Sean Curran

About

Sean Curran, PhD, is a Professor of Gerontology and Molecular and Computational Biology at the USC Leonard Davis School of Gerontology, where he also serves as Vice Dean, Dean of Faculty, and Dean of Research. He is co-director of the USC-Buck Nathan Shock Center of Excellence in the Basic Biology of Aging. His research group focuses on defining molecular, genetic, and environmental factors that impact health parameters such as resistance to environmental and dietary stress, mobility, metabolism, reproductive fitness, and mitochondrial function throughout life. The long-term goal of his work is to generate blueprints that enable individuals to maximize health over their lifespan, informed by genetics to predict ideal diets for a healthy life and identify diets to avoid. Curran developed the first PhD in Geroscience program, which recruited its inaugural class in 2024. His research is funded by the NIH and has received support from various foundations and organizations. He is a Fellow of the Gerontological Society of America and has received numerous awards for his research, including the AFAR Vincent Cristofalo Rising Star in Aging Research Award, the Paul F. Glenn Award, and the Nathan Shock New Investigator Award. Curran's mentoring has been recognized by the Mellon Foundation, and he received the USC Provost’s Mentoring Award in 2019. He earned his PhD from UCLA and completed post-doctoral training at Harvard Medical School and Massachusetts General Hospital.

Research topics

• Biology
• Genetics
• Cell biology
• Biochemistry
• Physiology
• Biotechnology
• Microbiology

Selected publications

• Bacterial diets differentially alter lifespan and healthspan trajectories in C. elegans

  Communications Biology · 2020 · 106 citations

  Senior authorCorresponding

  Diet is one of the more variable aspects in life due to the variety of options that organisms are exposed to in their natural habitats. In the laboratory, C. elegans are raised on bacterial monocultures, traditionally the E. coli B strain OP50, and spontaneously occurring microbial contaminants are removed to limit experimental variability because diet-including the presence of contaminants-can exert a potent influence over animal physiology. In order to diversify the menu available to culture C…

  DOI

• Loss of flavin adenine dinucleotide (FAD) impairs sperm function and male reproductive advantage in C. elegans

  eLife · 2020 · 45 citations

  Senior authorCorresponding

  loss-of-function mutants. These sperm-specific defects are suppressed by feeding diets that restore FAD levels. Our results define a cell autonomous role for mitochondrial proline catabolism and FAD homeostasis on sperm function and specify strategies to pharmacologically reverse these defects.

  DOI

• Incomplete proline catabolism drives premature sperm aging

  Aging Cell · 2021 · 36 citations

  Senior authorCorresponding

  Infertility is an increasingly common health issue, with rising prevalence in advanced parental age. Environmental stress has established negative effects on reproductive health, however, the impact of altering cellular metabolism and its endogenous reactive oxygen species (ROS) on fertility remains unclear. Here, we demonstrate the loss of proline dehydrogenase, the first committed step in proline catabolism, is relatively benign. In contrast, disruption of alh-6, which facilitates the second s…

  DOI

• Disrupting the SKN-1 homeostat: mechanistic insights and phenotypic outcomes

  Frontiers in Aging · 2024-03-04 · 25 citations

  reviewOpen accessSenior authorCorresponding

  The mechanisms that govern maintenance of cellular homeostasis are crucial to the lifespan and healthspan of all living systems. As an organism ages, there is a gradual decline in cellular homeostasis that leads to senescence and death. As an organism lives into advanced age, the cells within will attempt to abate age-related decline by enhancing the activity of cellular stress pathways. The regulation of cellular stress responses by transcription factors SKN-1/Nrf2 is a well characterized pathw…

  PublisherOA PDFDOI

• Serotonin deficiency from constitutive SKN-1 activation drives pathogen apathy

  Nature Communications · 2024-09-16 · 10 citations

  articleOpen accessSenior author

  When an organism encounters a pathogen, the host innate immune system activates to defend against pathogen colonization and toxic xenobiotics produced. C. elegans employ multiple defense systems to ensure survival when exposed to Pseudomonas aeruginosa including activation of the cytoprotective transcription factor SKN-1/NRF2. Although wildtype C. elegans quickly learn to avoid pathogens, here we describe a peculiar apathy-like behavior towards PA14 in animals with constitutive activation of SKN…

  PublisherOA PDFDOI

Recent grants

• NIH Grant K99AG032308

  NIH · $197k · 2011

• NIH Grant R01GM109028

  NIH · $1.8M · 2020

• Genomic Translation Across Species Core

  NIH · $11.2M · 2020–2026

Frequent coauthors

• Alexander A. Soukas

  Harvard University

  16 shared

• Nicole L. Stuhr

  University of Southern California

  16 shared

• Dana A. Lynn

  University of Southern California

  13 shared

• Gary Ruvkun

  Brandeis University

  12 shared

• Chia‐An Yen

  University of Southern California

  11 shared

• Chatrawee Duangjan

  University of Southern California

  10 shared

• Carla M. Koehler

  University of California, Los Angeles

  10 shared

• Lucydalila Cedillo

  Massachusetts General Hospital

  9 shared

Education

• Ph.D., Gerontology

  USC Leonard Davis School of Gerontology

  2026

Awards & honors

• AFAR Vincent Cristofalo Rising Star in Aging Research Award
• Paul F. Glenn Award
• Nathan Shock New Investigator Award (GSA)
• Ewald W. Busse Research Award
• USC Provost’s Mentoring Award (2019)

Similar researchers at University of Southern California

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• Eileen Crimminsh-89
• Jennifer Ailshireh-37