GATA Factor-Regulated Samd14 Enhancer Confers Red Blood Cell Regeneration and Survival in Severe Anemia

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Title
GATA Factor-Regulated Samd14 Enhancer Confers Red Blood Cell Regeneration and Survival in Severe Anemia
Author(s)
Kyle J. Hewitt; Koichi R. Katsumura; Daniel R. Matson; Prithvia Devadas; Nobuyuki Tanimura; Alexander S. Hebert; Joshua J. Coon; Jin-Soo Kim; Colin N. Dewey; Sunduz Keles; Siyang Hao; Robert F. Paulson; Emery H. Bresnick
Publication Date
2017-08
Journal
DEVELOPMENTAL CELL, v.42, no.3, pp.213 - 225.e4
Publisher
CELL PRESS
Abstract
An enhancer with amalgamated E-box and GATA motifs (+9.5) controls expression of the regulator of hematopoiesis GATA-2. While similar GATA-2-occupied elements are common in the genome, occupancy does not predict function, and GATA-2-dependent genetic networks are incompletely defined. A “+9.5-like” element resides in an intron of Samd14 (Samd14-Enh) encoding a sterile alpha motif (SAM) domain protein. Deletion of Samd14-Enh in mice strongly decreased Samd14 expression in bone marrow and spleen. Although steady-state hematopoiesis was normal, Samd14-Enh−/− mice died in response to severe anemia. Samd14-Enh stimulated stem cell factor/c-Kit signaling, which promotes erythrocyte regeneration. Anemia activated Samd14-Enh by inducing enhancer components and enhancer chromatin accessibility. Thus, a GATA-2/anemia-regulated enhancer controls expression of an SAM domain protein that confers survival in anemia. We propose that Samd14-Enh and an ensemble of anemia-responsive enhancers are essential for erythrocyte regeneration in stress erythropoiesis, a vital process in pathologies, including β-thalassemia, myelodysplastic syndrome, and viral infection. © 2017 Elsevier Inc
URI
https://pr.ibs.re.kr/handle/8788114/3648
ISSN
1534-5807
Appears in Collections:
Center for Genome Engineering(유전체 교정 연구단) > Journal Papers (저널논문)
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