Neurospora crassa

Neurospora crassa pioneered modern genetics with Beadle and Tatum's one-gene-one-enzyme hypothesis and continues contributing to aging research through its circadian rhythm system and replicative senescence. Unlike unicellular yeasts, Neurospora grows as a filamentous network (mycelium), providing a model for aging in multicellular fungal organization. Different parts of the same mycelium can have different ages, enabling study of how local aging affects connected tissue.

The Neurospora circadian clock has become central to understanding how daily rhythms affect aging. The fungus maintains robust ~22-hour cycles in gene expression, metabolism, and development. Clock mutants show altered lifespan, revealing connections between circadian regulation and longevity. These connections extend to mammals: disrupting circadian rhythms accelerates aging in mice and is associated with increased disease risk in humans. Neurospora's accessible genetics enabled molecular dissection of clock-aging interactions.

Replicative senescence in Neurospora involves mitochondrial dysfunction—a theme that resonates with mammalian aging. Aging mycelia accumulate damaged mitochondria that eventually prevent growth. The kalilo and maranhar plasmids insert into mitochondrial DNA, triggering senescence when copy number exceeds thresholds. Studying how Neurospora manages mitochondrial quality, and how this management fails in senescence, informs understanding of mitochondrial contributions to aging across species.