'; ?> geneimprint : Hot off the Press http://www.geneimprint.com/site/hot-off-the-press Daily listing of the most recent articles in epigenetics and imprinting, collected from the PubMed database. en-us Sun, 27 Sep 2020 18:51:16 EDT Sun, 27 Sep 2020 18:51:16 EDT jirtle@radonc.duke.edu james001@jirtle.com Promising biomarkers of human aging: in search of a multi-omics panel to understand the aging process from a multidimensional perspective. Rivero-Segura NA, Bello-Chavolla OY, Barrera-Vázquez OS, Gutierrez-Robledo LM, Gómez-Verjan JC
Ageing Res Rev (Sep 2020)

The aging process has been linked to the occurrence of chronic diseases and functional impairments, including cancer, sarcopenia, frailty, metabolic, cardiovascular, and neurodegenerative diseases. Nonetheless, aging is highly variable and heterogeneous and represents a challenge for its characterization. In this sense, intrinsic capacity (IC) stands as a novel perspective by the World Health Organization, which integrates the individual wellbeing, environment, and risk factors to understand aging. However, there is a lack of quantitative and qualitative attributes to define it objectively. Therefore, in this review we attempt to summarize the most relevant and promising biomarkers described in clinical studies at date over different molecular levels, including epigenomics, transcriptomics, proteomics, metabolomics, and the microbiome. To aid gerontologists, geriatricians, and biomedical researchers to understand the aging process through the IC. Aging biomarkers reflect the physiological state of individuals and the underlying mechanisms related to homeostatic changes throughout an individual lifespan; they demonstrated that aging could be measured independently of time (that may explain its heterogeneity) and to be helpful to predict age-related syndromes and mortality. In summary, we highlight the areas of opportunity and gaps of knowledge that must be addressed to fully integrate biomedical findings into clinically useful tools and interventions.]]>
Wed, 31 Dec 1969 19:00:00 EST
Impact of parental origin of X-chromosome on clinical and biochemical profile in Turner syndrome. Malhotra R, Shukla R, Kabra M, Gupta Y, Jyotsna VP, Khadgawat R
J Pediatr Endocrinol Metab (Sep 2020)

Objectives To evaluate if the parental origin of X-chromosome has an impact on the phenotype and biochemical profile in Turner syndrome (TS). Result of the previous studies have been equivocal and could be attributable to the multicentric study design with different experts examining heterogeneous TS population of various ethnic background. Methods A cross-sectional single center study from Northern India. Fifty nine diagnosed subjects of TS and their parents participated in the study. Parental origin of intact X-chromosome was determined using 12 highly polymorphic short tandem repeats (STR) on X-chromosome. For the evaluation of parent-of-origin effects, typical phenotypic traits including congenital malformations, anthropometry, body composition by dual energy X-ray absorptiometry (DXA) and biochemical profile were compared. Clinical stigmata of TS in all subjects were examined by a single expert. Results The intact X-chromosome was of maternal origin (Xm) in 49.1% subjects while 50.9% had paternal origin (Xp). Skeletal anomalies were more common in Xm group, out of which prevalence of short neck and short fourth metatarsal reached statistical significance (p=0.04 and 0.01 respectively). A strong correlation was observed between subject's baseline height standard deviation score (Ht SDS) and paternal height (r=0.593, p<0.001), maternal height (r=0.564, p<0.001) and mid-parental height (MPH) (r=0.372, p=0.047) in Xp group. This effect was not seen in Xm subjects whose baseline Ht SDS showed no significant correlation with maternal height, paternal height or MPH. No differences were detected between the groups with regard to biochemical profile or body composition. Conclusions We speculate that the differences in skeletal anomalies and height correlations between Xm and Xp groups could be due to the modifying effect of epigenetic signature on short stature homeobox (SHOX) gene of Xm. SHOX gene is not modified on Xp thereby explaining the paucity of skeletal changes and height correlations in Xp subjects.]]>
Wed, 31 Dec 1969 19:00:00 EST
Integrated Analysis of DNA Methylation, Hydroxymethylation, and Gene Expression Data Using ME-Class2. Singh MK, Edwards JR
Methods Mol Biol (2021)

