Ramon Lavado
Baylor University, TX·Ecology & Evolution
Some fish populations living in heavily polluted estuaries have evolved, over just a few generations, to survive chemical exposures that kill fish from clean sites. Understanding how they do it reveals both how quickly wildlife can adapt and what such adaptation costs.
- Fields
Ecology & Evolution
Pharmacology
Earth & Environmental Science
- Topics
Gulf killifish
Fundulus grandis
aryl hydrocarbon receptor
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Quantify how the aryl hydrocarbon receptor deletion in adapted Gulf killifish changes the rate and products of phase I and phase II biotransformation of benzo[a]pyrene, a model polycyclic aromatic hydrocarbon.
- Determine whether the altered metabolic routes in adapted fish generate less toxic or more toxic metabolites, distinguishing a fitness cost of adaptation from a compensatory alternative pathway.
- Test whether the receptor deletion lowers proinflammatory cytokine levels across tissues, using the immune response as an example of a receptor-linked pathway unrelated to biotransformation.
- Compare adapted Galveston Bay populations with sensitive populations using metabolomics and transcriptomics to identify compensatory changes that could explain cross-resistance to contaminants with different modes of action.
More about the research
This project uses Gulf killifish (Fundulus grandis) from Galveston Bay, which resist the heart defects normally caused by two widespread classes of industrial pollutants: polychlorinated biphenyls and polycyclic aromatic hydrocarbons, the latter formed whenever fuels burn.
Why it matters
Knowing which biochemical changes accompany pollutant resistance helps predict which wild populations are vulnerable to chemical stressors and which have hidden trade-offs, information useful for assessing contaminated estuaries such as Galveston Bay. Because the same biotransformation enzymes and the aryl hydrocarbon receptor operate in humans, the findings may also inform how differences in chemical metabolism translate into differences in susceptibility and immune response.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Shelley Tischkau
Southern Illinois University-Carbondale, IL·Physiology
Test whether restricted feeding, limiting food intake to set times of day, can reset circadian clock function and restore adipose tissue rhythms after the clock is disrupted by chronic activation of the aryl hydrocarbon receptor (AhR) by pollutants such as dioxins.
John Mountz
University of Alabama at Birmingham, AL·Microbiology & Immunology
Determine which IL-4-induced tryptophan metabolic signals block TLR7-driven autoantibody-precursor B cells in vivo, comparing wild-type mice with mice lacking the B-cell enzymes IL4i1 and Ido1 or the metabolite sensor AhR.
Collynn Woeller
University of Rochester, NY·Microbiology & Immunology
Define the molecular steps by which the aryl hydrocarbon receptor, a chemical-sensing transcription factor, blocks activation of orbital fibroblasts — the connective-tissue cells behind the eye that turn into fat cells and scar-forming myofibroblasts in thyroid eye disease.
The school
Baylor University: 5 labs on PI Pages, $135M a year on research, 280 research doctorates a year.
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