Updated project metadata. Nuclear pore complexes (NPCs) are giant cylindrical structures embedded into the nuclear envelope and mediate nucleocytoplasmic exchange. NPC longevity has been linked to aging but since they appear to rarely turn over, the underlying mechanisms remain understudied. Here, we show that upon nitrogen starvation and genetic interference with NPC architecture, Nups are rapidly degraded in budding yeast. We demonstrate that NPC turnover involves 25 vacuolar proteases and the core autophagic machinery. Autophagic degradation is mediated by the cytoplasmically exposed Nup159 that serves as intrinsic cargo receptor and directly binds to the autophagic marker protein Atg8. The inducible manner of this mechanism might explain why NPCs are long-lived under specific conditions