Transcription factor YY1 functions as a PcG protein in vivo

Atchison, Lakshmi; Ghias, Ayesha; Wilkinson, Frank H.; Bonini, Nancy M.; Atchison, Michael L.

doi:10.1093/emboj/cdg124

Cited by 184 publications

(206 citation statements)

References 69 publications

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“…The coincidental increase in H3K27me3 (Fig 3) suggests that the recruitment of Polycomb group complex (PcG) might contribute to establish marks of repressive chromatin, in cooperation with Brm-based SWI/SNF, as proposed by Ho & Crabtree [51]. Interestingly, the sequence of Ccnd1 promoter that is bound by Brm and is enriched in H3K27me3 contains both putative YY1 and E2F4/6 binding sites, which can mediate Brm recruitment, via PcG [52] or pRb [49,53], respectively.…”

Section: Discussionmentioning

confidence: 76%

Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis

et al. 2015

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Although the two catalytic subunits of the SWI/SNF chromatinremodeling complex-Brahma (Brm) and Brg1-are almost invariably co-expressed, their mutually exclusive incorporation into distinct SWI/SNF complexes predicts that Brg1-and Brm-based SWI/SNF complexes execute specific functions. Here, we show that Brg1 and Brm have distinct functions at discrete stages of muscle differentiation. While Brg1 is required for the activation of muscle gene transcription at early stages of differentiation, Brm is required for Ccnd1 repression and cell cycle arrest prior to the activation of muscle genes. Ccnd1 knockdown rescues the ability to exit the cell cycle in Brm-deficient myoblasts, but does not recover terminal differentiation, revealing a previously unrecognized role of Brm in the activation of late muscle gene expression independent from the control of cell cycle. Consistently, Brm null mice displayed impaired muscle regeneration after injury, with aberrant proliferation of satellite cells and delayed formation of new myofibers. These data reveal stage-specific roles of Brm during skeletal myogenesis, via formation of repressive and activatory SWI/SNF complexes.

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Section: Discussionmentioning

confidence: 76%

Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis

et al. 2015

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“…The search site predicted a series of transcription factors that might be involved in the transcriptional regulation of let-7a (Table 1). The transcription factor Yin Yang 1 (YY1), ranked first in the prediction, is a member of the polycomb group and has been shown to be involved in CXCR4 signaling (25)(26)(27)(28)(29).…”

Section: Figurementioning

confidence: 99%

CXCR4 downregulation of let-7a drives chemoresistance in acute myeloid leukemia

Chen¹,

Jácamo²,

Konopleva³

et al. 2013

J. Clin. Invest.

169

130

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We examined the role of microRNAs (miRNAs) in targeting the stromal-derived factor 1α/CXCR4 (SDF-1α/ CXCR4) axis to overcome chemoresistance of AML cells. Microarray analysis of OCI-AML3 cells revealed that the miRNA let-7a was downregulated by SDF-1α-mediated CXCR4 activation and increased by CXCR4 inhibition. Overexpression of let-7a in AML cell lines was associated with decreased c-Myc and BCL-XL protein expression and enhanced chemosensitivity, both in vitro and in vivo. We identified the transcription factor Yin Yang 1 (YY1) as a link between SDF-1α/CXCR4 signaling and let-7a, as YY1 was upregulated by SDF-1α and downregulated by treatment with a CXCR4 antagonist. ChIP assay confirmed the binding of YY1 to unprocessed let-7a DNA fragments, and treatment with YY1 shRNA increased let-7a expression. In primary human AML samples, high CXCR4 expression was associated with low let-7a levels. Xenografts of primary human AML cells engineered to overexpress let-7a exhibited enhanced sensitivity to cytarabine, resulting in greatly extended survival of immunodeficient mice. Based on these data, we propose that CXCR4 induces chemoresistance by downregulating let-7a to promote YY1-mediated transcriptional activation of MYC and BCLXL in AML cells.

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“…One mechanism of YY1-mediated transcriptional repression is through recruitment of PcG proteins (44,45). In situ hybrid- knockdown experiments (sets 1 and 2) using whole cell extracts of untransfected (Ϫ) or transfected P19 cells with either pSUPER-YY1 (YY1 siRNA) or pSUPER-CTRL (ctrl siRNA) vectors.…”

Section: Nucleosome Positioning and Remodeling At The Hoxd4 P1mentioning

confidence: 99%

Interplay between Chromatin and Trans-acting Factors Regulating the Hoxd4 Promoter during Neural Differentiation

Kobrossy

Rastegar

Featherstone

2006

Journal of Biological Chemistry

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Correct patterning of the antero-posterior axis of the embryonic trunk is dependent on spatiotemporally restricted Hox gene expression. In this study, we identified components of the Hoxd4 P1 promoter directing expression in neurally differentiating retinoic acid-treated P19 cells. We mapped three nucleosomes that are subsequently remodeled into an open chromatin state upon retinoic acid-induced Hoxd4 transcription. These nucleosomes spanned the Hoxd4 transcriptional start site in addition to a GC-rich positive regulatory element located 3 to the initiation site. We further identified two major cis-acting regulatory elements. An autoregulatory element was shown to recruit HOXD4 and its cofactor PBX1 and to positively regulate Hoxd4 expression in differentiating P19 cells. Conversely, the Polycomb group (PcG) protein Ying-Yang 1 (YY1) binds to an internucleosomal linker and represses Hoxd4 transcription before and during transcriptional activation. Sequential chromatin immunoprecipitation studies revealed that the PcG protein MEL18 was co-recruited with YY1 only in undifferentiated P19 cells, suggesting a role for MEL18 in silencing Hoxd4 transcription in undifferentiated P19 cells. This study links for the first time local chromatin remodeling events that take place during transcriptional activation with the dynamics of transcription factor association and DNA accessibility at a Hox regulatory region.Hox gene transcriptional activation marks the onset of an intricate series of events leading to proper embryonic patterning in all animals. The products of Hox genes, homeodomain-containing HOX transcription factors, are essential in specifying antero-posterior positional identity, hindbrain development, limb formation, and numerous additional morphogenetic and organogenetic events (1, 2). Given their crucial role in embryonic development, the genes encoding HOX proteins are highly conserved throughout the animal kingdom, and their expression is tightly regulated (3). In mammals, 39 Hox genes are organized into four clusters, each located on a different chromosome (1). Comparison of the clusters reveals 13 possible gene positions, although none of the clusters retains a full complement of 13 genes. Hox genes occupying the same positions are termed paralogs, sharing high sequence identity and functional redundancy. One can assign a 3Ј and a 5Ј end to a cluster since all genes are transcribed in the same direction. A unique feature of Hox gene clusters is a process termed "colinearity," correlating both the timing of transcriptional activation and the anterior expression borders with the position of a particular Hox gene along a cluster (4). Therefore, genes located more 3Ј are expressed earlier and have a more anterior expression border than genes located more 5Ј along the cluster. This observation and several other studies have led to the hypothesis that a sequential opening of chromatin, starting at the 3Ј end of a cluster and moving successively 5Ј, leads to the release of silencing, first at the 3Ј end, and seque...

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Transcription factor YY1 functions as a PcG protein in vivo

Cited by 184 publications

References 69 publications

Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis

Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis

CXCR4 downregulation of let-7a drives chemoresistance in acute myeloid leukemia

Interplay between Chromatin and Trans-acting Factors Regulating the Hoxd4 Promoter during Neural Differentiation

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