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Transcriptome Analysis Identifies Linc-Yy1, A Novel Functional LincRNA During Myogenesis

ABSTRACT: Little is known how lincRNAs are involved in skeletal myogenesis. Here we describe the discovery of a novel lincRNA, Linc-YY1 from the promoter of transcription factor (TF) Yin Yang 1 (YY1) gene. We demonstrate that Linc-YY1 is dynamically regulated during myogenesis in vitro and in vivo. Gain or loss of function of Linc-YY1 in C2C12 myoblast cells or satellite cells alters myogenic differentiation and in injured muscles impacts the course of regeneration. Further studies suggest LincYY1 may interact with YY1 through its middle domain to evict YY1

ORGANISM(S): Mus musculus

PROVIDER: GSE74049 | GEO | 2015/10/16

SECONDARY ACCESSION(S): PRJNA298863

REPOSITORIES: GEO

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A novel YY1-miR-1 regulatory circuit in skeletal myogenesis revealed by genome-wide prediction of YY1-miRNA network

Project description:microRNAs (miRNAs) are non-coding RNAs that regulate gene expression post-transcriptionally, and mounting evidences support the prevalence and functional significance of their interplay with transcription factors (TFs). Here we describe the identification of a regulatory circuit between muscle miRNAs (miR-1, miR-133 and miR-206) and Yin Yang 1 (YY1), an epigenetic repressor of skeletal myogenesis. Genome-wide identification of potential YY1 down-stream targets by combining computational prediction with expression profiling data reveals a large number of putative miRNA targets of YY1 during skeletal myoblasts differentiation into myotubes with muscle miRs rank on top of the list. Murine skeletal muscle cells (C2C12 cells) were differentiated for 0, 1 or 3 days. Total RNAs were isolated from the cells and used for array profiling of miRNA expression.

2011-12-31 | E-GEOD-32238 | biostudies-arrayexpress

A novel YY1-miR-1 regulatory circuit in skeletal myogenesis revealed by genome-wide prediction of YY1-miRNA network

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Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]

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Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]

Project description:Analysis of subcutaneous adipose tissue (IWAT) from Yin Yang 1 brown fat specific knockout mice fed a high fat diet for 2 weeks. The goal was to identify a gene signature of IWAT browning in YY1 mutant mice.

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Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]

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YY1 regulates DNA-DNA interaction

Project description:The DNA Guanine quadruplexes (G4) plays important roles in multiple cellular processes, including regulation of DNA replication, transcription and genome stability. Here, we show that Yin Yang-1 (YY1), a ubiquitously expressed and multifunctional transcription factor, can bind with G4 structures directly. Fluorescence anisotropy experiments shows that YY1 binds towards G4 structures with Kd in low nanomolar range (<100 nM) through the C terminal zinc finger domains. ChIP-seq results show that 81% of the YY1 ChIP-seq peaks contain G4 forming sequences, which is highly overlapped with the G4 ChIP-seq peaks. YY1 facilitate the DNA-DNA interaction through its binding with G4 structures in vivo and in vitro, which can be disturbed by G4 stabilizer treatment. In all, our studies identify a novel G4 structure binding protein-YY1, and reveal that G4 structure functions in DNA-DNA interaction.

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Project description:Ferroptosis is a type of programmed cell death caused by disruption of redox homeostasis, and is closely linked to amino acid metabolism. Yin Yang 2 (YY2) and its homolog Yin Yang 1 (YY1) are members of the YY family with high homology, especially in their zinc-finger domains. Furthermore, they share consensus DNA binding motif. In contrast with the oncogenic YY1, increasing evidences have demonstrated the tumor suppressive effect of YY2; however, at present, little is known about its biological and pathological functions. Here we found that YY2 induces tumor cells ferroptosis and subsequently, suppresses tumorigenesis, by inhibiting SLC7A11 transcription, leading to the decreased glutathione biosynthesis. Furthermore, we reveal that YY2 and YY1 bind competitively to SLC7A11 promoter and antagonistically regulate tumor cells ferroptosis, thus suggesting the molecular mechanism underlying their opposite regulation on tumorigenesis. Moreover, we showed that mutations of YY2 zinc-finger domains in clinical cancer patients abrogated YY2/SLC7A11 axis and tumor cells ferroptosis. Together, these results provide a new insight regarding the regulatory mechanism of ferroptosis, and a mechanistic explanation regarding the tumor suppressive effect of YY2. Furthermore, our findings demonstrate that homeostasis between YY1 and YY2 is crucial for maintaining redox homeostasis in tumor cells.

2022-05-11 | GSE184138 | GEO

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