Joel Meyer

Overview:

Dr. Meyer studies the effects of toxic agents and stressors on human and wildlife health. He is particularly interested in understanding the mechanisms by which environmental agents cause DNA damage, the molecular processes that organisms employ to protect prevent and repair DNA damage, and genetic differences that may lead to increased or decreased sensitivity to DNA damage. Mitochondrial DNA damage and repair, as well as mitochondrial function in general, are a particular focus. He studies these effects in the nematode Caenorhabditis elegans, in cell culture, and collaboratively in other laboratory model organisms as well as in human populations in the USA and globally.

Positions:

Truman and Nellie Semans/Alex Brown and Sons Associate Professor of Molecular Environmental Toxicology

Environmental Sciences and Policy
Nicholas School of the Environment

Associate Professor of Environmental Genomics in the Division of Environmental Sciences and Policy

Environmental Sciences and Policy
Nicholas School of the Environment

Faculty Network Member of The Energy Initiative

Nicholas Institute-Energy Initiative
Institutes and Provost's Academic Units

Affiliate, Duke Global Health Institute

Duke Global Health Institute
Institutes and Provost's Academic Units

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 1992

Juniata College

Ph.D. 2003

Duke University

Grants:

Center for Environmental Implications of Nanotechnology

Administered By
Pratt School of Engineering
Awarded By
National Science Foundation
Role
Investigator
Start Date
End Date

Fluoride and human health: Assessing novel biomarkers in detecting bone disorder

Administered By
Earth and Climate Sciences
Awarded By
National Institutes of Health
Role
Collaborator
Start Date
End Date

COPAS BIOSORT Worm Sorter

Administered By
Neurology, Headache and Pain
Awarded By
National Institutes of Health
Role
Collaborator
Start Date
End Date

Are mitochondria a major target of antimicrobial silver nanoparticles?

Administered By
Environmental Sciences and Policy
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

GW150184 Mitochondrial dysfunction and Gulf War Illness

Administered By
Environmental Sciences and Policy
Awarded By
United States Army Medical Research Acquisition Activity
Role
Principal Investigator
Start Date
End Date

Publications:

PCR-Based Determination of Mitochondrial DNA Copy Number in Multiple Species.

Mitochondrial DNA (mtDNA) copy number is a critical component of overall mitochondrial health. In this chapter, we describe methods for simultaneous isolation of mtDNA and nuclear DNA (nucDNA), and measurement of their respective copy numbers using quantitative PCR. Methods differ depending on the species and cell type of the starting material, and availability of specific PCR reagents. We also briefly describe factors that affect mtDNA copy number and discuss caveats to its use as a biomarker.
Authors
Leuthner, TC; Hartman, JH; Ryde, IT; Meyer, JN
MLA Citation
Leuthner, Tess C., et al. “PCR-Based Determination of Mitochondrial DNA Copy Number in Multiple Species.Methods in Molecular Biology (Clifton, N.J.), vol. 2310, Jan. 2021, pp. 91–111. Epmc, doi:10.1007/978-1-0716-1433-4_8.
URI
https://scholars.duke.edu/individual/pub1484742
PMID
34096001
Source
epmc
Published In
Methods in Molecular Biology (Clifton, N.J.)
Volume
2310
Published Date
Start Page
91
End Page
111
DOI
10.1007/978-1-0716-1433-4_8

Mitochondrial DNA Mutagenesis: Feature of and Biomarker for Environmental Exposures and Aging.

