c-Jun binding site identification in K562 cells

Minli Li; Qinyu Ge; Wei Wang; Jinke Wang; Zuhong Lu

doi:10.1016/j.jgg.2011.05.004

Volume 38 Issue 6

Jun. 2011

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Article Navigation > Journal of Genetics and Genomics > 2011 > 38(6): 235-242

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c-Jun binding site identification in K562 cells

doi: 10.1016/j.jgg.2011.05.004

a
State Key Laboratory of Bioelectronics, Southeast University, Nanjing 210096, China
b
Key Laboratory of Child Development and Learning Science, Ministry of Education, Southeast University, Nanjing 210096, China

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Corresponding author: E-mail address: zhlu@seu.edu.cn (Zuhong Lu)
Received Date: 2011-04-19
Accepted Date: 2011-05-10
Rev Recd Date: 2011-05-10

Available Online: 2011-05-17

Publish Date: 2011-06-20

Abstract

Abstract

Determining the binding sites of the transcription factor is important for understanding of transcriptional regulation. Transcription factor c-Jun plays an important role in cell growth, differentiation and development, but the binding sites and the target genes are not clearly defined in the whole human genome. In this study, we performed a ChIP-Seq experiment to identify c-Jun binding site in the human genome. Forty-eight binding sites were selected to process further evaluation by dsDNA microarray assay. We identified 283 c-Jun binding sites in K562 cells. Data analysis showed that 48.8% binding sites located within 100 kb of the upstream of the annotated genes, 28.6% binding sites comprised consensus TRE/CRE motif (5′-TGAC/GTCA-3′, 5′-TGACGTCA-3′) and variant sequences. Forty-two out of the selected 48 binding sites were found to bind the c-Jun homodimer in dsDNA microarray analysis. Data analysis also showed that 1569 genes are located in the neighborhood of the 283 binding sites and 191 genes in the neighborhood of the 42 binding sites validated by dsDNA microarray. We consulted 38 c-Jun target genes in previous studies and 16 among these 38 genes were also detected in this study. The identification of c-Jun binding sites and potential target genes in the genome scale may improve our fundamental understanding in the molecular mechanisms underlying the transcription regulation related to c-Jun.
- c-Jun,
- Chromatin immunoprecipitation,
- ChIP-Seq,
- dsDNA microarray

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References(53)

