Leo Pallanck


University of Washington, 

Developmental Biology, Stem Cells & Aging

Genetics, Genomics & Evolution


3720 15th Ave NE

Faculty Contact Information

Building: WH Foege Room: S-443 Box: 355065 Phone: 206-616-5997 Alt Phone: 206-616-5996

Lab Information

Location: University of Washington Building: WH Foege Room: s-443 Box: 355065 Phone: 206-616-5996

Accepting Students For:

Rotation, Autumn
Rotation, Spring
Rotation, Summer
Rotation, Winter


The following publications were retrieved from PubMed:

Autophagy accounts for approximately one-third of mitochondrial protein turnover and is protein selective.

Vincow ES, Thomas RE, Merrihew GE, Shulman NJ, Bammler TK, MacDonald JW, MacCoss MJ, Pallanck LJ.

Autophagy. 2019 Mar 13; 1-14

Deleterious mitochondrial DNA point mutations are overrepresented in Drosophila expressing a proofreading-defective DNA polymerase γ.

Samstag CL, Hoekstra JG, Huang CH, Chaisson MJ, Youle RJ, Kennedy SR, Pallanck LJ.

PLoS Genet. 2018 Nov; 11(14)e1007805

Lon protease inactivation in <i>Drosophila</i> causes unfolded protein stress and inhibition of mitochondrial translation.

Pareek G, Thomas RE, Vincow ES, Morris DR, Pallanck LJ.

Cell Death Discov. 2018; (4)51

Glucocerebrosidase deficiency promotes protein aggregation through dysregulation of extracellular vesicles.

Thomas RE, Vincow ES, Merrihew GE, MacCoss MJ, Davis MY, Pallanck LJ.

PLoS Genet. 2018 Sep; 9(14)e1007694

Research Summary

Mitochondrial dysfunction and protein aggregation are common neuropathological features of aging and neurodegenerative disease. My laboratory uses Drosophila to study these matters. In particular, we are interested in how damaged mitochondria are detected and degraded, whether there is selection against harmful mtDNA mutations, and how protein aggregates spread between tissues. We use genetic, genomic, proteomic and computational approaches to study these matters, thus offering multidisciplinary training opportunities for students interested in these problems.