ORC1 interacts with c‐Myc to inhibit E‐box‐dependent transcription by abrogating c‐Myc–SNF5/INI1 interaction

Takayama, Masa-aki; Taira, Takahiro; Tamai, Katsuyuki; Iguchi‐Ariga, Sanae M.M.; Ariga, Hiroyoshi

doi:10.1046/j.1365-2443.2000.00338.x

Cited by 37 publications

(33 citation statements)

References 46 publications

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“…In yeast and human cells, where ORC1 participates in gene silencing (13)(14)(15), changes in the histone modification status occur in the vicinity of the genomic region affected. We have found that Arabidopsis ORC1 also plays a role as a transcriptional regulator; but there are two novel features in its mechanism of action.…”

Section: Discussionmentioning

confidence: 99%

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Arabidopsis ORC1 is a PHD-containing H3K4me3 effector that regulates transcription

Sánchez

Gutiérrez

2009

Proc. Natl. Acad. Sci. U.S.A.

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Control of gene expression depends on a complex and delicate balance of various posttranslational modifications of histones. However, the relevance of specific combinations of histone modifications is not fully defined. Downstream effector proteins recognize particular histone modifications and transduce this information into gene expression patterns. Methylation of histone H3 at lysine 4 (H3K4me) is a landmark of gene expression control in eukaryotes. Its recognition depends on the presence in the effector protein of a motif termed plant homeodomain (PHD) that specifically binds to H3K4me3. Here, we establish that Arabidopsis ORC1, the large subunit of the origin recognition complex involved in defining origins of DNA replication, functions as a transcriptional activator of a subset of genes, the promoters of which are preferentially bound by ORC1. Arabidopsis ORC1 contains a PHD and binds to H3K4me3. In addition to H4 acetylation, ORC1 binding correlates with increased H4K20me3 in the proximal promoter region of ORC1 targets. This suggests that H4K20me3, unlike in animal cells, is associated with transcriptional activation in Arabidopsis. Thus, our data provide a molecular basis for the opposite role of ORC1 in transcriptional activation in plants and repression in animals. Since only ORC1 proteins of plant species contain a PHD, we propose that plant ORC1 constitutes a novel class of H3K4me3 effector proteins characteristic of the plant kingdom.cell cycle transcription ͉ histone H3 lysine 4 methylation ͉ ORC1 DNA replication ͉ plant homeodomain

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Section: Discussionmentioning

confidence: 99%

“…Thus, ORC1 participates in repression of yeast HMR and HML silent mating type loci (13), and human aldolase B (14) and c-Myc genes (15). Mutations of several ORC subunits in multicellular organisms cause pleiotropic phenotypes including chromosomal abnormalities, cell cycle arrest or zygotic lethality (16)(17)(18).…”

mentioning

confidence: 99%

Arabidopsis ORC1 is a PHD-containing H3K4me3 effector that regulates transcription

Sánchez

Gutiérrez

2009

Proc. Natl. Acad. Sci. U.S.A.

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“…This activation is at least in part due to the recruitment of the TRRAP-GCN5 histone acetylase complex (McMahon et al, 2000). Activation apparently also requires the presence of SNF5/INI1 and possibly the entire SWI/SNF complex (Cheng et al, 1999;Takayama et al, 2000). This observation suggests that loss of an intact SNF5/INI1 protein will cause down-regulation of c-MYC activation.…”

