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Alterations of autophagy in the peripheral neuropathy Charcot-Marie-Tooth type 2B

Colecchia, David, Stasi, Mariangela, Leonardi, Margherita, Manganelli, Fiore, Nolano, Maria, Veneziani, Bianca Maria, Santoro, Lucio, Eskelinen, Eeva-Liisa, Chiariello, Mario, Bucci, Cecilia·2018·Autophagy
DOI 10.1080/15548627.2017.1388475PMC PMC6103410
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Figure 1. Analysis of autophagy in HeLa cells expressing CMT2B-causing RAB7 mutant proteins. HeLa cells transfected for 48 h with empty vector or plasmids encoding HA-tagged RAB7WT, RAB7Q67L, RAB7T22N and CMT2B-causing RAB7 mutants (RAB7L129F, RAB7K157N, RAB7N161T, RAB7V162M), were incubated in full medium (FM) or starvation medium (ST) for 30 min, or in the presence of 100 nM bafilomycin A1 (BAF) for 3 h. (A) The colocalization rate between RAB7 and LC3B was analyzed for the each different RAB7 isoform and for each condition (FM, ST, BAF). (B) The number of LC3B-positive dots per cell was evaluated for each sample. (C) The autophagic flux was calculated as the ratio of LC3B dots between BAF and FM of the same sample and normalized on empty vector. Quantification of results was performed by unbiased intensitometric analysis of fluorescence using the Quantitation Module of Volocity software.69 Statistical analysis one-way ANOVA test was performed between the same conditions (FM, ST and BAF) selecting RAB7WT as the referring sample. All statistical comparisons are from the sample indicated with asterisks and RAB7WT. Means ± SEM for each value are shown in the graphs (n = 3). * = p < 0.05; ** = p < 0.01; *** = p < 0.001.
Figure 1. Analysis of autophagy in HeLa cells expressing CMT2B-causing RAB7 mutant proteins. HeLa cells transfected for 48 h with empty vector or plasmids encoding HA-tagged RAB7WT, RAB7Q67L, RAB7T22N and CMT2B-causing RAB7 mutants (RAB7L129F, RAB7K157N, RAB7N161T, RAB7V162M), were incubated in full medium (FM) or starvation medium (ST) for 30 min, or in the presence of 100 nM bafilomycin A1 (BAF) for 3 h. (A) The colocalization rate between RAB7 and LC3B was analyzed for the each different RAB7 isoform and for each condition (FM, ST, BAF). (B) The number of LC3B-positive dots per cell was evaluated for each sample. (C) The autophagic flux was calculated as the ratio of LC3B dots between BAF and FM of the same sample and normalized on empty vector. Quantification of results was performed by unbiased intensitometric analysis of fluorescence using the Quantitation Module of Volocity software.69 Statistical analysis one-way ANOVA test was performed between the same conditions (FM, ST and BAF) selecting RAB7WT as the referring sample. All statistical comparisons are from the sample indicated with asterisks and RAB7WT. Means ± SEM for each value are shown in the graphs (n = 3). * = p < 0.05; ** = p < 0.01; *** = p < 0.001.CC BY-NC-ND · PubMed Central
Figure 2. Analysis of autophagy in HeLa cells expressing CMT2B-causing RAB7 mutant proteins. HeLa cells transfected for 48 h with empty vector or plasmids encoding HA-tagged RAB7WT, RAB7Q67L, RAB7T22N and CMT2B-causing RAB7 mutants (RAB7L129F, RAB7K157N, RAB7N161T, RAB7V162M). Cells were incubated in full medium (FM) or starvation medium (ST) for 30 min, or in the presence of 100 nM bafilomycin A1 (BAF) for 3 h. (A) Cells were incubated in full medium or starvation medium for 30 min, or in the presence of BAF for 3 h. Immunoblot of LC3B, HA-RAB7, endogenous RAB7 and MAPK1. Representative images from 3 independent experiments are shown (n = 3). (B) Intensitometric analysis of LC3B and MAPK1 immunoblots shown in (A) were performed with NIH ImageJ. (C) The autophagic flux was calculated as the ratio of normalized LC3B-II between BAF and FM of the same sample. (D) Cells were incubated in full medium or in the presence of BAF for 24 h and next immunobloted for SQSTM1, GABARAP, HA-RAB7, endogenous RAB7 and MAPK1 proteins. Representative images from 3 independent experiments are shown (n = 3). (E) Intensitometric analysis of SQSTM1, GABARAP and MAPK1 immunoblots was used to calculate the autophagic flux as the ratio of LC3B dots between BAF and FM of the same sample. Statistical analysis one-way ANOVA test was performed between the same conditions (FM, ST and BAF) selecting RAB7WT as the referring sample. All statistical comparisons are from the sample indicated with asterisks and RAB7WT. Means ± SEM for each value are shown in the graphs. * = p < 0.05; ** = p < 0.01; *** = p < 0.001.
