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The histone code reader Spin1 controls skeletal muscle development

ABSTRACT: We report developmental defects in Spin1(Myf5-Cre) mice, in which Spin1 is ablated in skeletal muscle.

ORGANISM(S): Mus musculus

PROVIDER: GSE92539 | GEO | 2017/12/08

SECONDARY ACCESSION(S): PRJNA357994

REPOSITORIES: GEO

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The histone code reader Spin1 controls skeletal muscle development.

Project description:While several studies correlated increased expression of the histone code reader Spin1 with tumor formation or growth, little is known about physiological functions of the protein. We generated Spin1M5 mice with ablation of Spin1 in myoblast precursors using the Myf5-Cre deleter strain. Most Spin1M5 mice die shortly after birth displaying severe sarcomere disorganization and necrosis. Surviving Spin1M5 mice are growth-retarded and exhibit the most prominent defects in soleus, tibialis anterior, and diaphragm muscle. Transcriptome analyses of limb muscle at embryonic day (E) 15.5, E16.5, and at three weeks of age provided evidence for aberrant fetal myogenesis and identified deregulated skeletal muscle (SkM) functional networks. Determination of genome-wide chromatin occupancy in primary myoblast revealed direct Spin1 target genes and suggested that deregulated basic helix-loop-helix transcription factor networks account for developmental defects in Spin1M5 fetuses. Furthermore, correlating histological and transcriptome analyses, we show that aberrant expression of titin-associated proteins, abnormal glycogen metabolism, and neuromuscular junction defects contribute to SkM pathology in Spin1M5 mice. Together, we describe the first example of a histone code reader controlling SkM development in mice, which hints at Spin1 as a potential player in human SkM disease.

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The histone code reader SPIN1 controls RET signaling in liposarcoma.

Project description:The histone code reader Spindlin1 (SPIN1) has been implicated in tumorigenesis and tumor growth, but the underlying molecular mechanisms remain poorly understood. Here, we show that reducing SPIN1 levels strongly impairs proliferation and increases apoptosis of liposarcoma cells in vitro and in xenograft mouse models. Combining signaling pathway, genome-wide chromatin binding, and transcriptome analyses, we found that SPIN1 directly enhances expression of GDNF, an activator of the RET signaling pathway, in cooperation with the transcription factor MAZ. Accordingly, knockdown of SPIN1 or MAZ results in reduced levels of GDNF and activated RET explaining diminished liposarcoma cell proliferation and survival. In line with these observations, levels of SPIN1, GDNF, activated RET, and MAZ are increased in human liposarcoma compared to normal adipose tissue or lipoma. Importantly, a mutation of SPIN1 within the reader domain interfering with chromatin binding reduces liposarcoma cell proliferation and survival. Together, our data describe a molecular mechanism for SPIN1 function in liposarcoma and suggest that targeting SPIN1 chromatin association with small molecule inhibitors may represent a novel therapeutic strategy.

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The epigenetic reader protein SPIN1 controls proliferation and survival of liposarcoma by modulating the RET signaling pathway [RNA-Seq]

Project description:The aim of this study is to identify the SPIN1 target genes in liposarcoma cells

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The epigenetic reader protein SPIN1 controls proliferation and survival of liposarcoma by modulating the RET signaling pathway [ChIP-Seq]

Project description:The aim of this study is to identify the SPIN1 target genes in liposarcoma cells

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Next Generation Sequencing Analysis of Wild Type and SRSF2-MKO Skeletal Muscle Transcriptomes

Project description:We report skeletal muscle developmental defects in SRSF2 MyoD-Cre mice, in which SRSF2 is ablated in skeletal muscle.

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Gene expression signatures in SPIN1 siRNA- and negative control-transfected breast cancer cell line MCF-7/ADM

Project description:To screen potential target genes of SPIN1 in breast cancer, human gene expression microarray was performed to identify differentially expressed mRNAs in SPIN1 siRNA or negative control transfected MCF-7/ADM cells. After transfection with SPIN1 siRNA, 4409 genes were differentially expressed by >2-fold in MCF-7/ADM cells compared with negative control-transfected cells, of which 2413 were significantly downregulated and the other 1996 were upregulated. Differentially expressed genes were submitted to GO and KEGG pathway analysis.

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Distinct activities of Myf5 and MyoD indicate sequential roles in skeletal muscle lineage specification and differentiation (RNA-Seq)

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