Skip to main content
. 2015 Jan 15;128(2):232–238. doi: 10.1242/jcs.164152

Fig. 2.

Fig. 2.

TPC2 but not TPC1 mediates lysosomal morphology disturbances. (A–D) LAMP1 staining in fibroblasts from a healthy control (CTRL) (A) and a Parkinson disease patient (PD) (B–D) treated with either a control siRNA (Scr. siRNA) (A,B) or siRNA to TPC2 (C) or TPC1 (D). Scale bars: 5 µm. (E) Pooled data quantifying LAMP1 intensity for the cells shown in A–D (mean±s.e.m., n = 381–532 cells from six independent knockdowns from two patient and paired control lines). (F) Quantitative PCR analysis of TPC2 (left) and TPC1 (right) levels in cells treated with the indicated TPC siRNA. Data are from two patients and are normalised to TPC levels in cells treated with scrambled control siRNA. (G–I) Lysosomal morphology in control fibroblasts (G) or LRRK2-PD fibroblasts treated without (H) or with (I) the Rab7 GTPase inhibitor CID 1067700 (1 µM, 3 days). (J,K) Pooled data quantifying LAMP1 intensity (J) or the proportion of cells displaying perinuclear lysosome clustering (K) for the cells shown in G–I (mean±s.e.m., n = 237–281 cells from five independent platings of three patient and paired control lines). ***P<0.001. (L) Concentration–effect relationship (mean±s.e.m., n = 130–281 cells from five independent platings of three patient lines) for the Rab7 GTPase inhibitor on lysosome clustering in LRRK2-PD fibroblasts.