Siegfried Hekimi

In the Hekimi lab we are using mutants of Caenorhabditis elegans and mouse mutants to understand aging focusing on activities that affect mitochondrial function. We are using mutants of the microscopic nematode roundworm Caenorhabditis elegans, Saccharomyces cerevisiae, mice, and human cells to study aging, a crucial, profound, and poorly understood biological phenomenon. We hope to obtain insights that will also provide new ways for medical intervention on the aging process. We are particularly focusing on gene activities that affect mitochondrial function, and on mutants that enhance longevity. We are also interested in the biosynthesis and function of ubiquinone (UQ, Coenzyme Q, CoQ), the lipid-like the mitochondrial respiratory chain electron transporter. Here too we use mutants in both organisms to unravel the basic biochemical functions of ubiquinone and to develop drugs that can help alleviate the diseases linked to ubiquinone deficiency.

Wang Y, Noe A, Truong-Ong L, Hekimi S. (2026) Clarifying the molecular mechanisms underlying the lethal in vitro cellular effects and mild organismal phenotype of SOD1 loss. Scientific Reports. Lilienfeldt N, Tai Y, Sun H, Waddell B, Branicky R, Yang W, Hekimi S. (2026) Genetic analysis of sensitivity to temperature fluctuations identifies acclimation stress as a novel type of cellular stress in Caenorhabditis elegans. Genetics. iyag157. Wang Y, Hekimi S (2025) Elevated cellular accumulation of endogenous and exogenous CoQ by altered intracellular trafficking. Journal of Biological Chemistry 301(12). Pascal M, Cappadocia L, Hekimi S, Benard CY. (2025) Intragenic suppressors of the C. elegans clk-2(qm37) mutation. Micropublication Biology. 10.17912/micropub.biology.001828. Wang Y, Lilie