Fig. 4: Tethering proteins mediating mitochondria–lysosome contact are disrupted in GBA1-PD patient dopaminergic neurons. | Nature Communications

Fig. 4: Tethering proteins mediating mitochondria–lysosome contact are disrupted in GBA1-PD patient dopaminergic neurons.

From: Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease

Fig. 4

a–d Western blot analysis of b TBC1D15, c Rab7, and d Fis1 levels in PD patient-derived mutant GBA1 dopaminergic neurons (∆GBA) and its CRISPR-corrected isogenic control (Corr) neurons. Protein levels were normalized to loading control GAPDH. Values are expressed as fold-change compared to Corr (N = 3 independent experiments). Paired two-sided Student’s t-test; *p = 0.0442. e, f GST-RILP pull-down to measure GTP-bound Rab7 levels in ∆GBA and Corr neurons. f Rab7-GTP levels were normalized to total Rab7 normalized to GAPDH. Values are expressed as fold-change compared to Corr (N = 3 independent experiments). Paired two-sided Student’s t-test; *p = 0.0478. For all quantifications, data are means ± S.E.M., *p ≤ 0.05.

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