Figure 2. Analysis of autophagy in HeLa cells expressing CMT2B-causing RAB7 mutant proteins. HeLa cells transfected for 48 h with empty vector or plasmids encoding HA-tagged RAB7WT, RAB7Q67L, RAB7T22N and CMT2B-causing RAB7 mutants (RAB7L129F, RAB7K157N, RAB7N161T, RAB7V162M). Cells were incubated in full medium (FM) or starvation medium (ST) for 30 min, or in the presence of 100 nM bafilomycin A1 (BAF) for 3 h. (A) Cells were incubated in full medium or starvation medium for 30 min, or in the presence of BAF for 3 h. Immunoblot of LC3B, HA-RAB7, endogenous RAB7 and MAPK1. Representative images from 3 independent experiments are shown (n = 3). (B) Intensitometric analysis of LC3B and MAPK1 immunoblots shown in (A) were performed with NIH ImageJ. (C) The autophagic flux was calculated as the ratio of normalized LC3B-II between BAF and FM of the same sample. (D) Cells were incubated in full medium or in the presence of BAF for 24 h and next immunobloted for SQSTM1, GABARAP, HA-RAB7, endogenous RAB7 and MAPK1 proteins. Representative images from 3 independent experiments are shown (n = 3). (E) Intensitometric analysis of SQSTM1, GABARAP and MAPK1 immunoblots was used to calculate the autophagic flux as the ratio of LC3B dots between BAF and FM of the same sample. Statistical analysis one-way ANOVA test was performed between the same conditions (FM, ST and BAF) selecting RAB7WT as the referring sample. All statistical comparisons are from the sample indicated with asterisks and RAB7WT. Means ± SEM for each value are shown in the graphs. * = p < 0.05; ** = p < 0.01; *** = p < 0.001.CC BY-NC-ND · PubMed Central
Figure 3. Analysis of autophagic flux in EGFP-mCherry-LC3B HeLa cells expressing CMT2B-causing RAB7 mutant proteins. HeLa cells transfected for 48 h with empty vector or plasmids encoding HA-tagged RAB7WT, RAB7Q67L, RAB7T22N and CMT2B-causing RAB7 mutants (RAB7L129F, RAB7K157N, RAB7N161T, RAB7V162M), were incubated in full medium (FM) or starvation medium (ST) for 4 h. Scatter and singlet gates were used to eliminate debris, dead cells, and mitotic cells. For each experiment, voltages and gain on EGFP and mCherry detectors are set empirically on negative and positive controls to allow the best plot fit on the mCherry:EGFP ratio histogram. Statistical analysis one-way ANOVA test was performed between the same conditions (FM and ST) selecting RAB7WT as the referring sample. All statistical comparisons are from the sample indicated with asterisks and the corresponding RAB7WT. Means ± SEM for each value are shown in the graphs. * = p < 0.05; ** = p < 0.01; *** = p < 0.001. (A) Graph shows the percentage of cells with high autophagic flux (measured as mCherry:EGFP ratio) in FM and ST for each sample. (B) Histograms plotting cell counts versus mCherry:EGFP ratio with a bar indicating the gate for high autophagic flux cell population. Representative images from 3 independent experiments are shown (n = 3).
