| Aspect | Key findings (concise) | Evidence type | Best supporting sources (author year, journal) | URL/DOI | Notes/limitations |
|---|---|---|---|---|---|
| Identity | The target is the fission-yeast autophagy factor Atg13 encoded by atg13/mug78/SPAC4F10.07c (UniProt O36019), analyzed in S. pombe Atg1-complex studies rather than homologs from other organisms. It is treated as a core subunit of the S. pombe Atg1 initiation complex. (pqac-00000001, pqac-00000008) | Review synthesis; organism-specific biochemistry | Xu & Du 2022, *Cells*; Nanji et al. 2017, *Autophagy* | https://doi.org/10.3390/cells11071086; https://doi.org/10.1080/15548627.2017.1382782 | Identity is well supported in S. pombe literature, but many broader Atg13 papers are from other organisms and should not be overgeneralized to SCHPO. |
| Domains | Atg13 has an N-terminal HORMA domain (Atg13HORMA, residues 1–269) that binds Atg101 and a C-terminal region/CTD (reported as residues 392–758) that mediates Atg1 and Atg17 binding. Additional sequences flanking the putative MIM are required for stable Atg1 binding. (pqac-00000004, pqac-00000006, pqac-00000007, pqac-00000010) | Biochemical; structural inference; domain mapping | Nanji et al. 2017, *Autophagy* | https://doi.org/10.1080/15548627.2017.1382782 | Domain boundaries come from recombinant-fragment studies, not a full-length S. pombe Atg13 structure. |
| Interactions | Direct interactions are reported between Atg13 and Atg1, Atg13 and Atg17, and Atg13 HORMA and Atg101. Atg11 interacts strongly with Atg1 and weakly with Atg13. Atg101 does not bind Atg17 but can contact Atg1 CTD. (pqac-00000001, pqac-00000002, pqac-00000006, pqac-00000007, pqac-00000008, pqac-00000010) | Pairwise coprecipitation; pulldown; biochemical reconstitution; review | Nanji et al. 2017, *Autophagy*; Xu & Du 2022, *Cells* | https://doi.org/10.1080/15548627.2017.1382782; https://doi.org/10.3390/cells11071086 | Evidence is strong for physical association, but stoichiometry and dynamics in vivo are less completely resolved than in budding yeast or mammals. |
| Complex architecture/function | Atg13 functions as a scaffold/adaptor in the S. pombe Atg1 complex, helping anchor Atg1 to the Atg17 scaffold and coupling Atg101 into the initiation machinery; this places Atg13 upstream in autophagy initiation rather than acting as an enzyme. (pqac-00000000, pqac-00000001, pqac-00000006, pqac-00000008, pqac-00000010) | Biochemical; structural model; review | Nanji et al. 2017, *Autophagy*; Xu & Du 2022, *Cells* | https://doi.org/10.1080/15548627.2017.1382782; https://doi.org/10.3390/cells11071086 | The scaffold role is well supported; direct downstream substrates specifically controlled via Atg13 in S. pombe remain less defined. |
| Atg101 stabilization | Atg101 binds the Atg13 HORMA domain and stabilizes Atg13. DSF reported melting temperatures of ~43°C for Atg13HORMA, ~48°C for Atg101, and ~63°C for the heterodimer, indicating strong stabilization upon complex formation. (pqac-00000004, pqac-00000009, pqac-00000010) | Biochemical; DSF; crosslinking-MS | Nanji et al. 2017, *Autophagy*; Nanji 2021 thesis | https://doi.org/10.1080/15548627.2017.1382782; https://doi.org/10.14288/1.0378352 | The quantitative stabilization result is robust, but functional consequences beyond stability are not fully quantified in the cited excerpts. |
| Requirement for Atg1 kinase activity | In S. pombe, Atg13 is not required for detectable Atg1 autophosphorylation activity; Atg1 from atg13Δ cells showed autophosphorylation similar to wild type under nutrient-rich and 1 h nitrogen-starved conditions. Atg11, not Atg13/Atg17/Atg101, is the key requirement for Atg1 kinase activation. (pqac-00000002, pqac-00000005) | Genetic; in vitro kinase assay | Pan et al. 2020, *eLife*; Xu & Du 2022, *Cells* | https://doi.org/10.7554/elife.58073; https://doi.org/10.3390/cells11071086 | This is a major fission-yeast-specific divergence from the budding-yeast paradigm; lack of a kinase requirement does not mean Atg13 is dispensable for autophagy initiation complex assembly. |
| Regulation by TORC1 | The general fungal model is that TORC1-dependent hyperphosphorylation of Atg13 suppresses Atg1-complex assembly, and starvation-associated dephosphorylation promotes initiation. Reviews specific to S. pombe note Atg13 as a TORC1-dependent autophagy regulator/target, but specific S. pombe Atg13 phosphoresidues are still unknown in the cited 2024 phosphoproteomic work. (pqac-00000000, pqac-00000018) | Review; pathway inference; phosphoproteomics context | Fernández 2025; Bérard et al. 2024, *PLOS Biology* | https://doi.org/10.1371/journal.pbio.3002963 | Scope caveat: the TORC1→Atg13 mechanism is strongly established broadly in yeasts/mammals, but residue-level regulation of S. pombe Atg13 remains incompletely mapped in the provided evidence. |
