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Author Correction: HIC2 controls developmental hemoglobin switching by repressing BCL11A transcription - Nature Genetics

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By Peng Huang, Scott A. Peslak, Cheryl A. Keller, Belinda Giardine, Henry Bell, Malini Sharma, Osheiza Abdulmalik, Stella T Chou, Junwei Shi, Merlin Crossley, Ross C. Hardison, Xiaodong Cheng
| Nature Verified
Correction to: Nature Genetics https://doi.org/10.1038/s41588-022-01152-6. Published online 8 August 2022. In the version of this article originally published, the sixth paragraph of the Discussion did not include the following text: “Moreover, Dykes et al.47 [J. Mol. Cell. Cardiol.
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HIC2 controls developmental hemoglobin switching by repressing BCL11A transcription - Nature Genetics

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By Peng Huang, Scott A. Peslak, Cheryl A. Keller, Belinda Giardine, Henry Bell, Malini Sharma, Osheiza Abdulmalik, Stella T Chou, Junwei Shi, Merlin Crossley, Ross C. Hardison, Gerd A. Blobel
| Nature Verified
Abstract The fetal-to-adult switch in hemoglobin production is a model of developmental gene control with relevance to the treatment of hemoglobinopathies. The expression of transcription factor BCL11A, which represses fetal β-type globin (HBG) genes in adult erythroid cells, is predominantly controlled at the transcriptional level but the underlying mechanism is unclear. We identify HIC2 as a repressor of BCL11A transcription. HIC2 and BCL11A are reciprocally expressed during development.
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