About

Professor David L. Aylor is a researcher at North Carolina State University leading the Aylor Lab. His research focuses on understanding how genetic variation influences complex traits, susceptibility to disease, and molecular biology at the individual level. The lab investigates the genetic and environmental factors that contribute to prevalent human diseases, agriculturally important traits, and evolutionary fitness, all of which are complex traits affected by multiple factors. Aylor's work aims to identify quantitative trait loci (QTL), which are genetic variants that impact complex traits. His research addresses the challenges of small effect sizes of individual factors and their interactions with the environment and other genes. The lab develops and applies systems genetics approaches to discover QTL and elucidate their mechanisms, with the goal of translating findings from model organisms to humans and uncovering new principles of genetics and genome science.

Research topics

• Biology
• Genetics
• Medicine
• Bioinformatics
• Neuroscience
• Endocrinology
• Cell biology
• Pharmacology
• Food science
• Biochemistry
• Cardiology
• Internal medicine

Selected publications

• Early-Life Environmental Exposures Reprogram Epigenomic Aging to Alter Gene Expression Trajectories

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-04-22

  preprintOpen access

  ABSTRACT To understand how early-life environmental exposures shape health and disease risk across the lifecourse, the TaRGET II Consortium exposed mice to diverse toxicants from pre-conception through weaning, and followed individual animals into adulthood, generating over 800 epigenomic and transcriptomic profiles. These profiles revealed that early-life exposures induced persistent epigenomic reprogramming and significantly disrupted the adult transcriptome. Notably, despite their diverse mechanisms of action, the exposure signatures of the xenoestrogen BPA, obesogen TBT, dioxin TCDD, and air pollutant PM2.5, were all largely comprised of genes normally differentially expressed during liver aging. Epigenetic histone modifications at enhancers—and, to a lesser extent, promoters—emerged as key targets for this reprogramming. Despite differing mechanisms of action, these four toxicants imparted similar “fingerprints” on the adult liver, characterized by direction-and cell type-specific polarization of the transcriptome. Hepatocyte genes that typically increase with age, particularly those in metabolic pathways, were downregulated, while conversely, non-parenchymal cell genes that typically decrease with age, such as those involved in extracellular matrix production, were upregulated. A similar signature of anti-correlation with programmed aging aging was also found in the transcriptome of patients with liver disease and hepatocellular carcinoma (HCC), and was effective at distinguishing healthy from diseased human livers. These findings demonstrate that the plasticity of epigenomic aging is vulnerable to early-life environmental exposures, which can reprogram the epigenome with lasting impacts on the transcriptome, and disease risk, later in life.

  PublisherOA PDFDOI

• Toxicogenomic Insights into Environmental Toxicant Exposures: The TaRGET II Resource

  Research Square · 2025-08-20

  preprintOpen access
  PublisherOA PDFDOI

• Cross-tissue molecular responses in the liver and blood after toxicant exposures

  Research Square · 2025-10-10 · 1 citations

  preprintOpen access
  PublisherOA PDFDOI

• Plasticity of Epigenomic and Transcriptomic Aging Reveals Common Targets for Reprogramming by Environmental Exposures

  Research Square · 2025-09-19 · 1 citations

  preprintOpen access
  PublisherDOI

• Phenotype variability in diet-induced obesity and response to (−)-epigallocatechin gallate supplementation in a Diversity Outbred mouse cohort: A model for exploring gene x diet interactions for dietary bioactives

  Nutrition Research · 2024 · 2 citations

  • Biology
  • Genetics
  • Food science
  PublisherDOI

• Impacts of Gestational FireMaster 550 Exposure on the Neonatal Cortex Are Sex Specific and Largely Attributable to the Organophosphate Esters

  Neuroendocrinology · 2022-09-08 · 19 citations

  articleOpen access

  INTRODUCTION: Flame retardants (FRs) are common bodily and environmental pollutants, creating concern about their potential toxicity. We and others have found that the commercial mixture FireMaster® 550 (FM 550) or its individual brominated (BFR) and organophosphate ester (OPFR) components are potential developmental neurotoxicants. Using Wistar rats, we previously reported that developmental exposure to FM 550 or its component classes produced sex- and compound-specific effects on adult socioemotional behaviors. The underlying mechanisms driving the behavioral phenotypes are unknown. METHODS: To further mechanistic understanding, here we conducted transcriptomics in parallel with a novel lipidomics approach using cortical tissues from newborn siblings of the rats in the published behavioral study. Inclusion of lipid composition is significant because it is rarely examined in developmental neurotoxicity studies. Pups were gestationally exposed via oral dosing to the dam to FM 550 or the BFR or OPFR components at environmentally relevant doses. RESULTS: The neonatal cortex was highly sexually dimorphic in lipid and transcriptome composition, and males were more significantly impacted by FR exposure. Multiple adverse modes of action for the BFRs and OPFRs on neurodevelopment were identified, with the OPFRs being more disruptive than the BFRs via multiple mechanisms including dysregulation of mitochondrial function and disruption of cholinergic and glutamatergic systems. Disrupted mitochondrial function by environmental factors has been linked to a higher risk of autism spectrum disorders and neurodegenerative disorders. Impacted lipid classes included ceramides, sphingomyelins, and triacylglycerides. Robust ceramide upregulation in the OPFR females could suggest a heightened risk of brain metabolic disease. CONCLUSIONS: This study reveals multiple mechanisms by which the components of a common FR mixture are developmentally neurotoxic and that the OPFRs may be the compounds of greatest concern.

