brain pathologies using a linear mixed model adjusted for potential confounding factors and stratified by Results: 559 participants (69.1% female) had complete data for analysis. They were followed for a median of 7 years and a median of 3 years prior to dementia onset. LDL-C was associated with all measures of AD neuropathology (neurofibrillary tangles, beta-amyloid, Braak stage, modified CERAD score and global AD pathology) and cerebral amyloid angiopathy independent of Conclusions: These findings implicate LDL-C in the pathophysiology of AD independent of
Language	English
Publishing date	2022-06-30
Publishing country	England
Document type	Journal Article
ZDB-ID	3087-9
ISSN	1468-330X ; 0022-3050
ISSN (online)	1468-330X
ISSN	0022-3050
DOI	10.1136/jnnp-2021-328164
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Article ; Online: Identification of allelic imbalance with a statistical model for subtle genomic mosaicism.

Xia, Rui / Vattathil, Selina / Scheet, Paul

PLoS computational biology

2014 Volume 10, Issue 8, Page(s) e1003765

Abstract: Genetic heterogeneity in a mixed sample of tumor and normal DNA can confound characterization of the tumor genome. Numerous computational methods have been proposed to detect aberrations in DNA samples from tumor and normal tissue mixtures. Most of these ...

Abstract	Genetic heterogeneity in a mixed sample of tumor and normal DNA can confound characterization of the tumor genome. Numerous computational methods have been proposed to detect aberrations in DNA samples from tumor and normal tissue mixtures. Most of these require tumor purities to be at least 10-15%. Here, we present a statistical model to capture information, contained in the individual's germline haplotypes, about expected patterns in the B allele frequencies from SNP microarrays while fully modeling their magnitude, the first such model for SNP microarray data. Our model consists of a pair of hidden Markov models--one for the germline and one for the tumor genome--which, conditional on the observed array data and patterns of population haplotype variation, have a dependence structure induced by the relative imbalance of an individual's inherited haplotypes. Together, these hidden Markov models offer a powerful approach for dealing with mixtures of DNA where the main component represents the germline, thus suggesting natural applications for the characterization of primary clones when stromal contamination is extremely high, and for identifying lesions in rare subclones of a tumor when tumor purity is sufficient to characterize the primary lesions. Our joint model for germline haplotypes and acquired DNA aberration is flexible, allowing a large number of chromosomal alterations, including balanced and imbalanced losses and gains, copy-neutral loss-of-heterozygosity (LOH) and tetraploidy. We found our model (which we term J-LOH) to be superior for localizing rare aberrations in a simulated 3% mixture sample. More generally, our model provides a framework for full integration of the germline and tumor genomes to deal more effectively with missing or uncertain features, and thus extract maximal information from difficult scenarios where existing methods fail.
MeSH term(s)	Allelic Imbalance/genetics ; Cell Line, Tumor ; Gene Expression Profiling ; Genome/genetics ; Genomics ; Humans ; Models, Genetic ; Models, Statistical ; Mosaicism
Language	English
Publishing date	2014-08-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2193340-6
ISSN	1553-7358 ; 1553-734X
ISSN (online)	1553-7358
ISSN	1553-734X
DOI	10.1371/journal.pcbi.1003765
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Article ; Online: Rapid and powerful detection of subtle allelic imbalance from exome sequencing data with hapLOHseq.

San Lucas, F Anthony / Sivakumar, Smruthy / Vattathil, Selina / Fowler, Jerry / Vilar, Eduardo / Scheet, Paul

Bioinformatics (Oxford, England)

2016 Volume 32, Issue 19, Page(s) 3015–3017

Abstract: Motivation: The detection of subtle genomic allelic imbalance events has many potential applications. For example, identifying cancer-associated allelic imbalanced regions in low tumor-cellularity samples or in low-proportion tumor subclones can be used ...

Abstract	Motivation: The detection of subtle genomic allelic imbalance events has many potential applications. For example, identifying cancer-associated allelic imbalanced regions in low tumor-cellularity samples or in low-proportion tumor subclones can be used for early cancer detection, prognostic assessment and therapeutic selection in cancer patients. We developed hapLOHseq for the detection of subtle allelic imbalance events from next-generation sequencing data. Results: Our method identified events of 10 megabases or greater occurring in as little as 16% of the sample in exome sequencing data (at 80×) and 4% in whole genome sequencing data (at 30×), far exceeding the capabilities of existing software. We also found hapLOHseq to be superior at detecting large chromosomal changes across a series of pancreatic samples from TCGA. Availability and implementation: hapLOHseq is available at scheet.org/software, distributed under an open source MIT license. Contact: pscheet@alum.wustl.edu Supplementary information: Supplementary data are available at Bioinformatics online.
MeSH term(s)	Allelic Imbalance ; Exome ; Genomics ; High-Throughput Nucleotide Sequencing ; Humans ; Software
Language	English
Publishing date	2016-06-10
Publishing country	England
Document type	Journal Article
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btw340
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