Abstract
Nucleophagy, the selective subtype of autophagy that targets nuclear material for autophagic degradation, was not only shown to be a model system for the study of selective macroautophagy, but also for elucidating the role of the core autophagic machinery within microautophagy. Nucleophagy also emerged as a system associated with a variety of disease conditions including cancer, neurodegeneration and ageing. Nucleophagic processes are part of natural cell development, but also act as a response to various stress conditions. Upon releasing small portions of nuclear material, micronuclei, the autophagic machinery transfers these micronuclei to the vacuole for subsequent degradation. Despite sharing many cargos and requiring the core autophagic machinery, recent investigations revealed the aspects that set macro- and micronucleophagy apart. Central to the discrepancies found between macro- and micronucleophagy is the nucleus vacuole junction, a large membrane contact site formed between nucleus and vacuole. Exclusion of nuclear pore complexes from the junction and its exclusive degradation by micronucleophagy reveal compositional differences in cargo. Regarding their shared reliance on the core autophagic machinery, micronucleophagy does not involve normal autophagosome biogenesis observed for macronucleophagy, but instead maintains a unique role in overall microautophagy, with the autophagic machinery accumulating at the neck of budding vesicles.
Highlights
Autophagy is a highly conserved process that facilitates the degradation and recycling of intracellular components and plays a central role in the maintenance of cellular homeostasis
Starvation, rapamycin induced TORC1 inactivation, genotoxic stress, expansion of the nucleus vacuole junction (NVJ), as well as defects in the nuclear envelope and lamina lead to enhanced rates of nucleophagy [3,4,5,6,7]
While Atg39 does not contain an reticulon homology domain (RHD), initial bulging of the nuclear envelope for formation of micronuclei could be facilitated by curvature inducing factors that localise to the Outer nuclear membrane (ONM) in tandem with Atg39
Summary
Autophagy is a highly conserved process that facilitates the degradation and recycling of intracellular components and plays a central role in the maintenance of cellular homeostasis. Starvation, rapamycin induced TORC1 inactivation, genotoxic stress, expansion of the nucleus vacuole junction (NVJ), as well as defects in the nuclear envelope and lamina lead to enhanced rates of nucleophagy [3,4,5,6,7] Detailed investigations towards their initiation showed that macro- and micronucleophagy occur dependent on the Nem1/Spo7–Pah axis, a downstream process of TORC1 inactivation [8]. The Nem1/Spo7–Pah axis which is part of lipid metabolism, is involved in other autophagic processes, including endosomal sorting complexes required for transport (ESCRT)-dependent and autophagy independent micro-ER-phagy [9]. Nucleophagy occurs in both a macro- and micronucleophagic manner in the budding yeast Saccharomyces cerevisiae [4,5]. (INM and ONM) are targeted by nucleophagy, excluding nuclear pore complexes (NPCs), which are are tadreggerateddedbbyynauscpleeocipalhisaegdy,foerxmcloufdsienlegctnivueclaeuatropphoargey.coNmucpleleoxpelassm(N, PasCws)e,llwahsinchucaleroeladrepgrroatdeiends by a speciaarleisdeedgrfaodremd,owf hsieleleecxticvluedainugtorpibhoasogmy.alNDuNclAeo(prDlaNsAm),. aPsiewcemelleaalsmniucrcolaeuotloaprhpargoyteoifntshearneudcleegursaded, whiletaergxectlsutdhiensge croibmopsoonmenatlsDaNs wAel(lrDanNdAa)d.dPitiieocneamllyeadlegmraicdreosatuhteoptighhatglyy colafmthpeednunuclceleuusstvaargcueotslethese compjuonncetinotns(aNsVwJ)e, linl calnuddinadg daiptioorntiaolnlyofdveagcruaodlaersmtheme tbirgahntel.y clamped nucleus vacuole junction (NVJ), including a portion of vacuolar membrane
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