There is increasing interest in understanding the pathological role of DNA methylation changes in disease by profiling genome-wide methylation changes. This includes both 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC). The typical profiling study is designed to measure 5mC and/or 5hmC levels alongside gene expression in a set of samples and controls to determine a list of candidate genes whose 5mC and/or 5hmC changes are associated with expression changes. We recently showed that ME-Class2 substantially outperforms other bioinformatic approaches at accurately identify genes with highly associated methylation and expression changes. ME-Class2 further illuminated how synergistic changes in 5mC and 5hmC potentially contribute to gene silencing and activation. Here we present a detailed protocol for using ME-Class2 to analyze genome-wide methylation (5mC and/or 5hmC) and expression data. Further, we provide advice about extending ME-Class2 to study the relationships between other epigenetic marks.]]>
Wed, 31 Dec 1969 19:00:00 EST
IMPLICON: an ultra-deep sequencing method to uncover DNA methylation at imprinted regions. Klobučar T, Kreibich E, Krueger F, Arez M, Pólvora-Brandão D, von Meyenn F, da Rocha ST, Eckersley-Maslin M
Nucleic Acids Res (Sep 2020)

Genomic imprinting is an epigenetic phenomenon leading to parental allele-specific expression. Dosage of imprinted genes is crucial for normal development and its dysregulation accounts for several human disorders. This unusual expression pattern is mostly dictated by differences in DNA methylation between parental alleles at specific regulatory elements known as imprinting control regions (ICRs). Although several approaches can be used for methylation inspection, we lack an easy and cost-effective method to simultaneously measure DNA methylation at multiple imprinted regions. Here, we present IMPLICON, a high-throughput method measuring DNA methylation levels at imprinted regions with base-pair resolution and over 1000-fold coverage. We adapted amplicon bisulfite-sequencing protocols to design IMPLICON for ICRs in adult tissues of inbred mice, validating it in hybrid mice from reciprocal crosses for which we could discriminate methylation profiles in the two parental alleles. Lastly, we developed a human version of IMPLICON and detected imprinting errors in embryonic and induced pluripotent stem cells. We also provide rules and guidelines to adapt this method for investigating the DNA methylation landscape of any set of genomic regions. In summary, IMPLICON is a rapid, cost-effective and scalable method, which could become the gold standard in both imprinting research and diagnostics.]]>
Wed, 31 Dec 1969 19:00:00 EST
Mapping DNA Methylation in Mammals: The State of the Art. Lentini A, Nestor CE
Methods Mol Biol (2021)

A complete understanding of the dynamics and function of cytosine modifications in mammalian biology is lacking. Central to achieving this understanding is the availability of techniques that permit sensitive and specific genome-wide mapping of DNA modifications in mammalian DNA. The last decade has seen the development of a vast arsenal of novel profiling approaches enabling epigeneticists to tackle research questions that were previously out of reach. Here, we review the techniques currently available for profiling DNA modifications in mammals, discuss their strengths and weaknesses, and speculate on the future direction of DNA modification profiling technologies.]]>
Wed, 31 Dec 1969 19:00:00 EST
Prioritizing transcriptomic and epigenomic experiments by using an optimization strategy that leverages imputed data. Schreiber J, Bilmes J, Noble WS
Bioinformatics (Sep 2020)

Successful science often involves not only performing experiments well, but also choosing well among many possible experiments. In a hypothesis generation setting, choosing an experiment well means choosing an experiment whose results are interesting or novel. In this work, we formalize this selection procedure in the context of genomics and epigenomics data generation. Specifically, we consider the task faced by a scientific consortium such as the National Institutes of Health ENCODE Consortium, whose goal is to characterize all of the functional elements in the human genome. Given a list of possible cell types or tissue types ("biosamples") and a list of possible high throughput sequencing assays, where at least one experiment has been performed in each biosample and for each assay, we ask "Which experiments should ENCODE perform next?"]]>
Wed, 31 Dec 1969 19:00:00 EST
Profiling Chromatin Landscape at High Resolution and Throughput with 2C-ChIP. Wang XQD, Cameron CJF, Segal D, Paquette D, Blanchette M, Dostie J
Methods Mol Biol (2021)