Figure 3. Analysis of autophagic flux in EGFP-mCherry-LC3B HeLa cells expressing CMT2B-causing RAB7 mutant proteins. HeLa cells transfected for 48 h with empty vector or plasmids encoding HA-tagged RAB7WT, RAB7Q67L, RAB7T22N and CMT2B-causing RAB7 mutants (RAB7L129F, RAB7K157N, RAB7N161T, RAB7V162M), were incubated in full medium (FM) or starvation medium (ST) for 4 h. Scatter and singlet gates were used to eliminate debris, dead cells, and mitotic cells. For each experiment, voltages and gain on EGFP and mCherry detectors are set empirically on negative and positive controls to allow the best plot fit on the mCherry:EGFP ratio histogram. Statistical analysis one-way ANOVA test was performed between the same conditions (FM and ST) selecting RAB7WT as the referring sample. All statistical comparisons are from the sample indicated with asterisks and the corresponding RAB7WT. Means ± SEM for each value are shown in the graphs. * = p < 0.05; ** = p < 0.01; *** = p < 0.001. (A) Graph shows the percentage of cells with high autophagic flux (measured as mCherry:EGFP ratio) in FM and ST for each sample. (B) Histograms plotting cell counts versus mCherry:EGFP ratio with a bar indicating the gate for high autophagic flux cell population. Representative images from 3 independent experiments are shown (n = 3).CC BY-NC-ND · PubMed Central
Figure 4. Analysis of autophagy in CMT2B fibroblasts. Normal dermal human fibroblasts (NDHF) and CMT2B patient-derived fibroblasts were incubated with full medium or starvation medium for 30 min, or incubated with 400 nM bafilomycin A1 for 3 h. (A) Representative images (n = 3) for NDHF and CMT2B fibroblasts labeled for LC3B (green), RAB7 (red) and nuclei (blue). White squares indicated the area enlarged in the zoom. (B) Colocalization rate between RAB7 and LC3B was analyzed for each condition (FM, ST, BAF). (C) The number of autophagosomes (scored as LC3B-positive dots) per cell was evaluated for each sample. (D) The autophagic flux was calculated as the ratio of LC3B dots between FM and BAF of the same sample. Statistical analysis was performed using one-way ANOVA test where normal fibroblasts were selected as referring sample for each condition (FM, ST and BAF). Means ± SEM for each value are shown in the graphs. * = p < 0.05; ** = p < 0.01; *** = p < 0.001. Scale bars are 10 μm for FM and BAF and 25 μm for ST.
Figure 4. Analysis of autophagy in CMT2B fibroblasts. Normal dermal human fibroblasts (NDHF) and CMT2B patient-derived fibroblasts were incubated with full medium or starvation medium for 30 min, or incubated with 400 nM bafilomycin A1 for 3 h. (A) Representative images (n = 3) for NDHF and CMT2B fibroblasts labeled for LC3B (green), RAB7 (red) and nuclei (blue). White squares indicated the area enlarged in the zoom. (B) Colocalization rate between RAB7 and LC3B was analyzed for each condition (FM, ST, BAF). (C) The number of autophagosomes (scored as LC3B-positive dots) per cell was evaluated for each sample. (D) The autophagic flux was calculated as the ratio of LC3B dots between FM and BAF of the same sample. Statistical analysis was performed using one-way ANOVA test where normal fibroblasts were selected as referring sample for each condition (FM, ST and BAF). Means ± SEM for each value are shown in the graphs. * = p < 0.05; ** = p < 0.01; *** = p < 0.001. Scale bars are 10 μm for FM and BAF and 25 μm for ST.CC BY-NC-ND · PubMed Central
