Melissa Hoyer, Ph.D.
Assistant Professor, Department of Neurodegenerative Science
Areas of Expertise
Neurodegeneration, proteomics, neuronal development, cell biology, organelle dynamics, lysophagy, ER-phagy
Biography
Dr. Melissa Hoyer investigates the fundamental cellular processes that support neuronal health with a focus on organelle proteome landscapes. Her leading-edge research has deep implications for understanding the mechanisms that drive protein and organelle degradation, which are defective in neurodegenerative diseases.
Dr. Hoyer earned a B.S. in molecular biology and chemistry from University of Wyoming followed by a Ph.D. in molecular, cellular and developmental biology from University of Colorado (Adviser: Dr. Gia Voeltz). Her dissertation research helped elucidate the relationship between the endoplasmic reticulum and endosome fission, which has significant implications for signaling receptor sorting and degradation in the endocytic pathway. Her graduate work was supported in part by a National Science Foundation Graduate Research Fellowship.
She then joined the lab of Dr. J. Wade Harper at Harvard Medical School as a postdoctoral fellow, where she investigated organelle structure, function and quality control in stem cells as they differentiate to neurons. Her research has revealed powerful new insights into lysosomes and the endoplasmic reticulum, both of which are cellular organelles with links to protein aggregation in neurodegenerative diseases. She was awarded the Jane Coffin Child Fellowship (2019 –2022) and the Fred and Joan Goldberg Fellowship (2022–2024) in recognition of her scholarship.
In 2024, Dr. Hoyer joined Van Andel Institute’s Department of Neurodegenerative Science. Her lab explores the underlying mechanisms that control organelle protein levels in neurons to decipher how organelle proteome landscapes are linked to organelle structure, dynamics and function. Her research aims to better understand the establishment of neurons and maintenance of neuron cell health — both of which are dysregulated in neurodegenerative diseases.