YY1 Is a Structural Regulator of Enhancer-Promoter Loops

T helper 2 (Th2) cell differentiation, type 2 innate lymphoid cell (ILC2) development and regulation of interleukin-4 (IL-4) and IL-13 production.

There is considerable evidence that chromosome structure plays important roles in gene control, but we have limited understanding of the proteins that contribute to structural interactions between gene promoters and their enhancer elements. Large DNA loops that encompass genes and their regulatory elements depend on CTCF-CTCF interactions, but most enhancer-promoter interactions do not employ this structural protein. Here, we show that the ubiquitously expressed transcription factor Yin Yang 1 (YY1) contributes to enhancer-promoter structural interactions in a manner analogous to DNA interactions mediated by CTCF. YY1 binds to active enhancers and promoter-proximal elements and forms dimers that facilitate the interaction of these DNA elements. Deletion of YY1 binding sites or depletion of YY1 protein disrupts enhancer-promoter looping and gene expression. We propose that YY1-mediated enhancer-promoter interactions are a general feature of mammalian gene control.

The differential expression of IL-4 and IL-13 and its impact on type-2 immunity.

https://www.cell.com/immunity/pdf/S1074-7613(14)00225-8.pdf

GATA-3 function in innate and adaptive immunity

The Th2 locus control region (LCR) has been shown to be important in efficient and coordinated cytokine gene regulation during Th2 cell differentiation. However, the molecular mechanism for this is poorly understood. To study the molecular mechanism of the Th2 LCR, we searched for proteins binding to it. We discovered that transcription factor YY1 bound to the LCR and the entire Th2 cytokine locus in a Th2-specific manner. Retroviral overexpression of YY1 induced Th2 cytokine expression. CD4-specific knockdown of YY1 in mice caused marked reduction in Th2 cytokine expression, repressed chromatin remodeling, decreased intrachromosomal interactions, and resistance in an animal model of asthma. YY1 physically associated with GATA-binding protein-3 (GATA3) and is required for GATA3 binding to the locus. YY1 bound to the regulatory elements in the locus before GATA3 binding. Thus, YY1 cooperates with GATA3 and is required for regulation of the Th2 cytokine locus and Th2 cell differentiation.

https://www.pnas.org/content/pnas/110/1/276.full.pdf

Transcription factor YY1 is essential for regulation of the Th2 cytokine locus and for Th2 cell differentiation.

Attenuation of regulatory T cell function by type I IFN signaling in an MDA5 gain-of-function mutant mouse model.

GATA-binding protein-3 (GATA-3) regulates the T helper type 2 (Th2) cytokine locus through induction of chromatin remodelling. However, the molecular mechanism for this is poorly understood. To understand this mechanism better, we screened GATA-3 interacting proteins using affinity purification and mass spectrometry. We found that GATA-3 bound to metastasis-associated protein 2 (MTA-2), a component of the NuRD chromatin remodelling complex. GATA-3 and MTA-2 in turn bound to several regulatory regions of the Th2 cytokine locus and the ifng promoter. Cell transfection assay showed that MTA-2 acted as an antagonist with GATA-3 in the expression of Th2 cytokines, but co-operated with GATA-3 in the repression of the ifng gene expression. These results suggest that GATA-3 interacts with MTA-2 to co-ordinately regulate Th2 cytokine and ifng loci during T helper cell differentiation.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2567.2010.03271.x

GATA-binding protein-3 regulates T helper type 2 cytokine and ifng loci through interaction with metastasis-associated protein 2.

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Transcription factor YY1 is essential for regulation of the Th2 cytokine locus and for Th2 cell differentiation.

Attenuation of regulatory T cell function by type I IFN signaling in an MDA5 gain-of-function mutant mouse model.

GATA-binding protein-3 regulates T helper type 2 cytokine and ifng loci through interaction with metastasis-associated protein 2.