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Satb1 regulates the self-renewal of hematopoietic stem cells by promoting quiescence and repressing differentiation commitment
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Satb1 regulates the self-renewal of hematopoietic stem cells by promoting quiescence and repressing differentiation commitment
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Journal Article
Satb1 regulates the self-renewal of hematopoietic stem cells by promoting quiescence and repressing differentiation commitment
2013
Overview
How hematopoietic stem cells coordinate self-renewal and differentiation remains unclear. Steidl and colleagues show that the transcription factor and chromatin remodeler Satb1 is required for their self-renewal.
How hematopoietic stem cells (HSCs) coordinate the regulation of opposing cellular mechanisms such as self-renewal and differentiation commitment remains unclear. Here we identified the transcription factor and chromatin remodeler Satb1 as a critical regulator of HSC fate. HSCs lacking
Satb1
had defective self-renewal, were less quiescent and showed accelerated lineage commitment, which resulted in progressive depletion of functional HSCs. The enhanced commitment was caused by less symmetric self-renewal and more symmetric differentiation divisions of Satb1-deficient HSCs. Satb1 simultaneously repressed sets of genes encoding molecules involved in HSC activation and cellular polarity, including
Numb
and
Myc
, which encode two key factors for the specification of stem-cell fate. Thus, Satb1 is a regulator that promotes HSC quiescence and represses lineage commitment.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Cell Differentiation - genetics
/ Chromatin Assembly and Disassembly - genetics
/ Gene Expression Regulation, Developmental - genetics
/ Hematopoietic Stem Cells - physiology
/ Matrix Attachment Region Binding Proteins - genetics
/ Matrix Attachment Region Binding Proteins - metabolism
/ Membrane Proteins - genetics
/ Membrane Proteins - metabolism
/ Mice
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Proto-Oncogene Proteins c-myc - genetics
