Salsolinol　(1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline,　Sal)　is　a　catechol　isoquinoline　that　causes　neurotoxicity　and　shares　structural　similarity　with　1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,　an　environmental　toxin　that　causes　Parkinson＇s　disease.　However,　the　mechanism　by　which　Sal　mediates　dopaminergic　neuronal　death　remains　unclear.　In　this　study,　we　found　that　Sal　significantly　enhanced　the　global　level　of　N-6-methyladenosine　(m(6)A)　RNA　methylation　in　PC12　cells,　mainly　by　inducing　the　downregulation　of　the　expression　of　m(6)A　demethylases　fat　mass　and　obesity-associated　protein　(FTO)　and　alkB　homolog　5　(ALKBH5).　RNA　sequencing　analysis　showed　that　Sal　downregulated　the　Hippo　signaling　pathway.　The　m(6)A　reader　YTH　domain-containing　family　protein　2　(YTHDF2)　promoted　the　degradation　of　m(6)A-containing　Yes-associated　protein　1　(YAP1)　mRNA,　which　is　a　downstream　key　effector　in　the　Hippo　signaling　pathway.　Additionally,　downregulation　of　YAP1　promoted　autophagy,　indicating　that　the　mutual　regulation　between　YAP1　and　autophagy　can　lead　to　neurotoxicity.　These　findings　reveal　the　role　of　Sal　on　m(6)A　RNA　methylation　and　suggest　that　Sal　may　act　as　an　RNA　methylation　inducer　mediating　dopaminergic　neuronal　death　through　YAP1　and　autophagy.　Our　results　provide　greater　insights　into　the　neurotoxic　effects　of　catechol　isoquinolines　compared　with　other　studies　and　may　be　a　reference　for　assessing　the　involvement　of　RNA　methylation　in　the　pathogenesis　of　Parkinson＇s　disease.