Impaired in vitro erythropoiesis following deletion of the Scl (Tal1) +40 enhancer is largely compensated for in vivo despite a significant reduction in expression.

作者: Rita Ferreira , Dominik Spensberger , Yvonne Silber , Andrew Dimond , Juan Li

DOI: 10.1128/MCB.01525-12

关键词:

摘要: The Scl (Tal1) gene encodes a helix-loop-helix transcription factor essential for hematopoietic stem cell and erythroid development. +40 enhancer is situated downstream of Map17, the 3' flanking Scl, active in transgenic mice during primitive definitive erythropoiesis. To analyze vivo function within Scl/Map17 transcriptional domain, we deleted this element germ line. Scl(Δ40/Δ40) were viable with reduced numbers CFU both bone marrow spleen yet displayed normal response to stress hematopoiesis. Analysis embryonic (ES) cells revealed impaired differentiation, which was accompanied by failure upregulate when erythropoiesis initiated. Map17 expression also tissues differentiating ES cells, able enhance activity promoter. However, only but not could rescue phenotype. Together, these data demonstrate that an cell-specific regulates Map17. Moreover, deletion causes novel phenotype, can be rescued ectopic

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