🧪
hypothesis

LRRK2 G2019S Uncouples RAB29-Dependent Spatial Control from Kinase Activity (H7)

Hypothesis

LRRK2 G2019S Uncouples RAB29-Dependent Spatial Control from Kinase Activity (H7)

Normally RAB29 recruits LRRK2 specifically to stressed lysosomes for localized RAB10 phosphorylation.
🧬 LRRK2,RAB29🩺 neurodegeneration🎯 Composite 64%💱 $0.57▼10.5%proposed
EvidencePending (0%)📖 0 cit🗣 1 debates 3 support 2 oppose
✓ All Quality Gates Passed
Mechanistic 0.65 (15%) Evidence 0.62 (15%) Novelty 0.85 (12%) Feasibility 0.58 (12%) Impact 0.68 (12%) Druggability 0.45 (10%) Safety 0.62 (8%) Competition 0.78 (6%) Data Avail. 0.55 (5%) Reproducible 0.62 (5%) KG Connect 0.50 (8%) 0.640 composite
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arXiv PreprintNeurIPSNature MethodsPLOS ONE
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Composite64%

🧪 Overview

Normally RAB29 recruits LRRK2 specifically to stressed lysosomes for localized RAB10 phosphorylation. G2019S increases kinase activity even in cytosolic/untargeted LRRK2, creating diffuse RAB10 phosphorylation that disrupts normal endosomal trafficking. RAB29 overexpression rescuing G2019S phenotypes suggests spatial control not completely uncoupled.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
    A["LRRK2 Mutation<br/>G2019S Kinase Hyperactivity"]
    B["RAB29 Recruitment<br/>Lysosomal Membrane"]
    C["Enhanced Lysosomal<br/>Volume Sensing"]
    D["Signal Amplification<br/>Pathological Threshold"]
    E["Lysosomal<br/>Dysfunction"]
    F["Autophagy<br/>Impairment"]
    G["Neuronal Death<br/>PD Progression"]
    A --> B
    B --> C
    C --> D
    D --> E
    E --> F
    F --> G
    style A fill:#6a1b9a,stroke:#ce93d8,color:#ce93d8
    style G fill:#b71c1c,stroke:#ef9a9a,color:#ef9a9a

⚖️ Evidence

⚖️ Evidence Matrix3 supports2 contradicts
Supports
LRRK2:RAB29 cryo-EM structure shows specific binding interface
PMID:34519112
Supports
RAB29 overexpression rescues G2019S phenotypes
PMID:30635564
Supports
Combined Knockout of Lrrk2 and Rab29 Does Not Result in Behavioral Abnormalities in vivo.
J Parkinsons Dis2021PMID:33523017
Contradicts
R1078 is in WD40 domain, not RAB29 interface—mutation may confound results
PMID:34519112
Contradicts
If truly uncoupled, RAB29 overexpression would not rescue
PMID:30635564
📖 Linked Papers

No linked papers recorded for this hypothesis yet.

🏥 Translation

🧬 3D Protein Structure — LRRK2

🧬 PDB 6VP6 Click to expand

Experimental structure from RCSB PDB | Powered by Mol*

🧠 GTEx v10 Brain ExpressionJSON

Median TPM across 13 brain regions for LRRK2,RAB29 from GTEx v10.

Frontal Cortex BA93.5 Cortex3.3median TPM (GTEx v10)

💉 Clinical Trials

No clinical trials data linked to this hypothesis yet.

No curated ClinVar variants loaded for this hypothesis.

Run scripts/backfill_clinvar_variants.py to fetch P/LP/VUS variants.

🔍 Search ClinVar for LRRK2,RAB29 →

No DepMap CRISPR Chronos data found for LRRK2,RAB29.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

🏆 Tournament

🏆 Arenas / Elo

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📊 Market Indicators

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💾 Resource Usage

No resource usage or linked notebooks recorded for this hypothesis yet.

🔮 Predictions

🔎 Predictions vs Observations2 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
IF G2019S-associated phenotypes arise from cytosolic LRRK2 kinase activity uncoupled from RAB29-dependent recruitment, THEN selective pharmacological inhibition of LRRK2 (MLi-2, 100nM, 4h) will reduceRAB10-pT73 levels will decrease significantly (p<0.001, ANOVA with Tukey's) and distribution will shift from cytosolic to lysosome-associated puncta, matching w— no observation —pending0.72
IF LRRK2 G2019S neurons are transduced with RAB29 overexpression vector, THEN the rescued phenotype will include restoration of RAB10 phosphorylation to lysosome-proximal puncta (≥80% colocalization wRAB10-pT73 signal will show punctate lysosomal enrichment rather than diffuse cytosolic distribution, with retrograde transport of fluorescently-labeled BDNF or— no observation —pending0.75
🔮 Falsifiable Predictions (2)
pendingconf 75%
IF LRRK2 G2019S neurons are transduced with RAB29 overexpression vector, THEN the rescued phenotype will include restoration of RAB10 phosphorylation to lysosome-proximal puncta (≥80% colocalization with LAMP2) and normalization of endocytic cargo trafficking rates to wild-type levels within 7 days
Predicted outcome: RAB10-pT73 signal will show punctate lysosomal enrichment rather than diffuse cytosolic distribution, with retrograde transport of fluorescently-label
Falsification: If RAB29 overexpression fails to re-establish lysosomal RAB10 phosphorylation localization (remains >50% diffuse) OR endosomal trafficking defects persist unchanged, the hypothesis that spatial contro
pendingconf 72%
IF G2019S-associated phenotypes arise from cytosolic LRRK2 kinase activity uncoupled from RAB29-dependent recruitment, THEN selective pharmacological inhibition of LRRK2 (MLi-2, 100nM, 4h) will reduce total cellular RAB10-pT73 by ≥70% and restore lysosomal RAB10 localization without requiring RAB29
Predicted outcome: RAB10-pT73 levels will decrease significantly (p<0.001, ANOVA with Tukey's) and distribution will shift from cytosolic to lysosome-associated puncta,
Falsification: If MLi-2 treatment reduces total RAB10 phosphorylation but RAB10 remains diffusely distributed (cytosolic/cytoplasmic >50% of signal), the spatial uncoupling model is falsified, indicating kinase acti
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