  PublisherOA PDFDOI

• A cross-species approach using an in vivo evaluation platform in mice demonstrates that sequence variation in human RABEP2 modulates ischemic stroke outcomes

  The American Journal of Human Genetics · 2022 · 6 citations

  • Biology
  • Genetics
  • Bioinformatics
  PublisherOA PDFDOI

• A Neuroprotective Locus Modulates Ischemic Stroke Infarction Independent of Collateral Vessel Anatomy

  Frontiers in Neuroscience · 2021 · 6 citations

  • Biology
  • Genetics
  • Neuroscience

  Although studies with inbred strains of mice have shown that infarct size is largely determined by the extent of collateral vessel connections between arteries in the brain that enable reperfusion of the ischemic territory, we have identified strain pairs that do not vary in this vascular phenotype, but which nonetheless exhibit large differences in infarct size. In this study we performed quantitative trait locus (QTL) mapping in mice from an intercross between two such strains, WSB/EiJ (WSB) and C57BL/6J (B6). This QTL mapping revealed only one neuroprotective locus on Chromosome 8 (Chr 8) that co-localizes with a neuroprotective locus we mapped previously from F2 progeny between C3H/HeJ (C3H) and B6. The allele-specific phenotypic effect on infarct volume at the genetic region identified by these two independent mappings was in the opposite direction of the parental strain phenotype; namely, the B6 allele conferred increased susceptibility to ischemic infarction. Through two reciprocal congenic mouse lines with either the C3H or B6 background at the Chr 8 locus, we verified the neuroprotective effects of this genetic region that modulates infarct volume without any effect on the collateral vasculature. Additionally, we surveyed non-synonymous coding SNPs and performed RNA-sequencing analysis to identify potential candidate genes within the genetic interval. Through these approaches, we suggest new genes for future mechanistic studies of infarction following ischemic stroke, which may represent novel gene/protein targets for therapeutic development.

  PublisherDOI

• Integrative Genetic Analysis of Allergic Inflammation in the Murine Lung

  UNC Libraries · 2020-10-30

  articleOpen accessSenior author

  Airway allergen exposure induces inflammation among individuals with atopy that is characterized by altered airway gene expression, elevated levels of T helper type 2 cytokines, mucus hypersecretion, and airflow obstruction. To identify the genetic determinants of the airway allergen response, we employed a systems genetics approach. We applied a house dust mite mouse model of allergic airway disease to 151 incipient lines of the Collaborative Cross, a new mouse genetic reference population, and measured serum IgE, airway eosinophilia, and gene expression in the lung. Allergen-induced serum IgE and airway eosinophilia were not correlated. We detected quantitative trait loci (QTL) for airway eosinophilia on chromosome (Chr) 11 (71.802–87.098 megabases [Mb]) and allergen-induced IgE on Chr 4 (13.950–31.660 Mb). More than 4,500 genes expressed in the lung had gene expression QTL (eQTL), the majority of which were located near the gene itself. However, we also detected approximately 1,700 trans-eQTL, and many of these trans-eQTL clustered into two regions on Chr 2. We show that one of these loci (at 147.6 Mb) is associated with the expression of more than 100 genes, and, using bioinformatics resources, fine-map this locus to a 53 kb-long interval. We also use the gene expression and eQTL data to identify a candidate gene, Tlcd2, for the eosinophil QTL. Our results demonstrate that hallmark allergic airway disease phenotypes are associated with distinct genetic loci on Chrs 4 and 11, and that gene expression in the allergically inflamed lung is controlled by both cis and trans regulatory factors.

  PublisherDOI

• Genetic analysis of complex traits in the emerging Collaborative Cross

  UNC Libraries · 2020-11-02

  articleOpen access

  The Collaborative Cross (CC) is a mouse recombinant inbred strain panel that is being developed as a resource for mammalian systems genetics. Here we describe an experiment that uses partially inbred CC lines to evaluate the genetic properties and utility of this emerging resource. Genome-wide analysis of the incipient strains reveals high genetic diversity, balanced allele frequencies, and dense, evenly distributed recombination sites—all ideal qualities for a systems genetics resource. We map discrete, complex, and biomolecular traits and contrast two quantitative trait locus (QTL) mapping approaches. Analysis based on inferred haplotypes improves power, reduces false discovery, and provides information to identify and prioritize candidate genes that is unique to multifounder crosses like the CC. The number of expression QTLs discovered here exceeds all previous efforts at eQTL mapping in mice, and we map local eQTL at 1-Mb resolution. We demonstrate that the genetic diversity of the CC, which derives from random mixing of eight founder strains, results in high phenotypic diversity and enhances our ability to map causative loci underlying complex disease-related traits.

  PublisherDOI

Recent grants

• Epigenetics, environmental exposure, and reproduction in the Collaborative Cross

  NIH · $723k · 2014–2018

• Epigenetics, environmental exposure, and reproduction in the Collaborative Cross

  NIH · $176k · 2012–2014

• System Genetics of Male Infertility in the Collaborative Cross

  NIH · $96k · 2010–2012

• Systems Toxicogenomics of Endocrine Disrupting Chemicals in Brain

  NIH · $2.9M · 2016–2022

Frequent coauthors

• Fernando Pardo‐Manuel de Villena

  University of North Carolina at Charlotte

  29 shared

• Darla R. Miller

  22 shared

• David W. Threadgill

  Texas A&M University

  20 shared

• Timothy A. Bell

  19 shared

• Elissa J. Chesler

  Jackson Laboratory

  17 shared

• Gary A. Churchill

  16 shared

• Samir N. P. Kelada

  University of North Carolina at Chapel Hill

  14 shared

• Francis S. Collins

  National Institutes of Health

  13 shared

Labs

• Aylor LabPI