PURPOSE OF REVIEW: Mitochondrial dysfunction is a hallmark of aging. Mitochondrial genome (mtDNA) instability contributes to mitochondrial dysfunction, and mtDNA mutagenesis may contribute to aging. However, the origin of mtDNA mutations remains somewhat controversial. The goals of this review are to introduce and review recent literature on mtDNA mutagenesis and aging, address recent animal and epidemiological evidence for the effects of chemicals on mtDNA damage and mutagenesis, propose hypotheses regarding the contribution of environmental toxicant exposure to mtDNA mutagenesis in the context of aging, and suggest future directions and approaches for environmental health researchers. RECENT FINDINGS: Stressors such as pollutants, pharmaceuticals, and ultraviolet radiation can damage the mitochondrial genome or disrupt mtDNA replication, repair, and organelle homeostatic processes, potentially influencing the rate of accumulation of mtDNA mutations. Accelerated mtDNA mutagenesis could contribute to aging, diseases of aging, and sensitize individuals with pathogenic mtDNA variants to stressors. We propose three potential mechanisms of toxicant-induced effects on mtDNA mutagenesis over lifespan: (1) increased de novo mtDNA mutations, (2) altered frequencies of mtDNA mutations, or (3) both. There are remarkably few studies that have investigated the impact of environmental chemical exposures on mtDNA instability and mutagenesis, and even fewer in the context of aging. More studies are warranted because people are exposed to tens of thousands of chemicals, and are living longer. Finally, we suggest that toxicant-induced mtDNA damage and mutational signatures may be a sensitive biomarker for some exposures.
Authors
Leuthner, TC; Meyer, JN
MLA Citation
Leuthner, Tess C., and Joel N. Meyer. “Mitochondrial DNA Mutagenesis: Feature of and Biomarker for Environmental Exposures and Aging.Curr Environ Health Rep, Nov. 2021. Pubmed, doi:10.1007/s40572-021-00329-1.
URI
https://scholars.duke.edu/individual/pub1501344
PMID
34761353
Source
pubmed
Published In
Current Environmental Health Reports
Published Date
DOI
10.1007/s40572-021-00329-1

Early-life mitochondrial DNA damage results in lifelong deficits in energy production mediated by redox signaling in Caenorhabditis elegans.

The consequences of damage to the mitochondrial genome (mtDNA) are poorly understood, although mtDNA is more susceptible to damage resulting from some genotoxicants than nuclear DNA (nucDNA), and many environmental toxicants target the mitochondria. Reports from the toxicological literature suggest that exposure to early-life mitochondrial damage could lead to deleterious consequences later in life (the "Developmental Origins of Health and Disease" paradigm), but reports from other fields often report beneficial ("mitohormetic") responses to such damage. Here, we tested the effects of low (causing no change in lifespan) levels of ultraviolet C (UVC)-induced, irreparable mtDNA damage during early development in Caenorhabditis elegans. This exposure led to life-long reductions in mtDNA copy number and steady-state ATP levels, accompanied by increased oxygen consumption and altered metabolite profiles, suggesting inefficient mitochondrial function. Exposed nematodes were also developmentally delayed, reached smaller adult size, and were rendered more susceptible to subsequent exposure to chemical mitotoxicants. Metabolomic and genetic analysis of key signaling and metabolic pathways supported redox and mitochondrial stress-response signaling during early development as a mechanism for establishing these persistent alterations. Our results highlight the importance of early-life exposures to environmental pollutants, especially in the context of exposure to chemicals that target mitochondria.
Authors
Hershberger, KA; Rooney, JP; Turner, EA; Donoghue, LJ; Bodhicharla, R; Maurer, LL; Ryde, IT; Kim, JJ; Joglekar, R; Hibshman, JD; Smith, LL; Bhatt, DP; Ilkayeva, OR; Hirschey, MD; Meyer, JN
MLA Citation
Hershberger, Kathleen A., et al. “Early-life mitochondrial DNA damage results in lifelong deficits in energy production mediated by redox signaling in Caenorhabditis elegans.Redox Biol, vol. 43, July 2021, p. 102000. Pubmed, doi:10.1016/j.redox.2021.102000.
URI
https://scholars.duke.edu/individual/pub1482924
PMID
33993056
Source
pubmed
Published In
Redox Biology
Volume
43
Published Date
Start Page
102000
DOI
10.1016/j.redox.2021.102000

Analysis of Illumina 450K DNA Methylation in NEST Cord Blood Reveals Sex Differences at Mitochondrial Genes in the Nuclear Genome.

