ATAD3A PN Consistency Notes
- Generated: 2026-06-18
- Project: PROTEOSTASIS
- Scope: PN consistency rereview against local AIGR review and available deep-research artifacts
- UniProt: Q9NVI7
- AIGR review status: COMPLETE
- Review batch: proteostasis-batch-2026-06-03 (PR 1379)
- Batch change status: added
Source Files Checked
Deep Research Files
AIGR Review Snapshot
- Description: ATAD3A encodes a mitochondrial AAA+ ATPase that is anchored in the mitochondrial inner membrane, enriched at inner/outer membrane and mitochondria-ER contact regions, and associated with mitochondrial nucleoids. It supports mitochondrial network organization, mtDNA/nucleoid organization, and mitochondrial protein synthesis, and it can participate in stress-response signaling from mitochondria, including PERK modulation at mitochondria-ER contact sites and HRI-mediated integrated stress response signaling after mitochondrial DNA breaks.
- Existing/core annotation action counts: ACCEPT: 18; KEEP_AS_NON_CORE: 7; MARK_AS_OVER_ANNOTATED: 3; MODIFY: 1; NEW: 2
PN Consistency Summary
- Consistency: Consistent, with a deliberate, well-documented divergence from the projection. Deep research (manual synthesis), review YAML, and notes all describe ATAD3A as a mitochondrial inner-membrane AAA+ ATPase for network/nucleoid/mtDNA organization and mitochondrial translation, with secondary stress signaling (PERK, HRI/ISR). The PN mitophagy projection is explicitly evaluated and rejected in notes ("I did not add GO:0000423 mitophagy"). No internal contradiction.
- PN story / NEW pressure: PN asserts ATAD3A in mitophagy (GO:0000423, real term). PN Notes base this on a mouse Atad3a/Pink1 study (Nat Immunology) where Atad3a suppresses mitophagy. The review correctly declined to ADD mitophagy: human evidence shows ATAD3A normally restrains PINK1 accumulation, so a positive "involved_in mitophagy" annotation would mis-state directionality, and no direct cargo-marking/receptor role is shown. Verdict: PN story over-reaches; appropriately NOT added. Review instead ADDED GO:0032042 (mtDNA metabolic process) and GO:0032543 (mitochondrial translation) as NEW — both better-supported core functions.
- Evidence alignment: No overlap. PN cites one mouse mitophagy paper (Atad3a/Pink1, Nat Immunology); review is built on mitochondrial topology/nucleoid/translation papers (PMID:20154147, 17210950, 22453275, 18063578) plus stress-signaling papers (PMID:37832546, 39116259) — none shared with the PN row. The projection rests on evidence the review judged insufficient for a human mitophagy assertion.
- Verdict: Consistent; PN mitophagy projection correctly NOT added (over-reaches; directionally suppressive in source). No edits required.
Full Consistency Review
- UniProt: Q9NVI7 · batch: proteostasis-batch-2026-06-03 · review status: COMPLETE
- PN placement:
ALP|Autophagy substrate selection|Marking substrates for selective autophagy|Mitophagy|PINK/PRKN pathway ; PN-node mapping: PINK/PRKN subtype no_mapping; Mitophagy type mapped, ok_for_propagation_to_go → GO:0000423 mitophagy (new_to_goa).
- Consistency: Consistent, with a deliberate, well-documented divergence from the projection. Deep research (manual synthesis), review YAML, and notes all describe ATAD3A as a mitochondrial inner-membrane AAA+ ATPase for network/nucleoid/mtDNA organization and mitochondrial translation, with secondary stress signaling (PERK, HRI/ISR). The PN mitophagy projection is explicitly evaluated and rejected in notes ("I did not add GO:0000423 mitophagy"). No internal contradiction.
- PN story / NEW pressure: PN asserts ATAD3A in mitophagy (GO:0000423, real term). PN Notes base this on a mouse Atad3a/Pink1 study (Nat Immunology) where Atad3a suppresses mitophagy. The review correctly declined to ADD mitophagy: human evidence shows ATAD3A normally restrains PINK1 accumulation, so a positive "involved_in mitophagy" annotation would mis-state directionality, and no direct cargo-marking/receptor role is shown. Verdict: PN story over-reaches; appropriately NOT added. Review instead ADDED GO:0032042 (mtDNA metabolic process) and GO:0032543 (mitochondrial translation) as NEW — both better-supported core functions.