Figure 5. Analysis of autophagy in CMT2B fibroblasts. (A) Normal dermal human fibroblasts and CMT2B patient derived fibroblasts were incubated with full medium (FM) or starvation medium (ST) for 30 min, or incubated with 400 nM bafilomycin A1 (BAF) for 3 h. Immunoblot of LC3B, HA-RAB7 proteins and MAPK1. Representative images from 3 independent experiments are shown (n = 3). (B) Intensitometric analysis of LC3B and MAPK1 immunoblots shown in (A) were performed with NIH ImageJ. (C) The autophagic flux was calculated as the ratio of normalized LC3B-II between BAF and FM of the same sample. (D) Normal dermal human fibroblasts and CMT2B patient-derived fibroblasts were incubated with starvation medium with or without 400 nM BAF for 3 h. Immunoblot of LC3B, RAB7 proteins and MAPK1. Representative images from 3 independent experiments are shown (n = 3). (E) Intensitometric analysis of LC3B and MAPK1 immunoblots shown in (D) were performed with NIH ImageJ. The autophagic flux was calculated as the ratio of LC3B dots between BAF and FM of the same sample. (F) The autophagic flux was calculated as the ratio of normalized LC3B-II between BAF and FM of the same sample. (G) Normal dermal human fibroblasts and CMT2B patient derived fibroblasts were incubated with full medium or incubated with 400 nM BAF for 24 h. Immunoblot of SQSTM1, GABARAP, RAB7 and MAPK1 proteins. Representative images from 3 independent experiments are shown (n = 3). (H) Intensitometric analysis of SQSTM1 and MAPK1 immunoblots shown in (G) were performed with NIH ImageJ. (I) The autophagic flux was calculated as the ratio of normalized SQSTM1 between BAF and FM of the same sample. (J) Intensitometric analysis of GABARAP-II and MAPK1 immunoblots shown in (G) were performed with NIH ImageJ. (K) The autophagic flux was calculated as the ratio of normalized GABARAP-II between BAF and FM of the same sample. Statistical analysis was performed using one-way ANOVA test where normal fibroblasts were selected as referring sample for each condition (FM, ST and BAF). Means ± SEM for each value are shown in the graphs. * = p < 0.05; ** = p < 0.01; *** = p < 0.001.
Figure 5. Analysis of autophagy in CMT2B fibroblasts. (A) Normal dermal human fibroblasts and CMT2B patient derived fibroblasts were incubated with full medium (FM) or starvation medium (ST) for 30 min, or incubated with 400 nM bafilomycin A1 (BAF) for 3 h. Immunoblot of LC3B, HA-RAB7 proteins and MAPK1. Representative images from 3 independent experiments are shown (n = 3). (B) Intensitometric analysis of LC3B and MAPK1 immunoblots shown in (A) were performed with NIH ImageJ. (C) The autophagic flux was calculated as the ratio of normalized LC3B-II between BAF and FM of the same sample. (D) Normal dermal human fibroblasts and CMT2B patient-derived fibroblasts were incubated with starvation medium with or without 400 nM BAF for 3 h. Immunoblot of LC3B, RAB7 proteins and MAPK1. Representative images from 3 independent experiments are shown (n = 3). (E) Intensitometric analysis of LC3B and MAPK1 immunoblots shown in (D) were performed with NIH ImageJ. The autophagic flux was calculated as the ratio of LC3B dots between BAF and FM of the same sample. (F) The autophagic flux was calculated as the ratio of normalized LC3B-II between BAF and FM of the same sample. (G) Normal dermal human fibroblasts and CMT2B patient derived fibroblasts were incubated with full medium or incubated with 400 nM BAF for 24 h. Immunoblot of SQSTM1, GABARAP, RAB7 and MAPK1 proteins. Representative images from 3 independent experiments are shown (n = 3). (H) Intensitometric analysis of SQSTM1 and MAPK1 immunoblots shown in (G) were performed with NIH ImageJ. (I) The autophagic flux was calculated as the ratio of normalized SQSTM1 between BAF and FM of the same sample. (J) Intensitometric analysis of GABARAP-II and MAPK1 immunoblots shown in (G) were performed with NIH ImageJ. (K) The autophagic flux was calculated as the ratio of normalized GABARAP-II between BAF and FM of the same sample. Statistical analysis was performed using one-way ANOVA test where normal fibroblasts were selected as referring sample for each condition (FM, ST and BAF). Means ± SEM for each value are shown in the graphs. * = p < 0.05; ** = p < 0.01; *** = p < 0.001.CC BY-NC-ND · PubMed Central