Section: What About Snf5/ini1?mentioning

confidence: 99%

When the SWI/SNF complex remodels … the cell cycle

2001

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Mammalian cells contain several chromatin-remodeling complexes associated with the Brm and Brg1 helicaselike proteins. These complexes likely represent the functional homologs of the SWI/SNF and RSC complexes found in Saccharomyces cerevisiae. The mammalian chromatin-remodeling complexes are involved in both activation and repression of a variety of genes. Several lines of evidence also indicate that they play a speci®c role in the regulation of cell growth. Brm is down-regulated by ras signaling and its forced reexpression suppresses transformation by this oncogene. Besides, the Brg1 gene is silenced or mutated in several tumors cell lines and a Brg1-associated complex was recently found to co-purify with BRCA1, involved in breast and ovarian cancers. Finally, the gene encoding SNF5/Ini1, a subunit common to all mammalian SWI/ SNF complexes, is inactivated in rhabdoid sarcomas, a very aggressive form of pediatric cancer. The current review will address observations made upon inactivation of Brm, Brg1 and SNF5/Ini1 by homologous recombination in the mouse, as well as the possible implication of these factors in the regulation of the Retinoblastoma pRb-mediated repression of the transcription factor E2F. Oncogene (2001) 20, 3067 ± 3075.

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“…Since many candidate genes for transactivation have recently been identified by using the microarray method (7,8), identification of the bona fide target genes of c-Myc should be possible. For its versatile functions, c-Myc associates with various factors other than Max (5), including p107 (9, 10), TBP (11,12), Bin-1 (13), AMY-1 (14), TRRAP (15), PAM (16), ␣-tubulin (17), MM-1 (18), and Cdk inhibitor p21 (19), which bind to the N-proximal region of c-Myc, and also YY-1 (20), Miz-1 (21), AP2 (22), Nmi (23), BRCA1 (24), SNF5 (25), CBF-C/NF-YC (26), cdr2 (27), MSSP (28), CDC6 (29), and Orc1 (30), which bind to the Cproximal region. These binding proteins are thought to modulate c-Myc function, and mutation of the proteins or disregulated expression of their genes may lead to cell transformation by c-Myc.…”

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confidence: 99%

MM-1, a c-Myc-binding Protein, Is a Candidate for a Tumor Suppressor in Leukemia/Lymphoma and Tongue Cancer

Fujioka¹,

Taira²,

Maeda³

et al. 2001

Journal of Biological Chemistry

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The c-myc oncogene product (c-Myc) is a transcription factor that dimerizes with Max and recognizes the E-box sequence, and it plays key functions in cell proliferation, differentiation, and apoptosis. We previously showed that MM-1 bound to myc box II within the transactivation domain of c-Myc and repressed the E-box-dependent transcriptional activity of c-Myc. Here we report that MM-1 showed features of a tumor suppressor. In an EST data base search for cDNAs homologous to MM-1, we found a frequent substitution of amino acid 157 of MM-1, from alanine to arginine (A157R), and the substitution was observed more in tumor cells than in normal cells. A survey of the A157R mutation of MM-1 in 57 cultured cancer cells and 90 tissues from cancer patients showed that the A157R was present in about 50 -60% of leukemia/lymphoma cells and in more than 75% of squamous cell carcinoma of tongue cancer. Although both the A157R and the wild-type MM-1 bound to c-Myc, only A157R lost the activities to repress both the E-boxdependent transcriptional activity of c-Myc and the myc/ ras cooperative transforming activity in rat 3Y1 cells. Furthermore, the wild-type MM-1, but not A157R, arrested the growth of 3Y1 cells. The human MM-1 gene was mapped at chromosome 12q12-12q13, where many chromosome abnormalities in cancer cells have been reported. The results suggest that MM-1 is a novel candidate for a tumor suppressor that controls the transcriptional activity of c-Myc.

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ORC1 interacts with c‐Myc to inhibit E‐box‐dependent transcription by abrogating c‐Myc–SNF5/INI1 interaction

Cited by 37 publications

References 46 publications

Arabidopsis ORC1 is a PHD-containing H3K4me3 effector that regulates transcription

Arabidopsis ORC1 is a PHD-containing H3K4me3 effector that regulates transcription

When the SWI/SNF complex remodels … the cell cycle

MM-1, a c-Myc-binding Protein, Is a Candidate for a Tumor Suppressor in Leukemia/Lymphoma and Tongue Cancer

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