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Transcription Factor Yy1 OKDB#: 2949
 Symbols: YY1 Species: human
 Synonyms: DELTA, NF-E1, UCRBP, YIN-YANG-1,YIN YANG 1  Locus: 14q in Homo sapiens


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General Comment NCBI Summary: YY1 is a ubiquitously distributed transcription factor belonging to the GLI-Kruppel class of zinc finger proteins. The protein is involved in repressing and activating a diverse number of promoters. YY1 may direct histone deacetylases and histone acetyltransferases to a promoter in order to activate or repress the promoter, thus implicating histone modification in the function of YY1.
General function Chromosome organization, DNA binding , Epigenetic modifications
Comment The long noncoding Xist RNA inactivates one X chromosome in the female mammal. Current models posit that Xist induces silencing as it spreads along X and recruits Polycomb complexes. However, the mechanisms for Xist loading and spreading are currently unknown. Here, we define the nucleation center for Xist RNA and show that YY1 docks Xist particles onto the X chromosome. YY1 is a bivalent protein, capable of binding both RNA and DNA through different sequence motifs. Xist's exclusive attachment to the inactive X is determined by an epigenetically regulated trio of YY1 sites as well as allelic origin. Specific YY1-to-RNA and YY1-to-DNA contacts are required to load Xist particles onto X. YY1 interacts with Xist RNA through Repeat C. We propose that YY1 acts as adaptor between regulatory RNA and chromatin targets.
Cellular localization Nuclear
Comment
Ovarian function Primary follicle growth, Preantral follicle growth, Steroid metabolism, Luteolysis, Early embryo development
Comment Prostaglandin F2{alpha} Suppresses Rat Steroidogenic Acute Regulatory Protein Expression via Induction of Yin Yang 1 Protein and Recruitment of Histone Deacetylase 1 Protein. Liu Q et al. Prostaglandin F2alpha (PGF2alpha) plays a pivotal role in ovarian luteolysis by inhibiting the expression of StAR protein leading to a decrease in intracellular cholesterol transport and luteal steroid production. Previously we have demonstrated that the transcription factor YY1 bound to three regions in the StAR promoter in vitro and repressed promoter activity. This study further defined the YY1-mediated PGF2alpha effect on the inhibition of StAR protein expression through YY1 interaction with a single region in the StAR promoter in vivo. PGF2alpha consistently suppressed StAR mRNA and protein expression in cultured luteal cells in a dose dependent manner. PGF2alpha also enhanced YY1 protein expression and binding to its cis-element in a time-dependent pattern that preceded the decline in StAR protein levels. The StAR promoter region bound by YY1 was also associated with histone deacetylase 1 (HDAC1). PGF2alpha treatment promoted HDAC1 binding to and suppressed the histone H3 acetylation in this region. On the contrary, YY1 knockdown decreased HDAC1 binding, increased histone H3 acetylation, enhanced StAR protein expression, and negated PGF2alpha effect on StAR protein expression. Luciferase assays showed that YY1 overexpression inhibited StAR promoter activity and the addition of a HDAC inhibitor, Trichostatin A, abrogated the effect of YY1. Trichostatin A-treated luteal cells displayed increased StAR protein expression. These data indicate that PGF2alpha enhances a direct YY1/StAR promoter interaction and the recruitment of HDAC1 to the promoter, thereby preventing transcriptional activation of the StAR gene.
Expression regulated by
Comment
Ovarian localization Oocyte
Comment Expression of Polycomb-group genes in human ovarian follicles, oocytes and preimplantation embryos Hinkins M, et al . Mammalian oocytes possess unique properties with respect to their ability to regulate and reprogram chromatin structure and epigenetic information. Proteins containing the conserved chromodomain motif that is common to the Polycomb-group (Pc-G) proteins and the heterochromatin-associated protein HP1, play essential roles in these processes and more specifically, in X-chromosome inactivation in female zygotes and extra-embryonic tissues and in the regulation of genomic imprinting. To characterize the potential role of these proteins in the regulation of epigenetic events during early human development, we utilized a degenerate PCR priming assay to assess the expression of mRNAs of chromodomain proteins in cDNA samples derived from the human female germline and preimplantation embryos. Expression of mRNAs of HP1 genes was observed in ovarian follicles, (HP1 (HSalpha), HP1 (HSbeta), HP1 (HSgamma)), mature oocytes (HP1 (HSalpha), HP1 (HSbeta)), cleavage stage preimplantation embryos (HP1 (HSalpha), HP1 (HSbeta), HP1 (HSgamma)) and blastocysts (HP1 (HSalpha), HP1 (HSgamma)). Transcripts for three Pc-G genes, which are essential for early mammalian development (Yin Yang 1 (YY1), Enhancer of Zeste-2 (EZH2) and Embryonic Ectoderm Development (EED)) and that are essential for the regulation of X-inactivation and certain imprinted genes (EED) were revealed by gene-specific-PCR expression analysis of human ovarian follicles, oocytes and preimplantation embryos. YY1 and EZH2 transcripts were additionally detected in metaphase II oocytes.
Follicle stages
Comment Changes of maternal transcripts in oocytes from persistent follicles in cattle. Lingenfelter BM et al. A high incidence of early embryonic loss is associated with prolonged dominance of follicles. The objective of the present experiment was to determine if persistence of a follicle resulted in alterations in mRNA expression of important genes in the oocyte. Cows were assigned to four groups: growing follicles on day 6 (G0h) or day 8 (G48h) and persistent follicles on day 13 (P0h) or day 15 (P48h) of the estrous cycle (estrus = day 0). All cows were super-stimulated on day 1-4. Cows in G48h, P0h, and P48h groups received 25 mg prostaglandin (PG) F2alpha on day 6. Cows in P0h and P48h groups received progesterone from CIDR-B devices on day 5 through 13. Ovaries of cows in G0h, G48h, P0h, and P48h groups were removed on day 6, 8, 13, and 15, respectively. Oocytes were aspirated immediately after colpotomy and denuded of cumulus cells. Quantitative real-time PCR was used to measure the mRNA abundances of 10 selected genes important for early embryogenesis in oocytes obtained from growing and persistent follicles. Relative abundances of MSY2, PARN, and YY1 mRNA (P < 0.05) were significantly lower in oocytes from persistent than from growing follicles. Oocytes from persistent follicles, however, had greater abundances of PAP and eIF-4E transcripts (P < 0.05). The data indicate that persistence of a follicle leads to altered abundances of mRNA for genes important for regulation of transcription and protein translation in the oocyte, which could compromise development of early embryos in cows that ovulate a persistent follicle. Mol. Reprod. Dev. (c) 2006 Wiley-Liss, Inc.
Phenotypes
Mutations 1 mutations

