Increased oligomerization of mixtures of wild type LRRK2 and disease-associated LRRK2 variants (Supplementary Fig. 1a,b), as would be present in heterozygous patients with Parkinson’s disease, together with the inability of LRRK2 oligomers to sever actin (Fig. 3) suggest a mechanism for a dominant negative effect. Here, LRRK2 is linked to Parkinson disease.