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. 2022 Apr 6;13:1853. doi: 10.1038/s41467-022-29479-y

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — a HeLa DELE1^HA cells exposed to the specified sgRNAs or a non-targeting control (NTC). DELE1 processing and CHOP induction analyzed by immunoblotting as indicated. b HeLa WT and ΔDELE1 cells were transiently exposed to an sgRNA directed against PITRM1 (or NTC sgRNA) and induction of CHOP was analyzed by immunoblotting seven days post-transfection. c, d HAP1 DELE1 knockout (ΔDELE1) or stably reconstituted cells were infected with lentivirus encoding a NTC sgRNA or sgRNAs targeting PITRM1 (c) or PMPCB (d). CHOP levels were analyzed by immunoblotting seven (c) or six (d) days post transduction. (e) HeLa DELE1^HA WT, clonal PITRM1 knockout cells (ΔPITRM1) and clonal PITRM1 knockout cells reconstituted with PITRM1 or empty vector (ΔPITRM1 + PITRM1/vector) were analyzed for DELE1 cleavage and CHOP levels by immunoblotting. f HeLa DELE1^HA cells of the indicated genotypes were cultured in medium containing ISRIB or DMSO as control and cell growth was followed over time. Cells were passaged and counted every 3 days. Mean ± s.d. of n = 3 independent biological replicates (separately seeded and cultured wells for each genotype and treatment) is shown. Statistical significance was assessed using two-way ANOVA with Tukey’s multiple comparisons correction. Day 3: ns ≥ 0.1336; Day 6: **P = 0.0027, *P = 0.0396, ns = 0.5268; Day 9: ***P = 0.0002, *P = 0.0121, ns = 0.2491; Day 12: ****P < 0.0001, **P = 0.0081, ns = 0.1951. g HeLa DELE1^HA cells of the indicated genotypes were infected with lentivirus encoding sgRNAs directed against the specified genes or a non-targeting control together with tRFP. The fraction of tRFP-positive cells was followed over time. The percentage of sgDELE1 or sgHRI-containing cells was normalized to the non-targeting control and to day 7 for each cell line. Mean ± s.d. of n = 3 independent biological replicates (separately cultured wells for each sgRNA and genotype) is shown. h Model of the fates of DELE1 in the steady-state and in the context of different types of perturbed mitochondrial protein import and processing.