Chromatin immunoprecipitation (ChIP) is used to probe the presence of proteins and/or their posttranslational modifications on genomic DNA. This method is often used alongside chromosome conformation capture approaches to obtain a better-rounded view of the functional relationship between chromatin architecture and its landscape. Since the inception of ChIP, its protocol has been modified to improve speed, sensitivity, and specificity. Combining ChIP with deep sequencing has recently improved its throughput and made genome-wide profiling possible. However, genome-wide analysis is not always the best option, particularly when many samples are required to study a given genomic region or when quantitative data is desired. We recently developed carbon copy-ChIP (2C-ChIP), a new form of the high-throughput ChIP analysis method ideally suited for these types of studies. 2C-ChIP applies ligation-mediated amplification (LMA) followed by deep sequencing to quantitatively detect specified genomic regions in ChIP samples. Here, we describe the generation of 2C-ChIP libraries and computational processing of the resulting sequencing data.]]>
Wed, 31 Dec 1969 19:00:00 EST
Biomarkers of Fabry Nephropathy: Review and Future Perspective. Levstek T, Vujkovac B, Trebusak Podkrajsek K
Genes (Basel) (Sep 2020)

Progressive nephropathy is one of the main features of Fabry disease, which largely contributes to the overall morbidity and mortality burden of the disease. Due to the lack of specific biomarkers, the heterogeneity of the disease, and unspecific symptoms, diagnosis is often delayed. Clinical presentation in individual patients varies widely, even in patients from the same family carrying the same pathogenic variant. Therefore, it is reasonable to anticipate that additional genomic, transcriptomic, proteomic, and metabolomics factors influence the manifestation and progression of the disease. The aim of this article is to provide an overview of nephropathy in Fabry patients and the biomarkers currently used in the diagnosis and follow-up. Current biomarkers are associated with late signs of kidney damage. Therefore, there is a need to identify biomarkers associated with early stages of kidney damage that would enable early diagnosis, which is crucial for effective treatment and prevention of severe irreversible complications. Recent advances in sequencing and -omics technologies have led to several studies investigating new biomarkers. We will provide an overview of the novel biomarkers, critically evaluate their clinical utility, and propose future perspectives, which we believe might be in their integration.]]>
Wed, 31 Dec 1969 19:00:00 EST
GENETICS IN ENDOCRINOLOGY: Genetic etiologies of central precocious puberty and the role of imprinted genes. Roberts SA, Kaiser UB
Eur J Endocrinol (Oct 2020)

Pubertal timing is regulated by the complex interplay of genetic, environmental, nutritional and epigenetic factors. Criteria for determining normal pubertal timing, and thus the definition of precocious puberty, have evolved based on published population studies. The significance of the genetic influence on pubertal timing is supported by familial pubertal timing and twin studies. In contrast to the many monogenic causes associated with hypogonadotropic hypogonadism, only four monogenic causes of central precocious puberty (CPP) have been described. Loss-of-function mutations in Makorin Ring Finger Protein 3(MKRN3), a maternally imprinted gene on chromosome 15 within the Prader-Willi syndrome locus, are the most common identified genetic cause of CPP. More recently, several mutations in a second maternally imprinted gene, Delta-like noncanonical Notch ligand 1 (DLK1), have also been associated with CPP. Polymorphisms in both genes have also been associated with the age of menarche in genome-wide association studies. Mutations in the genes encoding kisspeptin (KISS1) and its receptor (KISS1R), potent activators of GnRH secretion, have also been described in association with CPP, but remain rare monogenic causes. CPP has both short- and long-term health implications for children, highlighting the importance of understanding the mechanisms contributing to early puberty. Additionally, given the role of mutations in the imprinted genes MKRN3 and DLK1 in pubertal timing, other imprinted candidate genes should be considered for a role in puberty initiation.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetic Assays in Purified Cardiomyocyte Nuclei. Hill MC, Martin JF
Methods Mol Biol (2021)

The adult mammalian heart's potential for regeneration is very inefficient. Importantly, adult mammalian cardiomyocytes (CMs) are characterized as a cell population with very limited mitotic potential. Conversely, the neonatal mouse heart possesses a brief, yet robust, regenerative capacity within the first week of life. Cell type-specific enrichment procedures are essential for characterizing the full spectrum of epigenomic landscapes and gene regulatory networks deployed by mammalian CMs. In this chapter, we describe a protocol useful for purifying CM nuclei from mammalian cardiac tissue. Furthermore, we detail a low-input procedure suitable for the parallel genome-wide profiling of chromatin accessibility, histone modifications, and transcription factor-binding sites. The CM nuclei purified using this process are suitable for multi-omic profiling approaches.]]>
Wed, 31 Dec 1969 19:00:00 EST
The epigenomics of sarcoma. Nacev BA, Jones KB, Intlekofer AM, Yu JSE, Allis CD, Tap WD, Ladanyi M, Nielsen TO
Nat Rev Cancer (Oct 2020)