- Mapping strategy: Gene is a defensible decline at this node (parallel to RAB7A/HSPA8 broader-rejection precedent): the Mitophagy type-leaf mapping is a class-level statement, but this gene's role is suppressive/indirect, so the projected term (GO:0000423) is broader/wrong-signed relative to the review's evidence.
- Evidence alignment: No overlap. PN cites one mouse mitophagy paper (Atad3a/Pink1, Nat Immunology); review is built on mitochondrial topology/nucleoid/translation papers (PMID:20154147, 17210950, 22453275, 18063578) plus stress-signaling papers (PMID:37832546, 39116259) — none shared with the PN row. The projection rests on evidence the review judged insufficient for a human mitophagy assertion.
- Verdict: Consistent; PN mitophagy projection correctly NOT added (over-reaches; directionally suppressive in source). No edits required.
PN Dossier Context
- review_batch: proteostasis-batch-2026-06-03
- review_yaml: genes/human/ATAD3A/ATAD3A-ai-review.yaml
- PN workbook rows: 1
PN row 1: Autophagy-Lysosome Pathway | Autophagy substrate selection | Marking substrates for selective autophagy | Mitophagy | PINK/PRKN pathway
- UniProt: Q9NVI7
- In branches: ALP
- Notes: AAA+ ATPase involved in mitochondrial dynamics. By homology with mouse: deletion of Atad3a hyperactivates mitophagy. Atad3a normally facilitates import and processing of Pink1, absence causes accumulation and activates mitophagy.
- PN references (titles):
- Atad3a suppresses Pink1-dependent mitophagy to maintain homeostasis of hematopoietic progenitor cells | Nature Immunology
- PN-node mapping records (path + ancestors):
- [subtype] Autophagy-Lysosome Pathway|Autophagy substrate selection|Marking substrates for selective autophagy|Mitophagy|PINK/PRKN pathway
status=no_mapping scope= GO=[]
rationale: Reviewed as a contextual PN role. The label is useful for curator triage, but by itself does not support a universal GO assertion for all member genes beyond curated ancestor or child mappings.
- [type] Autophagy-Lysosome Pathway|Autophagy substrate selection|Marking substrates for selective autophagy|Mitophagy
status=mapped scope=ok_for_propagation_to_go GO=[GO:0000423 mitophagy]
rationale: The PN marking category for mitophagy captures upstream cargo-marking steps that commit mitochondrial substrates to the mitophagy pathway. That supports propagation to mitophagy.
- [group] Autophagy-Lysosome Pathway|Autophagy substrate selection|Marking substrates for selective autophagy
status=no_mapping scope= GO=[]
rationale: Reviewed as a broad PN taxonomy container. The descendants mix components, regulators, context labels, and mechanistic leaves, so propagation should come only from narrower curated nodes.
- [class] Autophagy-Lysosome Pathway|Autophagy substrate selection
status=no_mapping scope= GO=[]
rationale: Reviewed as a broad substrate-selection container. GO has useful targets for specific receptor, cargo-adaptor, and selective-autophagy leaves, but this class mixes marking, recognition, receptor regulation, and unknown roles and should not propagate as one term.
- [branch] Autophagy-Lysosome Pathway
status=no_mapping scope= GO=[]
rationale: Reviewed as the top-level PN branch. It is a project taxonomy umbrella rather than a direct GO assertion; all propagation must come from manually curated child nodes.
Projected GO annotations (1)
- GO:0000423 mitophagy | scope=ok_for_propagation_to_go | goa_status=new_to_goa | from=Autophagy-Lysosome Pathway|Autophagy substrate selection|Marking substrates for selective autophagy|Mitophagy
Note
This file is generated from the current PROTEOSTASIS phase-1 dossier and local gene-review artifacts. Edit the source review, PN mapping, or dossier rather than this generated note when correcting the underlying curation.