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Erratum to: Repression of chimeric transcripts emanating from endogenous retrotransposons by a sequence-specific transcription factor

  • Ka Sin Mak1,
  • Jon Burdach1,
  • Laura J. Norton1,
  • Richard CM Pearson1,
  • Merlin Crossley1Email author and
  • Alister PW Funnell1
Genome Biology201617:119

https://doi.org/10.1186/s13059-016-0977-1

Received: 5 May 2016

Accepted: 5 May 2016

Published: 3 June 2016

The original article was published in Genome Biology 2014 15:3252

In the study [1] a gel depicted in Fig. 2a was labelled in a way which suggests that the sample comes from a Klf3 −/− knockout mouse. In fact, this sample comes from a Klf3 −/− ,Klf8 genetrap double mutant animal. The Klf8 genotype was not indicated as authors felt that it was not relevant for the conclusions of this paper; however, all authors now acknowledge that this information should have been included. Importantly, an equivalent result from single Klf3 −/− knockout mice is included and confirmed in the RNA-seq results presented in Figure 6 of the original article [1].
Fig. 2

A novel, internal Pu.1 promoter resides within an ORR1A0 LTR element and is repressed by KLF3. (a) RNA from Klf3 +/+ (WT) and Klf3 −/−, Klf8 genetrap TER119+ fetal liver cells was subjected to 5′ RACE using a reverse primer specific for exon 3 of Pu.1 and analyzed by agarose gel electrophoresis. The smaller band from a Klf3KO animal was sequenced and found to contain a novel exon (exon 2b). (b) The sequence of the ORR1A0 LTR, in which Pu.1 exon 2b is shown in bold. Sequences which fit the KLF binding consensus 5′-NCN CNC CCN-3′ are boxed, and the TATA box at −30 is underlined. (c) Schematic of the murine Pu.1 locus showing the position of exon 2b. Exons are represented by blue boxes, transcription start sites by arrowheads and splicing events by broken lines. Start points of translation (ATGs) for the two alternative transcripts are also shown. (d) Real-time RT-PCR quantification revealing that transcripts containing exon 2b spliced to exon 3 of Pu.1 (that is, Pu.2 transcripts) are upregulated in Klf3 −/− TER119+ E14.5 fetal liver cells compared to Klf3 +/− (HET) and Klf3 +/+. Values have been normalized to 18S rRNA and the Klf3 +/+ sample has been set to 1.0. n = 3 for each genotype. **, P <0.005 compared to both Klf3 +/+ and Klf3 +/− (Student’s two-tailedt-test). (e) ChIPs were performed on Klf3 +/+ and Klf3 −/− E14.5 fetal livers (n = 2 or 3 of each genotype per IP). Data are represented as the fold-change enrichment in Klf3 −/− cells compared to Klf3 +/+. The Fam132a and Klf8 promoters have been included as positive controls while Serpina9, Gapdh, and MyoD are negative control regions. *, P <0.05 compared to Gapdh (Student’s one-tailed t-test). In (d and e), error bars represent standard error of the mean

All other data described in the article were obtained from the Klf3 −/− single knockout mice, and as such the conclusions of the article remain unchanged. It is also critical to note that all other results in the article could not have been obtained from the double mutant mice, because Klf3,Klf8 deficient animals die in utero (as reported by the authors in [2]).

Figure 2 with the correct legend is published in this Erratum.

The authors apologize for this omission and any confusion and inconvenience it may have caused.

Notes

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
School of Biotechnology and Biomolecular Sciences, University of New South Wales, Kensington, Australia

References

  1. Mak KS, Burdach J, Norton LJ, Pearson RCM, Crossley M, Funnell APW. Repression of chimeric transcripts emanating from endogenous retrotransposons by a sequence-specific 35 transcription factor. Genome Biol. 2014;15:R58.View ArticlePubMedPubMed CentralGoogle Scholar
  2. Funnell APW, Mak KS, Twine NA, Pelka GJ, Norton LJ, Radziewic T, et al. Generation of Mice Deficient in both KLF3/BKLF and KLF8 Reveals a Genetic Interaction and a Role for These Factors in Embryonic Globin Gene Silencing. Mol Cell Biol. 2013;33(15):2976–87.Google Scholar

Copyright

© Mak et al. 2016

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