Epigenetic regulation is critical to physiological control of development, cell fate, cell proliferation, genomic integrity and, fundamentally, transcriptional regulation. This epigenetic control occurs at multiple levels including through DNA methylation, histone modification, nucleosome remodelling and modulation of the 3D chromatin structure. Alterations in genes that encode chromatin regulators are common among mesenchymal neoplasms, a collection of more than 160 tumour types including over 60 malignant variants (sarcomas) that have unique and varied genetic, biological and clinical characteristics. Herein, we review those sarcomas in which chromatin pathway alterations drive disease biology. Specifically, we emphasize examples of dysregulation of each level of epigenetic control though mechanisms that include alterations in metabolic enzymes that regulate DNA methylation and histone post-translational modifications, mutations in histone genes, subunit loss or fusions in chromatin remodelling and modifying complexes, and disruption of higher-order chromatin structure. Epigenetic mechanisms of tumorigenesis have been implicated in mesenchymal tumours ranging from chondroblastoma and giant cell tumour of bone to chondrosarcoma, malignant peripheral nerve sheath tumour, synovial sarcoma, epithelioid sarcoma and Ewing sarcoma - all diseases that present in a younger patient population than most cancers. Finally, we review current and potential future approaches for the development of sarcoma therapies based on this emerging understanding of chromatin dysregulation.]]>
Wed, 31 Dec 1969 19:00:00 EST
Imprinting analysis by droplet digital PCR coupled with locked nucleic acid TaqMan probes. Mitake M, Hirano S, Kishino T
Epigenetics (Sep 2020)

Imprinted genes are differentially expressed in a parent-of-origin-specific manner. Parental origin of the alleles is discriminated by intragenic DNA polymorphisms. Comparisons of parental allelic expression have been analysed by semiquantitative RT-PCR. Here, we developed a novel quantitative method for allelic expression of the imprinted gene , which inactivation and mutations cause Angelman syndrome and predominantly expressed by the maternal allele in neuronal tissues. In this method, cDNA was amplified by droplet digital PCR (ddPCR) coupled with allele-specific locked nucleic acid (LNA) TaqMan probes, which labelled by FAM and HEX were designed to detect the SNPs in the target regions. ddPCR assay demonstrated that the sense transcript of was equally expressed from both parental alleles in adult tissues except neuronal tissues, where expression from the paternal allele was about 10 to 14% of total expression in adult brain, and 20% in spinal cord. The antisense transcript of was expressed at 60% to 70% of the sense transcript of in adult brain. Changes in the transcripts during postnatal brain development were also evaluated by ddPCR. The ddPCR method is far more reliable and simpler to use than semiquantitative PCR to analyse skewed or faint allelic expression of imprinted genes.]]>
Wed, 31 Dec 1969 19:00:00 EST
Aberrant allelic-switch of antisense lncRNA IRAIN may be an early diagnostic marker in laryngeal cancer. Wang JY, Liu D, Di Meng Y, Guo YY, Zhao M
Oncol Lett (Oct 2020)

