TraitMech

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autophagy

traitmech:000638 · CLASS · PROPOSED

A physiological phenotype in which a microbial cell degrades intracellular material, including its own constituents or intracellular non-self cargo, by delivering that material to lysosomal or vacuolar compartments.

Trait evidence (5)

  • DOI:10.1083/jcb.119.2.301
    This is the first report that nutrient-deficient conditions induce extensive autophagic degradation of cytosolic components in the vacuoles of yeast cells.

    PMID:1400575, PMC2289660. Scientific Abstract directly read in Europe PMC XML. Saccharomyces cerevisiae protease-deficient mutants and PMSF-treated reference cells accumulate bodies containing cytosol and organelles; bodies disappear after inhibitor removal. Sequestration and subsequent degradation, not inhibited-body accumulation alone, support the phenotype. The study's starvation conditions are not a universal trigger requirement. The XML body is sparse; full methods, actual figures and natural strain provenance were not inspected.

  • DOI:10.1242/jcs.108.1.25
    there exist in P. pastoris at least two pathways for the sequestration of peroxisomes into the vacuole for degradation.

    PMID:7738102. Scientific Abstract directly read in Europe PMC metadata and publisher HTML. In historically named Pichia pastoris, carbon-source adaptation elicits peroxisome turnover through macroautophagy-like wrapping or microautophagy-like vacuolar engulfment. Enzyme activities, morphology and mutants support route diversity; proteinase-deficient cells accumulate undegraded cargo. This supports selective organelle turnover without requiring starvation or a double-membrane intermediate for every route. Publisher full text requires access; methods, actual figures and strain-specific modern taxonomy were not inspected.

  • DOI:10.1073/pnas.0813319106
    In both organisms, genetic inactivation of the autophagy pathway increases bacterial intracellular replication, decreases animal lifespan, and results in apoptotic-independent death.

    PMID:19667176, PMC2731839. Scientific Abstract directly read in Europe PMC core metadata with matching DOI. The two models are Dictyostelium discoideum and Caenorhabditis elegans. Only the microbial amoeba's intracellular-infection phenotype is relevant here; the abstract's combined animal-lifespan wording and nematode insulin-signaling results are not transferred to the amoeba. Genetic perturbation supports an autophagy-associated host-defense role, not direct proof of completed cargo degradation by itself. Full text, actual figures and strain provenance were not accessible in this review.

  • DOI:10.1371/journal.ppat.1006344
    Antagonistically, ESX-1 is also essential to block the autophagic flux and deplete the MCV of proteolytic activity.

    PMID:28414774, PMC5407849. Scientific Abstract, distinct from the Author summary, directly read in Europe PMC XML and PLOS. The flux Results, flux-assay Methods and Discussion were read; Figure 6 and supplemental S6 Figure were visually inspected. Dictyostelium discoideum is the autophagic cell, not the infecting Mycobacterium marinum. Protease-inhibitor comparisons and GFP-Atg8 processing distinguish formation from degradation; the infection-associated block is partial, not a complete absence of flux. Free GFP reduction alone is ambiguous in this assay. The paper frames intracellular-pathogen digestion as xenophagy, but its blockade result is boundary evidence, not a positive completed-clearance observation. Other actual figures and supplements were not visually audited.

  • DOI:10.1007/s00284-024-03838-y
    These results indicate that nuclei are engulfed in the autophagosomes as a whole and transported/released into the vacuolar lumen where they are degraded.

    PMID:39162852, PMC11335778. Scientific Abstract directly read in Europe PMC with matching DOI. Selected XML Methods, Results and Discussion support including nuclear cargo within autophagy. The nucleophagy child retains the assay and access limits. This repairs cytoplasmic to intracellular in the parent definition (#1754), without imposing this macro route on all autophagy or changing its stable identity.

Provenance

Identifier source
TraitMech local identifier
Definition source
DOI:10.1083/jcb.119.2.301

Parent traits (1)

Children (9)

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.

Retain catabolic scope without equating markers with completed flux.

CURATION TODO OPEN autophagy-scope-and-flux · 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 phenotype belongs to the microbial cell doing the degradation, not to a bacterium merely eliciting an animal host response. Selective and bulk turnover, macro- and microautophagic routes, and intracellular non-self cargo are within scope; no universal starvation trigger, double-membrane intermediate or ATG gene inventory is asserted. ATG genes, puncta, autophagic-body accumulation, cell death or reduced pathogen replication alone do not establish completed degradative flux. Nondegradative membrane repair or ejection using autophagy machinery is not sufficient. Extracellular uptake and ordinary phagolysosomal digestion alone do not distinguish autophagy. Existing endocytosis, phagocytosis, phagotrophy and extracellular proteolysis records are not equivalent or broader parents; their co-occurrence is not prohibited. GO:0006914 was resolved at https://www.ebi.ac.uk/QuickGO/services/ontology/go/terms/GO%3A0006914 and includes self and non-self material, but denotes a biological process rather than an equivalent organismal phenotype. Keep METPO:1000059 as parent and omit exact xrefs and synonyms pending human scope review. Nuclear cargo is included: DOI:10.1007/s00284-024-03838-y supports whole-nucleus autophagy in Aspergillus oryzae. The former cytoplasmic-only wording was too narrow (#1754); intracellular corrects that wording, not the identity of autophagy. Nucleophagy traitmech:000643 is a cargo-defined child. The original definition source supports the retained vacuolar catabolic genus; the added evidence supports nuclear cargo.

Resolve strain provenance and cargo-specific mechanism evidence.

KNOWLEDGE GAP OPEN autophagy-exemplar-and-mechanism · 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.

Canonical examples remain unset because reference-strain provenance and historical yeast taxonomy have not been independently verified. Do not infer natural or engineered origin from a mutant label. Retain the qualified experimental evidence without treating inhibited or knockout cells as positive completed-flux exemplars. Route-specific proteins, their accessions and taxon-paired functional evidence need review before adding a causal graph. The amoeba infection studies do not establish one universal microbial host-defense mechanism or prove that autophagy always eliminates an intracellular pathogen.

Curation history

  1. · MINTED_TRAITMECH_ID · codex

    Added autophagy with four DOI-backed scientific-abstract snippets and explicit route, cargo, flux and source-access limits. Ignored-and-hidden searches and pinned METPO review found no exact record. Reserved METPO:1059100 in v514. Deferred unverified examples, mappings and protein mechanisms; existing traits unchanged.

  2. · CURATED_WITH_LITERATURE · codex

    Corrected cytoplasmic to intracellular cargo using whole-nucleus autophagy evidence (#1754). Retained autophagy identity, prior evidence and route/flux limits; added the nucleophagy child and corrected parent context in proposal v519.