PRKN and Parkinson disease: C. elegans functional studies of other Mendelian PD genes and their orthologues, including PINK1, PARKIN, ATP13A2 and DJ-1, or PD risk genes, such as GBA1, have proven the strength of this invertebrate model, highlighting highly conserved functions of these genes and proteins in cellular pathways disrupted in PD, including mitophagy, lysosomal degradation and α-synuclein pathology [49,132,175,262–270].