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Roles of sumoylation of a reptin chromatin-remodelling complex in cancer metastasis
Kim, Jung Hwa,Choi, Hee June,Kim, Bogyou,Kim, Mi Hyang,Lee, Ji Min,Kim, Ik Soo,Lee, Moon Hee,Choi, Soo Joon,Kim, Keun Il,Kim, Su-Il,Chung, Chin Ha,Baek, Sung Hee Nature Publishing Group 2006 NATURE CELL BIOLOGY Vol.8 No.6
Defining the functional modules within transcriptional regulatory factors that govern switching between repression and activation events is a central issue in biology. Recently, we have reported the dynamic role of a β-catenin–reptin chromatin remodelling complex in regulating a metastasis suppressor gene KAI1 (ref.1), which is capable of inhibiting the progression of tumour metastasis. Here, we identify signalling factors that confer repressive function on reptin and hence repress the expression of KAI1. Biochemical purification of a reptin-containing complex has revealed the presence of specific desumoylating enzymes that reverse the sumoylation of reptin that underlies its function as a repressor. Desumoylation of reptin alters the repressive function of reptin and its association with HDAC1. Furthermore, the sumoylation status of reptin modulates the invasive activity of cancer cells with metastatic potential. These data clearly define a functional model and provide a novel link for SUMO modification in cancer metastasis.
Negative Regulation of Hypoxic Responses via Induced Reptin Methylation
Lee, Jason S.,Kim, Yunho,Kim, Ik Soo,Kim, Bogyou,Choi, Hee June,Lee, Ji Min,Shin, Hi-Jai R.,Kim, Jung Hwa,Kim, Ji-Young,Seo, Sang-Beom,Lee, Ho,Binda, Olivier,Gozani, Or,Semenza, Gregg L.,Kim, Minhyung Elsevier 2010 Molecular cell Vol.39 No.1
<P><B>Summary</B></P><P>Lysine methylation within histones is crucial for transcriptional regulation and thus links chromatin states to biological outcomes. Although recent studies have extended lysine methylation to nonhistone proteins, underlying molecular mechanisms such as the upstream signaling cascade that induces lysine methylation and downstream target genes modulated by this modification have not been elucidated. Here, we show that Reptin, a chromatin-remodeling factor, is methylated at lysine 67 in hypoxic conditions by the methyltransferase G9a. Methylated Reptin binds to the promoters of a subset of hypoxia-responsive genes and negatively regulates transcription of these genes to modulate cellular responses to hypoxia.</P> <P><B>Highlights</B></P><P>► Reptin is a target of G9a methyltransferase ► Reptin K67 methylation is induced by hypoxia ► Genome-wide identification of hypoxia target genes negatively regulated by Reptin ► Hypoxia-driven Reptin methylation negatively regulates tumorigenic behavior in vivo</P>