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  • 标题:Author Correction: Human WRN is an intrinsic inhibitor of progerin, abnormal splicing product of lamin A
  • 本地全文:下载
  • 作者:So‑mi Kang ; Min‑Ho Yoon ; Su‑Jin Lee
  • 期刊名称:Scientific Reports
  • 电子版ISSN:2045-2322
  • 出版年度:2021
  • 卷号:11
  • DOI:10.1038/s41598-021-97463-5
  • 语种:English
  • 出版社:Springer Nature
  • 摘要:Correction to: Scientific Reports 10.1038/s41598-021-88325-1, published online 27 April 2021 The original version of this Article contained an error in Figure 2G, where the legends for mouse models “Lmna +/+; Wrn +/-” and “Lmna G609/+; Wrn +/+” were interchanged. “Lmna +/+; Wrn +/- Lmna G609/+; Wrn +/+” now reads: “Lmna G609/+; Wrn +/+ Lmna +/+; Wrn +/-” In addition, the Supplementary Information file published with this Article contained an error in Figure S4B, where the x-axis “Genomic DNA” now reads: “cDNA gDNA” Finally, in the legend of Figure S4, “Analysis of lamin A genomic DNA in HGPS and WRN cells (at passage 12). An PCR screening using a specific primer to detect splice sites found in exon 11 of LMNA. A fragment under 300 bp in length was found in HGPS cells but not in WRN cells ( n = 3 independent experiments; two-tailed Student’s t-test).” now reads: “Analysis of lamin A genomic DNA (gDNA) in WRN cells (at passage 12). An intronic primer was designed for the PCR amplification of the LMNA exon 11 in WRN cells. The PCR product of HGPS cells was generated by amplification of cDNA using exon-specific primers ( n = 3 independent experiments; two-tailed Student’s t-test).” The original Figure  2 with accompanying legend and the Supplementary information file are provided below. The original Article and accompanying Supplementary Information file have been corrected. Figure 2 Fibroblasts derived from WRN patients express progerin. ( A) Analysis of lamin A cDNA in N9, HGPS, and WRN fibroblasts. RNA was extracted from HGPS, WRN and normal control cell lines (at passage 12) and RT-PCR was performed. A large amount of progerin was expressed in HGPS cells. A small amount of progerin was expressed in WRN cells. GAPDH was used as a loading control ( n  = 3 independent experiments; two-tailed Student’s  t-test). ( B) Analysis of progerin expression and nuclear aberrations in WRN and HGPS cells (at passage 11) by immunofluorescence (IF) assay. Progerin expression was detected by using an anti-progerin antibody. DAPI was used for nuclei staining. ( C) The box plot shows the relative expression of progerin in normal fibroblasts, HGPS, and WRN cells ( n  = 3 independent experiments; unpaired  t-test), Data are the mean ± SD. ( D) Expression of H3K9me3 was induced after the elimination of progerin in WRN cells (at passage 11) by an siRNA system. Knockdown of progerin induced H3K9me3 and reduced nuclear size in WRN cells. WRN cells were transfected with siRNA-control (Si-Con; nontarget sequence) or siRNA-progerin (Si-progerin) for 48 h and stained with anti-H3K9me3 antibody and DAPI ( n  = 3 independent experiments; unpaired  t-test). ( E) The box plot shows the intensity of H3K9me3 expression after transfection with siRNAs. ( F) The survival rate of  Lmna G609G/+  mice was not affected by deletion of the mouse  Wrn gene. Survival curves were determined by Kaplan–Meier analysis. ( G) The graph shows the change in body weight of 6 mouse models ( Lmna + /+   Wrn + /+ , Lmna + /+   Wrm + /- , Lmna + /+   Wrn −/− , Lmna G609G/+   Wrn + /+ , Lmna G609G/+   Wrn + /- , and  Lmna G609G/+   Wrn −/− ). There was no difference in body weight between  Lmna G609G/+  and  Lmna G609G/+ ;  Wrn −/−  mice or between  Wrn + /+  and  Wrn −/−  mice. ( H) Amino acid sequence analysis between human WRN (hWRN) and mouse WRN (mWRN). Twenty-eight amino acids are repeated in hWRN but not in mWRN. In hWRN, the sequences of exon 9 are repeated in exon 10. ** p  < 0.001. Data are the mean ± SD. Supplementary Information Supplementary Information.
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