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. 2014 Mar 11;9(3):e92635. doi: 10.1371/journal.pone.0092635

Correction: Epigenetic Control of SPI1 Gene by CTCF and ISWI ATPase SMARCA5

The PLOS ONE Staff
PMCID: PMC3950286

Figure 5 contains two extraneous graphs on the right-hand side. In addition, the error bars in Figures 4 and 5 are of inconsistent thickness. The authors have provided corrected versions here.

Figure 5. Binding of Cohesin complex members to SPI1 locus.

Figure 5

A: ChIP of RAD21 and SMC1 in mixed myeloid cells. B: ChIP of RAD21 and C: SMC1 in OCI-M2 without (OCI-M2) or with AZA (OCI-M2 AZA) treatment. Y-axis: ChIP enrichment. X-axis: amplicons (distance relative to SPI1 TSS). URE, Upstream Regulatory Element of SPI1 gene; ENH, enhancer; ELE, element. Error bars: the standard errors (SE). Asterisks: p-values (t-test, 0.05–0.005).

Figure 4. CTCF/SMARCA5 are recruited to SPI1 locus in myeloid cells and upon AZA treatment in AML.

Figure 4

A: Sequence conservation of human SPI1 locus (VISTA) generated by aligning with murine DNA. Regulatory regions and positions of ChIP amplicons are numbered in respect to human SPI1 TSS. B: ChIP of CTCF and SMARCA5 in mixed myeloid cells. C: ChIP of CTCF and D: SMARCA5 in OCI-M2 without (OCI-M2) or with AZA (OCI-M2 AZA) treatment. Y-axis: ChIP enrichment. X-axis: amplicons (distance relative to SPI1 TSS). URE, Upstream Regulatory Element of SPI1 gene; ENH, enhancer; ELE, element. Error bars: the standard errors (SE). Asterisks: p-values (t-test, 0.05–0.005).

Reference


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