Maxwell E. Miller

Marine Biodiscovery

Marine scientist and biochemist interested in bioprospecting in the deep sea and extreme marine habitats. Joining University of Florida’s Whitney Laboratory for Marine Bioscience in August 2026 to investigate biomineralization and help develop the sea anemone Nematostella vectensis as a platform for protein expression.

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Research directions

Marine natural products & biodiscovery

Discovering useful chemistry from underexplored marine life and connecting biological diversity to function.

Marine model systems & biological tools

Developing marine organisms, proteins, pathways, and processes into experimental and biotechnology tools.

Deep-sea & extreme marine habitats

Exploring environments where unusual conditions may drive distinctive biology, metabolism, and chemistry.

Incoming work at Whitney

Beginning August 2026

Beginning in August 2026, I will work with Drs. Mark Martindale and Sandra Loesgen at the Whitney Laboratory for Marine Bioscience. The project will investigate biomineralization pathways and help develop the sea anemone Nematostella vectensis as a platform for protein expression. The longer-term vision is to determine whether a genetically tractable anemone can reproduce aspects of coral-like biomineralization, informally, to “turn an anemone into a coral.” More broadly, I am interested in how marine organisms and their molecular machinery can become new research and biotechnology tools.

Working with Dr. Martindale will deepen my understanding of cnidarian development, evolution, and marine model systems. Dr. Loesgen’s expertise in natural products and organic chemistry will provide a complementary chemical perspective, creating a particularly strong environment for connecting organismal biology with marine biodiscovery.

Featured publication

Madison L. Sangster, Martha M. Bishop, Yizheng Yao, Jessica F. Feitor, Sanjid Shahriar, Maxwell E. Miller, Anil K. Chekuri, Bogdan Budnik, Fengfeng Bei, Yulia Grishchuk. (2024).

A blood-brain barrier-penetrant AAV gene therapy improves neurological function in symptomatic mucolipidosis IV mice

Molecular Therapy: Methods & Clinical Development, 32(2), 101269

doi:10.1016/j.omtm.2024.101269

Plain-language summary

Mucolipidosis IV is a rare inherited disorder that causes neurological impairment and progressive vision loss. This study tested a gene therapy designed to carry a functional copy of the affected gene across the blood-brain barrier in mice that were already showing symptoms. The treatment improved neurological function, reduced brain pathology, and prevented paralysis. Although the therapy reached the retina, it did not restore retinal thickness.

My contribution

I performed in vivo spectral-domain optical coherence tomography imaging of treated and control mice, segmented retinal layers, and analyzed retinal-thickness data to evaluate the therapy’s effects on retinal structure.

Methods spectral-domain OCT · retinal-layer segmentation · in vivo image acquisition · quantitative data analysis