The Curran lab seeks to understand the molecules, genes and cells that impact aging and age related diseases. Aging is a universal and inevitable process driven by diverse molecular pathways and surprisingly remains a fundamental mystery of biology. Among the genes that most potently influence the rate of aging in C. elegans are those that are essential for growth and development. More than 90% of these genes have conserved developmental roles from yeast to man and together may represent an evolutionarily conserved program to modulate lifespan. Many of these genes function independently of the canonical longevity-modulating pathways such as insulin/IGF-I signaling, dietary restriction, mitochondrial respiration and reproduction. Inactivation of one group of longevity modulators results in somatic cells with germ cell-like characteristics and increased lifespan. The idea that somatic cells maintain the potential to reacquire pathways lost during differentiation is tantalizing and suggests a mechanism for increasing lifespan through enhanced cellular repair and possibly regeneration. Since C. elegans longevity mutants are resistant to many age-related conditions and disease models, a better characterization of these pathways will provide a means to uncover new therapeutic strategies for the treatment of age-related pathologies in humans and provide insight into essential cellular pathways that regulate aging and development.