TOR1 Gene Review - Complete Curation Package

Overview

Comprehensive GO annotation curation review for yeast TOR1 (Serine/threonine-protein kinase TOR1, UniProt P35169), a master regulator of cell growth and nutrient sensing in response to nitrogen, carbon, and amino acid availability.

Files in This Directory

Core Review Files

• TOR1-ai-review.yaml - Main reviewed annotation file (VALIDATED)
• 67 GO annotations with detailed curation actions
• 3 core molecular functions identified
• Evidence-based justification for all actions

Summary and Analysis Documents

• TOR1-REVIEW-COMPLETE.md - Comprehensive final report
• Executive summary of curation results
• Detailed findings by functional category
• Evidence quality assessment
• Literature references

• Recommendations for further annotation

• TOR1-CURATION-SUMMARY.md - Detailed analysis table

• Annotation breakdown by evidence code
• Action distribution (ACCEPT, NON-CORE, OVER-ANNOTATED)
• Specific rationale for each curation decision

• Reference mapping

• INDEX.md - This file

Reference Materials

• TOR1-uniprot.txt - UniProt record (official source)
• TOR1-goa.tsv - Original GOA annotations
• generate_tor1_reviews.py - Script documenting curation logic
• update_tor1_reviews.py - Script used to apply reviews

Quick Reference

Curation Statistics

Evidence Code Distribution

• IEA: 16 (Electronic)
• IDA: 14 (Direct Assay)
• IMP: 13 (Mutant Phenotype)
• IPI: 7 (Protein Interaction)
• IBA: 6 (Phylogenetic)
• IGI: 5 (Genetic Interaction)
• NAS: 4 (Non-traceable)
• EXP: 1 (Experimental)
• HDA: 1 (Homology)

Core Functions

1. Protein serine/threonine kinase activity (GO:0004674)
2. ATP binding (GO:0005524)
3. Protein-containing complex binding (GO:0044877)

Key Findings

ACCEPT Annotations (52 total)

Master Regulatory Pathways
- TORC1 signaling (GO:0038202, GO:0031929)
- TORC1 complex membership (GO:0031931)
- Nutrient sensing and response

Critical Growth Control Functions
- Negative regulation of autophagy (GO:0016242, GO:0010507)
- Ribosome biogenesis (GO:0042254)
- Translational initiation (GO:0006413)
- Cell growth regulation (GO:0001558)
- Cell cycle regulation (GO:0051726)

Subcellular Localizations (8 locations)
- Nucleus, cytoplasm, vacuolar/plasma membranes, endosome, Golgi

KEEP_AS_NON_CORE Annotations (9 total)

Peripheral Stress Response and Metabolic Outputs
- ER stress response, oxidative stress, heat response
- DNA damage response
- Cell wall organization, sphingolipid biosynthesis
- snRNA pseudouridylation
- Mitochondrial retrograde signaling

MARK_AS_OVER_ANNOTATED Annotations (6 total)

Generic Protein Binding Terms
- GO:0005515 (protein binding) with multiple IPI references
- Recommendation: Consolidate into GO:0031931 (TORC1 complex) and GO:0044877 (complex binding)

How to Use This Review

For GO Annotation Updates

1. Read TOR1-ai-review.yaml for the structured curation data
2. Review TOR1-REVIEW-COMPLETE.md for evidence-based justification
3. Check specific annotations in TOR1-CURATION-SUMMARY.md for detailed rationale

For Reference Literature

See TOR1-REVIEW-COMPLETE.md Literature References section for:
- PMID:12408816 - TORC1/TORC2 discovery
- PMID:9461583 - Autophagy control
- PMID:8741837 - Translation and G1 control
- And 7 additional key references

For Further Research

Recommended research areas for annotation enhancement:
1. Substrate-specific phosphorylation terms (Tap42, Sch9, Ypk3, S6)
2. Nutrient-specific sensing pathways (nitrogen, carbon, amino acids)
3. Complex composition refinement
4. Consolidation of generic protein-binding annotations

Validation Status

✓ PASSED - All 67 annotations reviewed and validated
- Schema validation: SUCCESS
- Evidence quality: HIGH (multiple evidence codes per function)
- Completeness: COMPREHENSIVE (all annotations addressed)

Generation Information

• Generated: December 31, 2025
• Organism: Saccharomyces cerevisiae (strain ATCC 204508 / S288c)
• Gene: TOR1 (Target of Rapamycin 1)
• UniProt ID: P35169
• Protein Size: 2470 amino acids
• EC Number: 2.7.11.1 (Serine/threonine kinase)

For questions about this curation, see the detailed analysis documents or original publication references cited throughout.