Species: mouse
Mutation name: None
type: null mutation
fertility: infertile - ovarian defect
Comment: Yin-Yang1 Is Required in the Mammalian Oocyte for Follicle Expansion. Griffith GJ et al. The multifaceted polycomb group gene Yin-Yang1 (Yy1) has been implicated in a variety of transcriptional regulatory roles--both as an activator and silencer of gene expression. Here we have examined the role of Yy1 during oocyte growth by conditional deletion of the locus in the growing oocyte. Our results indicate that YY1 is required for oocyte maturation and granulosa cell expansion. In mutant oocytes we observe severely reduced expression of both Gdf9 and Bmp15, suggesting a mechanism underlying the failure of granulosa cell expansion. Consequently, we observe infertility, failure of estrus cycling and altered reproductive hormone levels in mutant females. Additionally we find that YY1-deficient oocytes exhibit altered levels of several oocyte specific factors including Pou5f1, Figla, Lhx8, Oosp1 and Sohlh2. These results document YY1's involvement in folliculogenesis and ovarian function in the mouse, and indicate that YY1 is required specifically in the oocyte for oocyte-granulosa cell communication.

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created: Dec. 7, 2005, 10:03 a.m. by: hsueh   email:
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last update: July 10, 2011, 11:45 a.m. by: hsueh    email:



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