The American Society for Cell Biology (ASCB) recently selected Vlad Denic, a Professor in the Department of Molecular and Cellular Biology, as the recipient of this year’s Early Career Life Scientist Award. The award is presented to an outstanding scientist who earned his or her doctorate no more than 12 years prior and who has served as an independent investigator for no more than seven years. Denic will speak at the ASCB Annual Meeting and receive a monetary prize.
“I am extremely grateful for the intellectual support from my colleagues in the department and for the financial support from Harvard University that helped get my lab started 8 years ago,” said Denic. “But most of all, this award is a testament to how bright and hard-working members of my lab have been during this time.”
In their announcement, the ASCB award committee noted two significant contributions Denic has made to the fields of membrane protein biogenesis and autophagy—a vesicular transport process that captures unwanted intracellular structures and targets them to the cell’s recycling compartment. Notably, he discerned the journey tail-anchored proteins make from the ribosome to insertion in the endoplasmic reticulum—which he and colleagues dubbed the guided entry of tail-anchored proteins (GET) pathway—and discovered that certain autophagy targets signal they are ready to be recycled by activating the enzyme responsible for initiating vesicle formation.
“I am very pleased that the ASCB shares the department’s appreciation of Vlad’s originality and creativity,” said MCB Chair Alex Schier.
Denic is currently interested in how cells detect damaged organelles and toxic protein aggregates for autophagy to mark them for destruction while sparing innocent bystanders. “Many neurodegenerative diseases are caused by defects in this kind of quality control,” he said. His lab is applying new gene editing and control technologies, such as CRISPR/Cas9, to model these disease processes.
Denic also studies the molecular mechanisms of age-related deterioration in budding yeast. “Young cells know how to make more chaperones to balance out excessive protein unfolding. Old cells seem to have lost this ability.” he said. “We are using insights from transcription factors that sense protein unfolding to create synthetic transcriptional programs that have the potential to promote longevity by delaying protein unfolding in old cells.” He hopes to uncover universal themes in cellular aging and eventually develop better pharmacological approaches for extending human lifespan.