Laryngeal carcinoma is a common head and neck malignancy, however, the molecular mechanism of the disease has not yet been elucidated. The present study aimed to investigate the role of IGF1R antisense imprinted non-protein coding RNA (IRAIN) long non-coding (lnc)RNA in laryngeal carcinoma. In total, specimens of healthy pharynx tissue from 6 healthy individuals, carcinoma tissue and paracancerous tissue from 37 patients with laryngeal carcinoma were used in this study. The single nucleotide polymorphism (SNP) rs8034564 was used to distinguish the two parental alleles of IRAIN. DNA and RNA were extracted from tissue specimens and the IRAIN allelic gene was sequenced. Reverse transcription-quantitative PCR was used to determine the expression levels of IRAIN and Insulin-like growth factor 1 receptor (IGF1R) in laryngeal carcinoma and paracancerous tissue. Bisulfite genomic sequencing was used to determine IRAIN promoter DNA methylation status in laryngeal carcinoma tissue. The expression of IRAIN was di-allelic in healthy pharynx tissue, laryngeal carcinoma tissue and paracancerous tissue. Moreover, IRAIN expression in laryngeal carcinoma tissue was lower compared with paracancerous tissue (P<0.05). IRAIN expression was not associated with age, histological type, tumor stage and grade and lymph node metastasis. IRAIN allelic expression imbalance was present in laryngeal carcinoma and paracancerous tissue, but not in healthy pharynx tissue. SNP analysis (rs8034564) indicated there was an allelic-switch of the two parental alleles. Furthermore, epigenetic analysis revealed no extensive DNA methylation of CpG islands in the IRAIN gene promoter of laryngeal carcinoma. Therefore, it was suggested that IRAIN allele was non-imprinted in laryngeal carcinoma and healthy pharynx tissue. It was also demonstrated that IRAIN may be a potential tumor suppressor in laryngeal carcinoma, and that DNA methylation is not involved in the regulation of IRAIN gene immobilization in laryngeal carcinoma tissue. Thus, detection of IRAIN allelic expression imbalance and aberrant allele-switch may serve as an early diagnostic marker of laryngeal carcinoma.]]>
Wed, 31 Dec 1969 19:00:00 EST
Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex. Laukoter S, Pauler FM, Beattie R, Amberg N, Hansen AH, Streicher C, Penz T, Bock C, Hippenmeyer S
Neuron (Sep 2020)

In mammalian genomes, a subset of genes is regulated by genomic imprinting, resulting in silencing of one parental allele. Imprinting is essential for cerebral cortex development, but prevalence and functional impact in individual cells is unclear. Here, we determined allelic expression in cortical cell types and established a quantitative platform to interrogate imprinting in single cells. We created cells with uniparental chromosome disomy (UPD) containing two copies of either the maternal or the paternal chromosome; hence, imprinted genes will be 2-fold overexpressed or not expressed. By genetic labeling of UPD, we determined cellular phenotypes and transcriptional responses to deregulated imprinted gene expression at unprecedented single-cell resolution. We discovered an unexpected degree of cell-type specificity and a novel function of imprinting in the regulation of cortical astrocyte survival. More generally, our results suggest functional relevance of imprinted gene expression in glial astrocyte lineage and thus for generating cortical cell-type diversity.]]>
Wed, 31 Dec 1969 19:00:00 EST
Longitudinal Characteristics of Glioblastoma in Genome-Wide Studies. Kraboth Z, Kalman B
Pathol Oncol Res (Oct 2020)

Glioblastoma is one of the deadliest tumors with barely over one-year median survival despite intensive efforts in defining its molecular characteristics and searching for innovative treatment strategies. While major progress has been made in cataloging cross-sectional genomic, transcriptomic and epigenomic features of the tumor, and inferring its main molecular pathways and niches for potential targeted intervention, we still do not have sufficient knowledge concerning evolutionary patterns and dynamics of molecular changes or the treatment-induced effects affecting glioblastoma biology. In this review, we summarize the results of recent longitudinal genomic, transcriptomic and epigenomic studies that brought us closer to a better understanding of this lethal disease. Evidence suggests that neuronal / glioma stem cells with accumulating mutations initiate glioblastoma development and recurrence, but the hypothetical models describing the courses that lead to established tumors have not been fully proven. Moving from the histopathological phenotype to the results of high resolution OMICS studies, we try to synthesize the currently available information from sequential glioblastoma analyses in order to highlight its multifaceted features and heterogenetity, as well as the expected complexity of potential treatment strategies that might once succeed.]]>
Wed, 31 Dec 1969 19:00:00 EST
Patent highlights April-May 2020. Mucke HA
Pharm Pat Anal (Sep 2020)

A snapshot of noteworthy recent developments in the patent literature of relevance to pharmaceutical and medical research and development.]]>
Wed, 31 Dec 1969 19:00:00 EST
Histone Modifications and their Role in Colorectal Cancer (Review). Qin J, Wen B, Liang Y, Yu W, Li H
Pathol Oncol Res (Oct 2020)

