About

Jessica S. Plavicki is an Associate Professor of Pathology and Laboratory Medicine at Brown University. Her research focuses on cardiac, cardiovascular, neuroscience, neurovascular diseases, toxicology, vascular biology, and zebrafish models. She has contributed to understanding the cellular complexity of zebrafish gonads, the effects of environmental pollutants such as dioxins on development, and the molecular mechanisms underlying neural connectivity and heart malformation. Her work often involves assessing the impact of toxic substances on embryonic development and vascular formation, utilizing zebrafish as a model organism. Dr. Plavicki holds a PhD from the University of Wisconsin at Madison and a BA from the University of Texas at Austin. She has received numerous awards for her research, mentoring, and teaching, including the NIH Outstanding New Environmental Scientist Award and the Brown University Graduate School Faculty Award for Advising & Mentoring. Her contributions extend to advancing understanding in developmental biology, toxicology, and environmental health, with a particular emphasis on the molecular pathways affected by environmental toxins.

Research topics

• Biology
• Biochemistry
• Cell biology
• Neuroscience
• Genetics
• Chemistry

Selected publications

• THRESHOLD: a comprehensive transcriptomic analysis tool for evaluating gene saturation and impact in disease progression

  NAR Cancer · 2025-09-09

  articleOpen access

  Abstract Gene expression studies are fundamental in molecular biology, offering insights into development, disease progression, and therapeutic targets. To address the need for precise analysis of large datasets, we developed THRESHOLD, a novel tool that introduces the concept of gene saturation. Unlike traditional methods focused on absolute or binary expression levels, THRESHOLD quantifies the consistency of gene expression across patients, revealing co-regulation patterns critical for understanding disease mechanisms and stratifying patients by molecular signatures. The tool offers several features, including user-defined parameters, statistical comparisons, and interactive data visualization. THRESHOLD has uncovered compelling insights into disease progression using TCGA cancer datasets. For instance, bladder urothelial carcinoma demonstrated increasing upregulated gene saturation in progressive cancer stages (P < .00001). Moreover, THRESHOLD identified heightened gene saturation in patients with earlier onset of prostate adenocarcinoma (P < .0001) and revealed a critical fusion transcript, SLC45A2-AMACR, implicated in prostate adenocarcinoma progression, recurrence, and metastasis. Additionally, novel biomarkers and potential candidates for drug therapies were identified through protein–protein interaction networks and functional analyses of saturation data in colon adenocarcinoma and breast invasive carcinoma. THRESHOLD offers a new approach for studying gene expression dynamics and patient stratification. The tool is publicly available at Zenodo: https://zenodo.org/records/15287195.

  PublisherOA PDFDOI

• Erratum: “Evaluation of Neural Regulation and Microglial Responses to Brain Injury in Larval Zebrafish Exposed to Perfluorooctane Sulfonate”

  Environmental Health Perspectives · 2025-06-01 · 1 citations

  erratumOpen accessSenior author
  PublisherOA PDFDOI

• Metabolomic Changes Following Genx and Pfbs Exposure in Developing Zebrafish

  SSRN Electronic Journal · 2024-01-01

  preprintOpen access
  PublisherDOI

• THRESHOLD: A Comprehensive Transcriptomic Analysis Tool for Evaluating Gene Saturation and Impact in Disease Progression

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-10-22

  preprintOpen access

  Abstract Gene expression studies serve as a foundational tool in molecular biology, providing insights into developmental, physiological, and pathological processes. Variations in gene expression can indicate disease states, which are vital in understanding disease progression, subtype manifestations, and identifying therapeutic targets based on detailed expression patterns. To effectively investigate gene expression patterns, especially in large datasets, a robust and precise analysis tool is crucial. In response to this critical analytical need, we developed THRESHOLD, a novel tool that goes beyond traditional gene expression analysis by introducing the concept of gene saturation. Unlike conventional methods that focus on absolute expression levels or binary differential expression, THRESHOLD quantifies the consistency of gene expression across patients, revealing co-regulation patterns that may otherwise be overlooked. This novel metric offers a unique perspective on gene expression patterns by highlighting consistent trends across patient samples, which are critical for understanding disease mechanisms and stratifying patients based on molecular signatures. The tool offers several features, including user-defined parameters, statistical comparisons, and interactive data visualization. THRESHOLD has uncovered compelling insights into disease progression using TCGA Cancer Datasets. For instance, bladder urothelial carcinoma demonstrated increasing upregulated gene saturation in progressive cancer stages (p < 0.00001). Moreover, THRESHOLD identified heightened gene saturation in patients with earlier onset of prostate adenocarcinoma (p < 0.0001) and revealed a critical fusion transcript, SLC45A2-AMACR, implicated in prostate adenocarcinoma progression, recurrence, and metastasis. Additionally, novel biomarkers and potential candidates for drug therapies were identified through protein-protein interaction networks and functional analyses of saturation data in colon adenocarcinoma and breast invasive carcinoma. Collectively, THRESHOLD advances our understanding of patient stratification and molecular signatures by offering a more detailed view of gene expression dynamics. The THRESHOLD tool is publicly available at: https://github.com/alperuzun/THRESHOLD .