Authors
King, D; Martinez, M; Lloyd, D; Maguire, R; Hoyo, C; Meyer, JN; Murphy, SK
MLA Citation
King, D., et al. “Analysis of Illumina 450K DNA Methylation in NEST Cord Blood Reveals Sex Differences at Mitochondrial Genes in the Nuclear Genome.Environmental and Molecular Mutagenesis, vol. 61, 2020, pp. 34–35.
URI
https://scholars.duke.edu/individual/pub1467214
Source
wos-lite
Published In
Environmental and Molecular Mutagenesis
Volume
61
Published Date
Start Page
34
End Page
35

Evaluation of Peruvian Government Interventions to Reduce Childhood Anemia.

<h4>Background</h4>In Peru, anemia has been a persistent health problem that is known to lead to irreversible cognitive and developmental deficits in children. The Peruvian government has recently made anemia a primary health concern by passing legislation in 2017 that makes anemia an intersectoral priority. This new legislation fortifies previous programs while creating new programs that target specific age groups.<h4>Objectives</h4>Evaluate the effectiveness of government programs in Madre de Dios, Peru to reduce anemia prevalence and increase hemoglobin levels among children ages 2-11 years old.<h4>Methods</h4>Propensity scores are used to match 688 children enrolled in 2018, after the legislation, and 2,140 children enrolled in previous studies our team conducted in the region between 2014 and 2017, based on sex, age (years), intervention status (prior/post), community income, presence of a health post in the community (yes/no), community type (indigenous, non-indigenous rural, non-indigenous urban) and road access (fraction of the number of months out of the year with road access). A pseudo matched case-control analysis to evaluate changes in anemia prevalence and hemoglobin was conducted using t-tests and multivariate models. Program effectiveness is evaluated overall, by age groups (2-4, 5-7 and 8-11 years old), and community type (indigenous vs. urban).<h4>Findings</h4>The adjusted odds ratio indicated lower odds of anemia (OR = 0.31, 95%CI 0.17-0.54) for children exposed to the anemia prevention programs vs. those not exposed. The effect was not significantly different across age groups; however, the intervention effects significantly differed by community type among children 8-11 years old, with urban children less likely to benefit from anemia interventions (OR = 0.69, 95% CI 0.38-1.25) compared to indigenous children (OR = 0.21, 95% CI 0.08-0.56).<h4>Conclusion</h4>Government programs to reduce anemia in Madre de Dios were found to be associated with reduced anemia prevalence in the study communities. However, the lack of program monitoring precludes the attribution of anemia decline to specific interventions or program components. In addition, regional anemia prevalence remains high according to the 2019 Demographic and Health Survey, suggesting impaired population impact. Program monitoring and evaluation is a key component of health interventions to improve program implementation effectiveness.
Authors
Berky, AJ; Robie, E; Ortiz, EJ; Meyer, JN; Hsu-Kim, H; Pan, WK
MLA Citation
Berky, Axel J., et al. “Evaluation of Peruvian Government Interventions to Reduce Childhood Anemia.Annals of Global Health, vol. 86, no. 1, Aug. 2020, p. 98. Epmc, doi:10.5334/aogh.2896.
URI
https://scholars.duke.edu/individual/pub1457432
PMID
32864350
Source
epmc
Published In
Annals of Global Health
Volume
86
Published Date
Start Page
98
DOI
10.5334/aogh.2896

Research Areas:

Abnormalities, Drug-Induced
Aldehydes
Benzopyrans
Calcium
Calibration
Cell Survival
DNA Replication
Dose-Response Relationship, Drug
Energy Metabolism
Fluorenes
Genotype
Half-Life
HeLa Cells
Heart
Heart Defects, Congenital
Humic Substances
Laboratories
Larva
Molecular Structure
Mutation
Neoplasm Proteins
Phosphorylation
Ponds
Proteolysis
Silver Nitrate
Solubility
Structure-Activity Relationship
Sulfides
Toxicity Tests
Transcriptome