Marina Ezcurra

This study shows that a defined microbial community remodels host metabolism and pathogen resistance in C. elegans by altering transcriptional pathways and physiological traits.

The paper shows that in C. elegans, lifespan is limited by competing senescent pathologies, and removing one can unmask another, indicating lifespan extension may not reflect reduced aging rate.

This study identifies a gut microbiota-muscle axis in C. elegans that protects against age-related motor decline by regulating mitochondrial fission through DRP-1.

This paper introduces a low-cost respirometry assay for C. elegans using optical oxygen sensors and fluorescence readers, showing it can accurately measure OCR and identify issues with sequential respiratory inhibitor use.

This paper develops tools to study Pseudomonas aeruginosa infection and biofilm formation in vivo using C. elegans, identifying RhlR as a potential antimicrobial target.

The paper uses machine learning to predict lifespan and causes of death in aging C. elegans by analyzing senescent pathology and genetic factors.

This study identifies SKN-1B in C. elegans as a central food-responsive node that controls satiety and metabolic homeostasis by modulating endocrine pathways and mitochondrial networks.

The paper shows that C. elegans hermaphrodites undergo reproductive death after reproduction, which is suppressed by germline removal and linked to lifespan extension.

This study identifies ETS transcription factors as conserved regulators of longevity across species, showing their roles in modulating lifespan through gene expression programs.

The paper investigates uterine tumors in C. elegans as a senescent pathology caused by quasi-programs, showing similarities to teratomas and senescence.

This study identifies autophagy-mediated gut-to-yolk biomass conversion as a cause of visceral pathologies and polymorbidity in aging C. elegans, and shows that inhibiting this process extends lifespan.