The development of colorectal cancer is a complex and multistep process mediated by a variety of factors including the dysregulation of genetic and epigenetic under the influence of microenvironment. It is evident that epigenetics that affects gene activity and expression has been recognized as a critical role in the carcinogenesis. Aside from DNA methylation, miRNA level, and genomic imprinting, histone modification is increasingly recognized as an essential mechanism underlying the occurrence and development of colorectal cancer. Aberrant regulation of histone modification like acetylation, methylation and phosphorylation levels on specific residues is implicated in a wide spectrum of cancers, including colorectal cancer. In addition, as this process is reversible and accompanied by a plethora of deregulated enzymes, inhibiting those histone-modifying enzymes activity and regulating its level has been thought of as a potential path for tumor therapy. This review provides insight into the basic information of histone modification and its application in the colorectal cancer treatment, thereby offering new potential targets for treatment of colorectal cancer.]]>
Wed, 31 Dec 1969 19:00:00 EST
Multi-omics study for interpretation of genome-wide association study. Akiyama M
J Hum Genet (Sep 2020)

Genome-wide association studies (GWASs) have identified thousands of genetic loci associated with complex traits, including a wide variety of diseases. Despite the successful identification of associated loci, interpreting GWAS findings remains challenging and requires other biological resources. Omics, including genomics, transcriptomics, proteomics, metabolomics, and epigenomics, are increasingly used in a broad range of research fields. Integrative analyses applying GWAS with these omics data are expected to expand our knowledge of complex traits and provide insight into the pathogenesis of complex diseases and their causative factors. Recently, associations between genetic variants and omics data have been comprehensively evaluated, providing new information on the influence of genetic variants on omics. Furthermore, recent advances in analytic methods, including single-cell technologies, have revealed previously unknown disease mechanisms. To advance our understanding of complex traits, integrative analysis using GWAS with multi-omics data is needed. In this review, I describe successful examples of integrative analyses based on omics and GWAS, discuss the limitations of current multi-omics analyses, and provide a perspective on future integrative studies.]]>
Wed, 31 Dec 1969 19:00:00 EST
Single-Cell Genomics and Epigenomics: Technologies and Applications in Plants. Luo C, Fernie AR, Yan J
Trends Plant Sci (Oct 2020)

The development of genomics and epigenomics has allowed rapid advances in our understanding of plant biology. However, conventional bulk analysis dilutes cell-specific information by providing only average information, thereby limiting the resolution of genomic and functional genomic studies. Recent advances in single-cell sequencing technology concerning genomics and epigenomics open new avenues to dissect cell heterogeneity in multiple biological processes. Recent applications of these approaches to plants have provided exciting insights into diverse biological questions. We highlight the methodologies underlying the current techniques of single-cell genomics and epigenomics before covering their recent applications, potential significance, and future perspectives in plant biology.]]>
Wed, 31 Dec 1969 19:00:00 EST
Neonatal Lead (Pb) Exposure and DNA Methylation Profiles in Dried Bloodspots. Montrose L, Goodrich JM, Morishita M, Kochmanski J, Klaver Z, Cavalcante R, Lumeng JC, Peterson KE, Dolinoy DC
Int J Environ Res Public Health (Sep 2020)

Lead (Pb) exposure remains a major concern in the United States (US) and around the world, even following the removal of Pb from gasoline and other products. Environmental Pb exposures from aging infrastructure and housing stock are of particular concern to pregnant women, children, and other vulnerable populations. Exposures during sensitive periods of development are known to influence epigenetic modifications which are thought to be one mechanism of the Developmental Origins of Health and Disease (DOHaD) paradigm. To gain insights into early life Pb exposure-induced health risks, we leveraged neonatal dried bloodspots in a cohort of children from Michigan, US to examine associations between blood Pb levels and concomitant DNA methylation profiles ( = 96). DNA methylation analysis was conducted via the Infinium MethylationEPIC array and Pb levels were assessed via high resolution inductively coupled plasma mass spectrometry (HR-ICP-MS). While at-birth Pb exposure levels were relatively low (average 0.78 µg/dL, maximum of 5.27 ug/dL), we identified associations between DNA methylation and Pb at 33 CpG sites, with the majority (82%) exhibiting reduced methylation with increasing Pb exposure (q < 0.2). Biological pathways related to development and neurological function were enriched amongst top differentially methylated genes by -value. In addition to increases/decreases in methylation, we also demonstrate that Pb exposure is related to increased variability in DNA methylation at 16 CpG sites. More work is needed to assess the accuracy and precision of metals assessment using bloodspots, but this study highlights the utility of this unique resource to enhance environmental epigenetics research around the world.]]>
Wed, 31 Dec 1969 19:00:00 EST