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标题：Author Correction: Generation of somatic mitochondrial DNA-replaced cells for mitochondrial dysfunction treatment
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作者：Hideki Maeda ; Daisuke Kami ; Ryotaro Maeda 等
期刊名称：Scientific Reports
电子版ISSN：2045-2322
出版年度：2021
卷号：11
DOI：10.1038/s41598-021-99936-z
语种：English
出版社：Springer Nature
摘要：Correction to: Scientific Reports 10.1038/s41598-021-90316-1, published online 25 May 2021 The original version of this Article contained an error in the long term culture of Figure 2(g). As a result, "ρ(-)". now reads: "Mock". Consequently, Figure 2(g) legend has been modified accordingly, “MirCs were generated from mitochondrial disease patient-derived (7S) fibroblasts. ( a) mtDNA CN during the procedure of MirC generation. Fibroblasts that received gene transfer, designated as 7S_ρ(-) were cultivated with or without isolated mitochondria. Mock transfectants that received a plasmid without the endonuclease, designated as 7S_Mock, were subjected to the same protocol. (n = 9, respectively). ( b) TaqMan qPCR SNP genotyping assay demonstrated the dominance of exogenous mtDNA. MirCs derived from 7S fibroblasts were designated as 7S_MirC. (n = 3, respectively). ( c) Heteroplasmic sc-ddPCR discriminated three different populations: healthy homoplasmic cells (Cluster 1: CL1, red), heteroplasmic cells (CL2, brown), and mutated homoplasmic cells (CL3, blue) for mtDNA. Representative analyses are shown in the quadrant plotting, and the averages are depicted as a bar graph. Donor mitochondria for MirCs were isolated from EPC100 cells. (n = 3, respectively). ( d) Cell growth of MirCs compared with the original cells and ρ(-) cells by using time-lapse imaging recorder from day 7 to day 12 in the protocol. The confluency was automatically calculated by JuLI STAT software. ( e) Microscopic photographs of cell cultures following mitochondrial replacement 5 days after replating at a concentration of 1 × 10 5 cells on day 12 in the protocol. ( f) The yield of cells and the doubling time of MirCs were similar to those of 7S fibroblasts. The black bar indicates 200 µm. (n = 3, respectively). ( g) Long-term culture showed the lifespan extension of MirCs. (n = 3, respectively). ( h) The cell size of MirCs was maintained during culture, whereas that of the original cells was significantly enlarged from early PDL with time. (n = 3, respectively). ( i) Short tandem repeats (STRs) demonstrated no contamination of the original MirCs by EPC100 cells that provided the donor mitochondria for MirCs. ( j) TERT expression in MirCs to deny carcinogenic transformations. The full-length gel of cropped gels is shown in Supplementary Fig. S4. mtDNA, mitochondrial DNA. CNT, no treatment control cell. ρ(-), rho minus, indicates cells with a low mtDNA number. CN, copy number. MC, medium change. DT, doubling time. PDL, population doubling level.” now reads: “MirCs were generated from mitochondrial disease patient-derived (7S) fibroblasts. ( a) mtDNA CN during the procedure of MirC generation. Fibroblasts that received gene transfer, designated as 7S_ρ(-) were cultivated with or without isolated mitochondria. Mock transfectants that received a plasmid without the endonuclease, designated as 7S_Mock, were subjected to the same protocol. (n = 9, respectively). ( b) TaqMan qPCR SNP genotyping assay demonstrated the dominance of exogenous mtDNA. MirCs derived from 7S fibroblasts were designated as 7S_MirC. (n = 3, respectively). ( c) Heteroplasmic sc-ddPCR discriminated three different populations: healthy homoplasmic cells (Cluster 1: CL1, red), heteroplasmic cells (CL2, brown), and mutated homoplasmic cells (CL3, blue) for mtDNA. Representative analyses are shown in the quadrant plotting, and the averages are depicted as a bar graph. Donor mitochondria for MirCs were isolated from EPC100 cells. (n = 3, respectively). ( d) Cell growth of MirCs compared with the original cells and ρ(-) cells by using time-lapse imaging recorder from day 7 to day 12 in the protocol. The confluency was automatically calculated by JuLI STAT software. ( e) Microscopic photographs of cell cultures following mitochondrial replacement 5 days after replating at a concentration of 1 × 10 5 cells on day 12 in the protocol. ( f) The yield of cells and the doubling time of MirCs were similar to those of 7S fibroblasts. The black bar indicates 200 µm. (n = 3, respectively). ( g) Long-term culture showed the lifespan extension of MirCs. (n = 3, respectively). Mock means cells that received gene transfection procedure without plasmid and subsequently were co-incubated with isolated mitochondria with the same protocol as MirC generation. ( h) The cell size of MirCs was maintained during culture, whereas that of the original cells was significantly enlarged from early PDL with time. (n = 3, respectively). ( i) Short tandem repeats (STRs) demonstrated no contamination of the original MirCs by EPC100 cells that provided the donor mitochondria for MirCs. ( j) TERT expression in MirCs to deny carcinogenic transformations. The full-length gel of cropped gels is shown in Supplementary Fig. S4. mtDNA, mitochondrial DNA. CNT, no treatment control cell. ρ(-), rho minus, indicates cells with a low mtDNA number. CN, copy number. MC, medium change. DT, doubling time. PDL, population doubling level.” The original Figure 2 and accompanying legend appear below. The original Article has been corrected. Figure 2 MirCs were generated from mitochondrial disease patient-derived (7S) fibroblasts. ( a) mtDNA CN during the procedure of MirC generation. Fibroblasts that received gene transfer, designated as 7S_ρ(-) were cultivated with or without isolated mitochondria. Mock transfectants that received a plasmid without the endonuclease, designated as 7S_Mock, were subjected to the same protocol. (n = 9, respectively). ( b) TaqMan qPCR SNP genotyping assay demonstrated the dominance of exogenous mtDNA. MirCs derived from 7S fibroblasts were designated as 7S_MirC. (n = 3, respectively). ( c) Heteroplasmic sc-ddPCR discriminated three different populations: healthy homoplasmic cells (Cluster 1: CL1, red), heteroplasmic cells (CL2, brown), and mutated homoplasmic cells (CL3, blue) for mtDNA. Representative analyses are shown in the quadrant plotting, and the averages are depicted as a bar graph. Donor mitochondria for MirCs were isolated from EPC100 cells. (n = 3, respectively). ( d) Cell growth of MirCs compared with the original cells and ρ(-) cells by using time-lapse imaging recorder from day 7 to day 12 in the protocol. The confluency was automatically calculated by JuLI STAT software. ( e) Microscopic photographs of cell cultures following mitochondrial replacement 5 days after replating at a concentration of 1 × 10 5 cells on day 12 in the protocol. ( f) The yield of cells and the doubling time of MirCs were similar to those of 7S fibroblasts. The black bar indicates 200 µm. (n = 3, respectively). ( g) Long-term culture showed the lifespan extension of MirCs. (n = 3, respectively). ( h) The cell size of MirCs was maintained during culture, whereas that of the original cells was significantly enlarged from early PDL with time. (n = 3, respectively). ( i) Short tandem repeats (STRs) demonstrated no contamination of the original MirCs by EPC100 cells that provided the donor mitochondria for MirCs. ( j) TERT expression in MirCs to deny carcinogenic transformations. The full-length gel of cropped gels is shown in Supplementary Fig. S4. mtDNA, mitochondrial DNA. CNT, no treatment control cell. ρ(-), rho minus, indicates cells with a low mtDNA number. CN, copy number. MC, medium change. DT, doubling time. PDL, population doubling level.