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autophagic glycogen degradation

traitmech:000647 · CLASS · PROPOSED

An autophagy phenotype in which a microbial cell degrades intracellular glycogen by delivering it to lysosomal or vacuolar compartments.

Trait evidence (4)

  • DOI:10.4161/auto.6.4.11736
    Our results indicate that autophagy and Sga1 act cooperatively in vacuolar glycogen breakdown

    PMID:20383057. DOI-matched scientific abstract directly read in Europe PMC metadata. Supports autophagy-associated vacuolar glycogen hydrolysis in Magnaporthe oryzae during asexual development. The reported breakdown supports conidia formation but is dispensable for pathogenicity. Cytoplasmic retargeting of GFP-Sga1 is an engineered rescue, not a natural vacuolar-flux exemplar. Full Methods, actual figures and independent strain provenance were not inspected.

  • DOI:10.3390/cells13060467
    vacuolar delivery of Glg1-GFP and its processing to free GFP were strictly dependent on autophagic machinery and vacuolar proteolysis.

    PMID:38534311, PMC10969688. Scientific abstract, XML Methods 2.1, Results 3.2-3.4 and Discussion were read. The authors conclude nonselective glycogen autophagy in nitrogen-starved Komagataella phaffii using glycogen-bound, nonbinding and cytosolic reporters. Atg11 independence alone is not the selectivity argument. TCA extraction under-recovers the bound reporter; raw free-GFP/total-fusion ratios are unreliable. Reporter proteolysis is not a direct polymer-hydrolysis assay. Actual panels and independent strain provenance remain uninspected.

  • DOI:10.3390/ijms252111772
    The K. phaffii Gsy1-GFP marked the GGs and reported on their autophagic degradation during nitrogen starvation, as expected.

    PMID:39519320, PMC11546884. DOI-matched scientific abstract and XML Results 2.2-2.3 and Discussion were read. GGs means glycogen granules. This follow-up uses Gsy1 and CBM20 reporters to support neutral cargo behavior in nitrogen-starved K. phaffii; it is not independent-laboratory replication. Early Gsy1-GFP dot disappearance is autophagy-independent and is not positive flux evidence. A human STBD1 domain used as a reporter does not establish a native human mechanism in yeast. Complete Methods, actual panels and strain provenance were not inspected.

  • DOI:10.1016/j.isci.2024.109810
    glycophagy may play a role in the suppression of glycogen consumption, rather than enhancing degradation.

    PMID:38832010, PMC11145338. Exact XML Results sec2.7 span, not an abstract quote. Scientific Summary, Results, Discussion, Limitations and selected yeast, GFP-cleavage and glycogen-assay Methods were read. Boundary evidence: Atg45-dependent vacuolar delivery during Saccharomyces cerevisiae sporulation can preserve glycogen. Do not score that delivery alone as degradation. Receptor recruitment and prolonged-starvation reporter turnover do not make storage and hydrolysis interchangeable. Actual panels, supplements and independent strain provenance remain unread.

Provenance

Identifier source
TraitMech local identifier
Definition source
DOI:10.4161/auto.6.4.11736

Parent traits (1)

kg-microbe context

No kg-microbe node embedding matched this record in the 2026-04-25 deepwalk.

Discussions and Knowledge Gaps (2)

Open questions attached to this trait. Seeded by just knowledge-gap-scan and curated; see the corpus-wide index.

Distinguish degradation from broader glycophagy usage.

CURATION TODO OPEN autophagic-glycogen-degradation-scope · raised by codex · 2026-10-06

Not yet attached to a section of this record — a curator sets attaches_to (e.g. causal_graphs#some_edge) so the gap shows beside the mechanism it concerns.

The explicit degradative endpoint narrows autophagy traitmech:000638 without changing that parent's identity. This is intracellular cargo recycling, not growth on glycogen, extracellular amylolysis, granule possession or a gene inventory. The Cells paper introduces glycophagy as selective but reports nonselective K. phaffii turnover; the iScience paper also uses glycophagy for vacuolar preservation during sporulation. Those source-attributed usages are not exact synonyms of this endpoint-defined record. GO:0061723 was directly resolved at https://www.ebi.ac.uk/QuickGO/services/ontology/go/terms/GO%3A0061723 as a nonobsolete biological process for selective glycogen degradation by macroautophagy. It is narrower on selectivity and route, and is not an exact organismal phenotype. Omit exact xrefs and synonyms. Broader delivery/storage and selective subtype relationships require human review, not silent normalization of conflicting terminology.

Resolve polymer turnover, natural exemplars and mechanisms.

KNOWLEDGE GAP OPEN autophagic-glycogen-degradation-assays-and-exemplars · raised by codex · 2026-10-06

Not yet attached to a section of this record — a curator sets attaches_to (e.g. causal_graphs#some_edge) so the gap shows beside the mechanism it concerns.

Keep glycogen-bound reporter cleavage, vacuolar localization, glycogen content and polymer hydrolysis as distinct readouts. Do not impose universal Sga1, Atg45, Atg11, starvation, sporulation, selectivity or a macroautophagic route. Yeast species and nutrient conditions can differ. The Atg45 storage result is a boundary, not positive evidence of this endpoint. Canonical examples remain unset pending independent natural-strain provenance and direct endpoint support; reporter and deletion strains are qualified evidence, not natural exemplars. Protein graphs require native taxon-paired accessions and functional evidence. Human disease models and an Aspergillus enzyme used as an assay reagent are not microbial observations of this trait. Inspect actual panels before protein-level curation.

Curation history

  1. · MINTED_TRAITMECH_ID · codex

    Added autophagic glycogen degradation with four DOI-backed source-matched snippets and explicit storage, selectivity and reporter limits. Fresh ignored-and-hidden searches, seed and METPO inventories found no exact record. Reserved METPO:1060000 in v523 with unchanged corrected autophagy parent context. Deferred broad glycophagy equivalence, natural exemplars and protein mechanisms.