Correction to: Scientific Reports https://doi.org/10.1038/s41598-017-04535-6, published online 29 June 2017
In the original version of this Article, the authors neglected to cite a previously-published paper which reports prior in vitro analysis of the transcriptional activity of grs357/s357 mutant line. As a result, in the Discussion section under subheading ‘Divergence in GRE-independent target gene transcription in the two mutant lines’.
“Divergent transcriptomic responses were observed with DEX suppression of the DSS-induced transcription of the cytokine genes il1β, il8 and il6 and of the metalloproteinase genes mmp-13 and DSS-unchallenged mmp-9 in grs357/s357 mutants, but not in the other ones. Hence, the grs357/s357 line directly reveals GRE-independent GC-GR transcribing activities due to their persistence, while the gr−/− line indirectly confirms their occurrence due to their absence with consequent effects on the phenotype, as discussed in details below.”
Now reads:
“Divergent transcriptomic responses were observed with DEX suppression of the DSS-induced transcription of the cytokine genes il1β, il8 and il6 and of the metalloproteinase genes mmp-13 and DSS-unchallenged mmp-9 in grs357/s357 mutants, but not in the other ones. Transcriptional activity of grs357/s357 mutant line was in vitro analysed by Ziv and co-workers (2013)31 that found lack of Gr genomic activity including transcriptional repression linked to AP1 or NF-kB transcription factors. However, these data are not in conflict with our definition of grs357/s357 as being partially silenced: Gr can regulate gene repression either by binding directly to a GRE and interacting with other transcription factors32 (and this way is lost also in grs357/s357) or by tethering with other DNA binding proteins, a way lost in the gr−/− null line while possibly retained in the grs357/s357 mutant. Hence, the grs357/s357 line directly reveals GRE-independent GC-GR transcribing activities due to their persistence, while the gr−/− line indirectly confirms their occurrence due to their absence with consequent effects on the phenotype, as discussed in details below.”
Additionally, a supplementary table containing the primers used was omitted from the original version of this Article. These errors have been corrected in the HTML version and the PDF version of the Article.
Author information
Authors and Affiliations
Corresponding author
Additional information
The original article can be found online at https://doi.org/10.1038/s41598-017-04535-6.
The original article can be found online at https://doi.org/10.1038/s41598-017-04535-6.
Rights and permissions
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/.
About this article
Cite this article
Facchinello, N., Skobo, T., Meneghetti, G. et al. Author Correction: nr3c1 null mutant zebrafish are viable and reveal DNA-binding-independent activities of the glucocorticoid receptor. Sci Rep 8, 4445 (2018). https://doi.org/10.1038/s41598-018-21745-8
Published:
DOI: https://doi.org/10.1038/s41598-018-21745-8
Comments
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.