| Other signaling inputs (PKA/MAPK) | 2023 work showed glucose-limitation autophagy in S. pombe is strongly controlled transcriptionally by cAMP-PKA and Sty1-Atf1/Rst2 pathways. This study did not directly map Atg13 regulation, but it provides current context for how initiation is integrated with nutrient/stress signaling in S. pombe. pka1-δ altered ~21% of genes (1106/5130), with 65% of induced genes Rst2-dependent and 33% Atf1-dependent. (pqac-00000023) | Genetics; transcriptomics; autophagic-flux assays | Pérez-Díaz et al. 2023, *Autophagy* | https://doi.org/10.1080/15548627.2022.2125204 | Important for pathway context, but evidence is indirect for Atg13 specifically. |
| Localization | The provided evidence places Atg13 function at the autophagy initiation site/PAS as part of the Atg1 complex architecture, but the gathered excerpts do not provide a direct microscopy-based localization result for S. pombe Atg13 itself. (pqac-00000000, pqac-00000010) | Structural/functional inference | Nanji et al. 2017, *Autophagy*; Fernández 2025 | https://doi.org/10.1080/15548627.2017.1382782 | Localization should be stated cautiously: PAS association is inferred from complex role and architecture, not directly demonstrated in the extracted passages. |
| Phenotypes/autophagy role | Atg13 is a core initiation-complex component critical for autophagy initiation according to S. pombe autophagy machinery synthesis, but the specific excerpts available here do not provide a standalone numeric flux defect for atg13Δ. The strongest direct phenotype in the gathered primary data concerns kinase independence rather than flux magnitude. (pqac-00000001, pqac-00000002, pqac-00000005) | Review; genetics; kinase assay | Xu & Du 2022, *Cells*; Pan et al. 2020, *eLife* | https://doi.org/10.3390/cells11071086; https://doi.org/10.7554/elife.58073 | Absence of quantitative atg13Δ flux data in the retrieved excerpts is a key limitation. |
| Assays used in Atg13 studies | Evidence for Atg13 function comes from pairwise coprecipitation/pulldown mapping, recombinant purification, DSF, crosslinking-MS, and Atg1 kinase assays. The Nanji thesis also lists CFP-Atg8 cleavage and Pho8Δ60 assays among methods relevant to Atg-complex function. (pqac-00000003, pqac-00000004, pqac-00000005, pqac-00000009, pqac-00000010) | Biochemical; structural; genetic; autophagy assay methods | Nanji et al. 2017, *Autophagy*; Nanji 2021 thesis; Pan et al. 2020, *eLife* | https://doi.org/10.1080/15548627.2017.1382782; https://doi.org/10.14288/1.0378352; https://doi.org/10.7554/elife.58073 | Some assays are documented as methods in the thesis without extracted Atg13-specific results in the available context. |
| Recent 2023–2024 developments | Recent S. pombe studies refined the signaling context of autophagy initiation rather than Atg13 biochemistry directly: (i) 2023 established major transcriptional control by PKA/SAPK during glucose limitation; (ii) 2024 phosphoproteomics showed TORC1 is reactivated during sexual differentiation by pheromone signaling, with Atg13 still discussed as a proposed TORC1 target but without mapped residues. In the 2024 study, Atg1 was not absolutely required for residual CFP-Atg8 cleavage in MSL medium, underscoring environmental dependence of autophagy readouts. (pqac-00000018, pqac-00000019, pqac-00000023) | Genetics; phosphoproteomics; autophagy flux | Pérez-Díaz et al. 2023, *Autophagy*; Bérard et al. 2024, *PLOS Biology* / bioRxiv | https://doi.org/10.1080/15548627.2022.2125204; https://doi.org/10.1371/journal.pbio.3002963; https://doi.org/10.1101/2024.06.04.597361 | Recent literature is valuable for pathway context, but there remains a gap in 2023–2024 residue-level or imaging-focused Atg13-specific data for S. pombe. |


*Table: This table summarizes the best available organism-specific evidence for Schizosaccharomyces pombe Atg13/O36019, including domain organization, interactions, signaling context, and assay support. It is useful for distinguishing directly demonstrated S. pombe findings from broader Atg13 models inferred from other systems.*