Arne Gennerich

Energetic ResearchInside cells, tiny molecular machines called kinesin and cytoplasmic dynein transport essential components(including organelles, mRNA, chromosomes and vesicles) along a network of molecular “highways” called microtubules. Dysfunction of these biomolecular machines can cause devastating neurological diseases such as motor neuron degeneration and lissencephaly. For over a decade, experts have debated the amount of force that single molecules of dynein can generate. In a recent paper in the February issue of Nature Communications, Dr. Arne Gennerich and colleagues explain why mammalian dynein produces less force and travels shorter distances than similarly structured yeast dynein. The researchers investigated the CT-cap--the terminal part of the mammalian motor protein that is absent in the yeast version of dynein. With the CT-cap removed, mammalian dynein generated greater forces and traveled longer distances, similar to yeast dynein. This is the first study to identify an element of dynein that controls force production. The CT-cap could potentially be a target to regulate dynein’s numerous and diverse cellular functions. Dr. Gennerich is an assistant professor of anatomy and structural biology and a member of the Gruss-Lipper Biophotonics Center. First author on the paper was Matthew Nicholas, an M.D.-Ph.D. candidate who defended his thesis in 2013 and is a member of the class of 2016.