  PublisherDOI

• Building methodological consensus to ensure rigor and reproducibility in zebrafish fertility research

  Aquatic Toxicology · 2024-04-26 · 3 citations

  reviewOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Loss of developmentally derived Irf8+ macrophages promotes hyperinnervation and arrhythmia in the adult zebrafish heart

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-04-20

  preprintOpen accessSenior authorCorresponding

  SUMMARY Recent developments in cardiac macrophage biology have broadened our understanding of the critical functions of macrophages in the heart. As a result, there is further interest in understanding the independent contributions of distinct subsets of macrophage to cardiac development and function. Here, we demonstrate that genetic loss of interferon regulatory factor 8 (Irf8)-positive embryonic-derived macrophages significantly disrupts cardiac conduction, chamber function, and innervation in adult zebrafish. At 4 months post-fertilization (mpf), homozygous irf8 st96/st96 mutants have significantly shortened atrial action potential duration and significant differential expression of genes involved in cardiac contraction. Functional in vivo assessments via electro- and echocardiograms at 12 mpf reveal that irf8 mutants are arrhythmogenic and exhibit diastolic dysfunction and ventricular stiffening. To identify the molecular drivers of the functional disturbances in irf8 null zebrafish, we perform single cell RNA sequencing and immunohistochemistry, which reveal increased leukocyte infiltration, epicardial activation, mesenchymal gene expression, and fibrosis. Irf8 null hearts are also hyperinnervated and have aberrant axonal patterning, a phenotype not previously assessed in the context of cardiac macrophage loss. Gene ontology analysis supports a novel role for activated epicardial-derived cells (EPDCs) in promoting neurogenesis and neuronal remodeling in vivo . Together, these data uncover significant cardiac abnormalities following embryonic macrophage loss and expand our knowledge of critical macrophage functions in heart physiology and governing homeostatic heart health.

  PublisherOA PDFDOI

• Metabolomic changes following GenX and PFBS exposure in developing zebrafish

  Aquatic Toxicology · 2024-04-03 · 11 citations

  articleOpen accessCorresponding
  PublisherOA PDFDOI

• Exposure to the persistent organic pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) disrupts development of the zebrafish inner ear

  Aquatic Toxicology · 2023-04-12 · 9 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Metabolomic Changes Following Genx and Pfbs Exposure in Developing Zebrafish

  SSRN Electronic Journal · 2023-01-01

  preprintOpen access
  PublisherDOI

• Exposure to the persistent organic pollutant 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, dioxin) disrupts development of the zebrafish inner ear

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-03-15 · 2 citations

  preprintOpen accessSenior authorCorresponding

  Abstract Dioxins are a class of highly toxic and persistent environmental pollutants that have been shown through epidemiological and laboratory-based studies to act as developmental teratogens. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most potent dioxin congener, has a high affinity for the aryl hydrocarbon receptor (AHR), a ligand activated transcription factor. TCDD-induced AHR activation during development impairs nervous system, cardiac, and craniofacial development. Despite the robust phenotypes previously reported, the characterization of developmental malformations and our understanding of the molecular targets mediating TCDD-induced developmental toxicity remains limited. In zebrafish, TCDD-induced craniofacial malformations are produced, in part, by the downregulation of SRY-box transcription factor 9b ( sox9b ), a member of the SoxE gene family. sox9b , along with fellow SoxE gene family members sox9a and sox10 , have important functions in the development of the otic placode, the otic vesicle, and, ultimately, the inner ear. Given that sox9b in a known target of TCDD and that transcriptional interactions exist among SoxE genes, we asked whether TCDD exposure impaired the development of the zebrafish auditory system, specifically the otic vesicle, which gives rise to the sensory components of the inner ear. Using immunohistochemistry, in vivo confocal imaging, and time-lapse microscopy, we assessed the impact of TCDD exposure on zebrafish otic vesicle development. We found exposure resulted in structural deficits, including incomplete pillar fusion and altered pillar topography, leading to defective semicircular canal development. The observed structural deficits were accompanied by reduced collagen type II expression in the ear. Together, our findings reveal the otic vesicle as a novel target of TCDD-induced toxicity, suggest that the function of multiple SoxE genes may be affected by TCDD exposure, and provide insight into how environmental contaminants contribute to congenital malformations. Highlights The zebrafish ear is necessary to detect changes in motion, sound, and gravity. Embryos exposed to TCDD lack structural components of the developing ear. TCDD exposure impairs formation of the fusion plate and alters pillar topography. The semicircular canals of the ear are required to detect changes in movement. Following TCDD exposure embryos fail to establish semicircular canals.

  PublisherOA PDFDOI

Recent grants

• Hemorrhage and Thrombosis in Extracorporeal Life Support

  NIH · $42.3M · 2022–2025

• Ahr2 activation and sox9b function in forebrain and cerebral vascular development

  NIH · $724k · 2017–2020

• Ahr2 activation and sox9b function in forebrain and cerebral vascular development

  NIH · $198k · 2014–2016

Frequent coauthors

• Nathan R. Martin

  Brown University

  33 shared

• Katherine E. Manz

  University of Michigan–Ann Arbor

  25 shared

• Kurt D. Pennell

  Providence College

  23 shared

• Michelle E. Kossack

  John Brown University

  22 shared

• Ratna Patel

  Providence College

  21 shared

• Layra G. Cintrón-Rivera

  21 shared

• Nicole Burns

  University of Colorado Denver

  17 shared

• Manuel Camarillo

  Brown University

  16 shared

Education

• Ph.D., Neuroscience

  University of Wisconsin Madison

  2009

• B.A., Psychology

  University of Texas at Austin

  2000

Awards & honors

• Graduate School Faculty Award for Advising & Mentoring, Brow…
• New-Career Scientist Award, Reproductive & Developmental Spe…
• Paper of the Year Award, Northeast Chapter of the Society of…
• National Institute of Environmental Health Sciences Outstand…
• Named the Manning Assistant Professor of Pathology and Labor…