About

Dr. Anya Brown is an Assistant Professor in the Department of Evolution and Ecology at UC Davis, based at the Bodega Marine Lab. Her research focuses on marine community ecology in both temperate and tropical systems. She has a particular interest in the interactions among hosts, microbes, and the environment, exploring how these relationships shape marine ecosystems. Dr. Brown leads a lab that investigates these complex ecological dynamics, contributing to a deeper understanding of marine biology and the factors influencing community structure and function in ocean habitats.

Research topics

• Biology
• Genetics
• Medicine
• Cell biology
• History
• Chemistry
• Evolutionary biology
• Neuroscience
• Immunology
• Organic chemistry
• Chromatography
• Computational biology

Selected publications

• Persistent transcriptomic changes following repeated exposure to wood smoke in non-human primate airway epithelial cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-16

  preprintOpen access

  Exposure to wildfire smoke is a significant public health concern with the respiratory system heavily impacted. Wildfire events are increasing in number and severity, and inhalation of wildfire smoke can lead to airway inflammation, oxidative stress-induced lung injury, impaired mucociliary clearance, and exacerbation of respiratory conditions such as asthma and chronic obstructive pulmonary disease (COPD). Despite these well-documented health risks, the molecular mechanisms underlying the respiratory effects of wildfire smoke exposure and recovery remain incompletely understood. In this study, we utilized transcriptomic and epigenomic analyses to investigate how exposure to wood smoke (WS) influences the expression patterns of gene networks in differentiated tracheobronchial epithelial cells. Our analysis identified exposure-induced differentially methylated regions, differentially expressed genes and gene networks that are implicated in lung disease, including dysregulation of immune responses, oxidative stress and cell death, compromise of epithelial barrier integrity and function, and epigenetic remodeling. Strikingly, significant transcriptomic changes were still detected one week after exposure cessation, enriched in pathways involved in inflammation, wound healing and tissue repair. Despite these transcriptomic and epigenomic perturbations, histology staining revealed no significant changes in epithelial tissue morphology following WS exposure. However, we found a significant number of pulmonary disease-associated genes and pathways whose transcription were affected by WS exposure. Our study enhances understanding of the molecular basis of wildfire smoke-induced respiratory effects and highlights the potential for WS to leave a lasting imprint on airway epithelium, with important implications for respiratory health in exposed populations.

  PublisherDOI

• Single-cell RNA-seq analysis reveals novel cell-cell communication interactions responsive to house dust mite and subject to TET1 regulation in the lung 9322

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description Epigenetic regulator, Tet1, protects against house dust mite (HDM)-induced allergic airway inflammation. We previously showed this may partially be due to the regulation of several stress response pathways by Tet1 in the airway epithelium. However, responses to HDM and the contribution of Tet1 in other lung cell types are unknown. A murine model of HDM-induced lung inflammation was established in Tet1 knockout and littermate wildtype mice. Total lung cells, as well as EpCAM+ airway epithelial cells, were subject to 10X Genomics single-cell RNA-seq workflow. ScRNA-seq analysis was performed using Cell Ranger, scAlign, and Seurat. Cell types were labeled using scMCA and confirmed using known markers. After 20 cell types were identified, cell communication networks were constructed using CellChat. While B cells were the most abundant immune cell type, macrophages had the most differentially expressed genes following HDM challenges. Loss of Tet1 and HDM challenges led to similar changes in cell-cell communication networks. Specifically, we observed an increased cell communication probability between innate lymphoid cells and both eosinophils and neutrophils via the CD40lg-(Itgam+Itgb2) interaction. Overall, exposure to HDM leads to cell-type-specific transcriptional changes which influence cross-talk between cell types in the lung, and such responses are regulated by Tet1. Funding Sources Supported by NIH/NIAID R01AI141569-01A1; T32 HL007013 Topic Categories Immediate Hypersensitivity, Asthma, and Allergic Responses (HYP)

  PublisherOA PDFDOI

• Silencing <i>TET1</i> expression alters the epigenomic landscape and amplifies transcriptomic responses to allergen in airway epithelial cells

