Abstract
AbstractMutations in Leucine-rich repeat kinase 2 (LRRK2) are responsible for late-onset autosomal dominant Parkinson’s disease (PD). LRRK2 has been implicated in a wide range of physiological processes including membrane repair in the endolysosomal system. Here, we report that purified LRRK2 directly binds acidic lipid bilayers in a cell-free system and can deform them into narrow tubules in a guanylnucleotide-dependent but ATP-independent way. Moreover, we found that LRRK2 shows preferential assembly on highly curved lipid nanotubes relative to spherical liposomes. We suggest that an interplay between the membrane remodeling and signaling properties of LRRK2 may be key to its physiological function. LRRK2, via its kinase activity, may achieve its signaling role at sites where membrane remodeling occurs.
Publisher
Cold Spring Harbor Laboratory
Cited by
5 articles.
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