Figure 6. Analysis of autophagosome biogenesis in CMT2B fibroblasts. Statistical analysis was performed using one-way ANOVA test where normal fibroblasts were selected as referring sample for each condition (full medium [FM] and serum starved [ST]). Means ± SEM for each value are shown in the graphs. (A) Normal dermal human fibroblasts and CMT2B patient-derived fibroblasts were incubated with full medium or serum starved medium for 6 sec. Immunoblots of ATG5, ATG12 and MAPK1 proteins. Representative images from 3 independent experiments are shown (n = 3). (B) Intensitometric analysis of ATG12–ATG5 complex (labeled with ATG5) and MAPK1 immunoblots shown in (A) were performed with NIH ImageJ. (C) Intensitometric analysis of ATG12–ATG5 complex (labeled with ATG12) and MAPK1 immunoblots shown in (A) were performed with NIH ImageJ. (D) Representative images (n = 3) for NDHF and CMT2B fibroblasts labeled for ATG12 (green) and nuclei (blue). Scale bars are 25 μm. (E) The number of ATG12 puncta per cell was evaluated for each sample. (F) Representative images (n = 3) for NDHF and CMT2B fibroblasts labeled for ATG5 (green) and nuclei (blue). (G) The number of ATG5 puncta per cell was evaluated for each sample. Scale bars are 25 μm except for starved CMT2B where they are 10 μm.
Figure 6. Analysis of autophagosome biogenesis in CMT2B fibroblasts. Statistical analysis was performed using one-way ANOVA test where normal fibroblasts were selected as referring sample for each condition (full medium [FM] and serum starved [ST]). Means ± SEM for each value are shown in the graphs. (A) Normal dermal human fibroblasts and CMT2B patient-derived fibroblasts were incubated with full medium or serum starved medium for 6 sec. Immunoblots of ATG5, ATG12 and MAPK1 proteins. Representative images from 3 independent experiments are shown (n = 3). (B) Intensitometric analysis of ATG12–ATG5 complex (labeled with ATG5) and MAPK1 immunoblots shown in (A) were performed with NIH ImageJ. (C) Intensitometric analysis of ATG12–ATG5 complex (labeled with ATG12) and MAPK1 immunoblots shown in (A) were performed with NIH ImageJ. (D) Representative images (n = 3) for NDHF and CMT2B fibroblasts labeled for ATG12 (green) and nuclei (blue). Scale bars are 25 μm. (E) The number of ATG12 puncta per cell was evaluated for each sample. (F) Representative images (n = 3) for NDHF and CMT2B fibroblasts labeled for ATG5 (green) and nuclei (blue). (G) The number of ATG5 puncta per cell was evaluated for each sample. Scale bars are 25 μm except for starved CMT2B where they are 10 μm.CC BY-NC-ND · PubMed Central

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Metadata

Authors
Colecchia, D., Stasi, M., Leonardi, M., Manganelli, F., Nolano, M., Veneziani, B. M., Santoro, L., Eskelinen, E.-L., Chiariello, M., & Bucci, C.
Affiliations
  • Consiglio Nazionale delle Ricerche, Istituto di Fisiologia Clinica and Istituto Toscano Tumori-Core Research Laboratory, Signal Transduction Unit, AOU Senese, Siena, Italy
  • Department of Biological and Environmental Sciences and Technologies (DiSTeBA), University of Salento, Lecce, Italy
  • Department of Neurosciences, University of Naples “Federico II”, Naples, Italy
  • Salvatore Maugeri Foundation, Institute of Telese Terme, Benevento, Italy
  • Department of Molecular Medicine and Medical Biotechnologies, University of Naples “Federico II”, Naples, Italy
  • Department of Biosciences, Division of Biochemistry and Biotechnology, University of Helsinki, Helsinki, Finland
ORCID
Venue
Autophagy
Publisher
Informa UK Limited
Published
2018-05-04
Pages
1-12
ISSN
  • 1554-8627
  • 1554-8635
DOI
10.1080/15548627.2017.1388475
PMC
PMC6103410
Cited by
10
References
2
Language
en
Funders
  • Italian Association for Cancer Research (AIRC) (IG2016 N.19068)
  • Telethon Italy (GGP16037)

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