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Polycomb Group Protein YY1 Is an Essential Regulator of Hematopoietic Stem Cell Quiescence.


ABSTRACT: Yin yang 1 (YY1) is a ubiquitous transcription factor and mammalian polycomb group protein (PcG) with important functions to regulate embryonic development, lineage differentiation, and cell proliferation. YY1 mediates stable PcG-dependent transcriptional repression via recruitment of PcG proteins that catalyze histone modifications. Many questions remain unanswered regarding how cell- and tissue-specificity is achieved by PcG proteins. Here, we demonstrate that a conditional knockout of Yy1 in hematopoietic stem cells (HSCs) decreases long-term repopulating activity and ectopic YY1 expression expands HSCs. Although the YY1 PcG domain is required for Ig? chain rearrangement in B cells, the YY1 mutant lacking the PcG domain retained the capacity to stimulate HSC self-renewal. YY1 deficiency deregulated the genetic network governing HSC cell proliferation and impaired stem cell factor/c-Kit signaling, disrupting mechanisms conferring HSC quiescence. These results reveal a mechanism for how a ubiquitously expressed transcriptional repressor mediates lineage-specific functions to control adult hematopoiesis.

SUBMITTER: Lu Z 

PROVIDER: S-EPMC6140794 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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Polycomb Group Protein YY1 Is an Essential Regulator of Hematopoietic Stem Cell Quiescence.

Lu Zhanping Z   Hong Courtney C CC   Kong Guangyao G   Assumpção Anna L F V ALFV   Ong Irene M IM   Bresnick Emery H EH   Zhang Jing J   Pan Xuan X  

Cell reports 20180201 6


Yin yang 1 (YY1) is a ubiquitous transcription factor and mammalian polycomb group protein (PcG) with important functions to regulate embryonic development, lineage differentiation, and cell proliferation. YY1 mediates stable PcG-dependent transcriptional repression via recruitment of PcG proteins that catalyze histone modifications. Many questions remain unanswered regarding how cell- and tissue-specificity is achieved by PcG proteins. Here, we demonstrate that a conditional knockout of Yy1 in  ...[more]

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