  Current Zoology · 2025-01-01 · 1 citations

  articleOpen access1st authorCorresponding

  Abstract Previous studies have demonstrated that ten-eleven translocation methylcytosine dioxygenase 1 (TET1) plays a protective role against house dust mite (HDM)-induced allergic airway inflammation. TET1 transcriptionally responded to HDM extract and regulated the expression of genes involved in asthma in human bronchial epithelial cells (HBECs). How TET1 regulates the expression of these genes, however, is unknown. To this end, we measured mRNA expression, DNA methylation, chromatin accessibility, and histone modifications in control and TET1 knockdown HBECs treated or untreated with HDM extract. Throughout our analyses of multiomics data, we detected significant similarities between the effects of TET1 knockdown alone and the effects of HDM treatment alone, all enriched for asthma-related genes and pathways. One especially striking pattern was that both TET1 knockdown and HDM treatment generally led to decreased chromatin accessibility at many of the same genomic loci. Transcription factor enrichment analyses indicated that altered chromatin accessibility following the loss of TET1 may affect, or be affected by, CCCTC-binding factor and CCAAT-enhancer-binding protein binding. Analysis of H3K27ac levels and comparison with existing datasets suggested a potential impact of TET1 on enhancer activity. TET1 loss also led to changes in DNA methylation, but these changes were generally in regions where accessibility was not changing. Lastly, more significant transcriptomic changes were observed in HBEC cells with TET1 knockdown compared to control cells following HDM challenges. Collectively, our data suggest that TET1 regulates gene expression through distinct mechanisms across various genomic regions in airway epithelial cells, restricting transcriptomic responses to allergen and potentially protecting against the development of asthma.

  PublisherOA PDFDOI

• Contributors

  Elsevier eBooks · 2024-11-22

  book-chapterOpen access
  PublisherDOI

• The role of epigenetic mechanisms in lung diseases and environmental exposure

  Elsevier eBooks · 2024-11-22

  book-chapter
  PublisherDOI

• Integrative analyses of convergent adaptation in sympatric extremophile fishes

  Current Biology · 2024-10-11 · 12 citations

  articleOpen access
  PublisherOA PDFDOI

• The “epiTet” of Air Pollution: Epigenetic Regulation of Airway Inflammation by Tet1

  International Archives of Allergy and Immunology · 2023-01-01 · 4 citations

  articleOpen access
  PublisherOA PDFDOI

• E-Cigarette Vaping Causes Mucociliary Dysfunction Through Impaired Autophagy

  2023-05-01

  article
  PublisherDOI

• TET1 regulates responses to house dust mite by altering chromatin accessibility, DNA methylation, and gene expression in airway epithelial cells

  Research Square · 2023-12-13 · 2 citations

  preprintOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Serum plays an important role in reprogramming the seasonal transcriptional profile of brown bear adipocytes

  iScience · 2022-09-21 · 17 citations

  articleOpen access

  Understanding how metabolic reprogramming happens in cells will aid the progress in the treatment of a variety of metabolic disorders. Brown bears undergo seasonal shifts in insulin sensitivity, including reversible insulin resistance in hibernation. We performed RNA-sequencing on brown bear adipocytes and proteomics on serum to identify changes possibly responsible for reversible insulin resistance. We observed dramatic transcriptional changes, which depended on both the cell and serum season of origin. Despite large changes in adipocyte gene expression, only changes in eight circulating proteins were identified as related to the seasonal shifts in insulin sensitivity, including some that have not previously been associated with glucose homeostasis. The identified serum proteins may be sufficient for shifting hibernation adipocytes to an active-like state.

  PublisherOA PDFDOI

Frequent coauthors

• Joanna L. Kelley

  University of California, Santa Cruz

  22 shared

• Michael Tobler

  Saint Louis Zoo

  22 shared

• Lenin Arias‐Rodríguez

  Universidad Juárez Autónoma de Tabasco

  20 shared

• Ryan Greenway

  Kansas State University

  16 shared

• Kerry L. McGowan

  14 shared

• Hong Ji

  14 shared

• Lucy P. Cai

  University of California, Davis

  14 shared

• Matthew T. Weirauch

  Cincinnati Children's Hospital Medical Center

  12 shared

Labs

• Brown LabPI

Education

• PhD, Biology, School of Biological Sciences

  Washington State University

  2019

• Bachelor of Science, Biochemistry and Molecular Biology

  University of California, Davis

  2013