References

[1]	Arts, J., Grimbergen, J., Toet, K. et al. Arterioscler. Thromb. Vasc. Biol., 19 (1999),pp. 39-46
[2]	Bakiri, L., Lallemand, D., Bossy-Wetzel, E. et al. Cell cycle-dependent variations in c-Jun and JunB phosphorylation: a role in the control of cyclin D1 expression EMBO J., 19 (2000),pp. 2056-2068
[3]	Borde-Chiche, P., Diederich, M., Morceau, F. et al. Phorbol ester responsiveness of the glutathione S-transferase P1 gene promoter involves an inducible c-Jun binding in human K562 leukemia cells Leuk. Res., 25 (2001),pp. 241-247
[4]	Bulyk, M.L., Huang, X., Choo, Y. et al. Exploring the DNA-binding specificities of zinc fingers with DNA microarrays Proc. Natl. Acad. Sci. USA, 98 (2001),pp. 7158-7163
[5]	Bulyk, M.L., Johnson, P.L., Church, G.M. Nucleotides of transcription factor binding sites exert interdependent effects on the binding affinities of transcription factors Nucleic Acids Res., 30 (2002),pp. 1255-1261
[6]	Carroll, J.S., Liu, X.S., Brodsky, A.S. et al. Chromosome-wide mapping of estrogen receptor binding reveals long-range regulation requiring the forkhead protein FoxA1 Cell, 122 (2005),pp. 33-43
[7]	Chen, J., Panchanathan, R., Choubey, D. Immunol. Lett., 118 (2008),pp. 13-20
[8]	Chen, X., Xu, H., Yuan, P. et al. Integration of external signaling pathways with the core transcriptional network in embryonic stem cells Cell, 133 (2008),pp. 1106-1117
[9]	Chen, K.C., Chiou, Y.L., Chang, L.S. J. Cell Biochem., 108 (2009),pp. 612-620
[10]	Chinenov, Y., Kerppola, T.K. Close encounters of many kinds: fos-Jun interactions that mediate transcription regulatory specificity Oncogene, 20 (2001),pp. 2438-2452
[11]	Cooper, S.J., Trinklein, N.D., Anton, E.D. et al. Comprehensive analysis of transcriptional promoter structure and function in 1% of the human genome Genome Res., 16 (2006),pp. 1-10
[12]	Daubeuf, S., Duvoix, A., Wellman-Rousseau, M. et al. Biochem. Biophys. Res. Commun., 313 (2004),pp. 300-307
[13]	Dong, L.Y., Wang, X.N., Song, Z.G. et al. Identification of human hepatic stimulator substance gene promoter and demonstration of dual regulation of AP1/AP4 cis-acting element in different cell lines Int. J. Biochem. Cell Biol., 39 (2007),pp. 181-196
[14]	Elagib, K.E., Xiao, M., Hussaini, I.M. et al. Jun blockade of erythropoiesis: role for repression of GATA-1 by HERP2 Mol. Cell. Biol., 24 (2004),pp. 7779-7794
[15]	Eriksson, M., Arminen, L., Karjalainen-Lindsberg, M.L. et al. AP-1 regulates alpha2beta1 integrin expression by ERK-dependent signals during megakaryocytic differentiation of K562 cells Exp. Cell Res., 304 (2005),pp. 175-186
[16]	Farnham, P.J. Insights from genomic profiling of transcription factors Nat. Rev. Genet., 10 (2009),pp. 605-616
[17]	Gu, Q., Tan, M., Sun, Y. SAG/ROC2/Rbx2 is a novel activator protein-1 target that promotes c-Jun degradation and inhibits 12-O-tetradecanoylphorbol-13-acetate-induced neoplastic transformation Cancer Res., 67 (2007),pp. 3616-3625
[18]	Hatzis, P., van der Flier, L.G., van Driel, M.A. et al. Genome-wide pattern of TCF7L2/TCF4 chromatin occupancy in colorectal cancer cells Mol. Cell. Biol., 28 (2008),pp. 2732-2744
[19]	Humbert, O., Achour, I., Lautier, D. et al. Nucleic Acids Res., 31 (2003),pp. 5627-5634
[20]	Ivanov, V.N., Bhoumik, A., Krasilnikov, M. et al. Cooperation between STAT3 and c-Jun suppresses Fas transcription Mol. Cell, 7 (2001),pp. 517-528
[21]	Johnson, D.S., Mortazavi, A., Myers, R.M. et al. Science, 316 (2007),pp. 1497-1502
[22]	Kasibhatla, S., Brunner, T., Genestier, L. et al. Mol. Cell, 1 (1998),pp. 543-551
[23]	Klampfer, L., Lee, T.H., Hsu, W. et al. Mol. Cell. Biol., 14 (1994),pp. 6561-6569
[24]	Kovacic-Milivojevic, B., Gardner, D.G. Divergent regulation of the human atrial natriuretic peptide gene by c-Jun and c-fos Mol. Cell. Biol., 12 (1992),pp. 292-301
[25]	Lamb, R.F., Hennigan, R.F., Turnbull, K. et al. AP-1-mediated invasion requires increased expression of the hyaluronan receptor CD44 Mol. Cell. Biol., 17 (1997),pp. 963-976
[26]	Lee, T.I., Johnstone, S.E., Young, R.A. Chromatin immunoprecipitation and microarray-based analysis of protein location Nat. Protoc., 1 (2006),pp. 729-748
[27]	Macpherson, P., Humbert, O., Karran, P. Frameshift mismatch recognition by the human MutS alpha complex Mutat. Res., 408 (1998),pp. 55-66
[28]	Miao, Z.H., Ding, J. Cancer Res., 63 (2003),pp. 4527-4532
[29]	Oka, T., Rairkar, A., Chen, J.H. Oncogene, 6 (1991),pp. 2077-2083
[30]	Okazaki, M., Maeda, G., Chiba, T. et al. Identification of GATA3 binding sites in Jurkat cells Gene, 445 (2009),pp. 17-25
[31]	Paliogianni, F., Raptis, A., Ahuja, S.S. et al. J. Clin. Invest., 91 (1993),pp. 1481-1489
[32]	Park, J.M., Adam, R.M., Peters, C.A. et al. AP-1 mediates stretch-induced expression of HB-EGF in bladder smooth muscle cells Am. J. Physiol., 277 (1999),pp. 294-301
[33]	Qian, X.X., Mata-Greenwood, E., Liao, W.X. et al. Transcriptional regulation of endothelial nitric oxide synthase expression in uterine artery endothelial cells by c-Jun/AP-1 Mol. Cell. Endocrinol., 279 (2007),pp. 39-51
[34]	Rabinovich, A., Jin, V.X., Rabinovich, R. et al. Genome Res., 18 (2008),pp. 1763-1777
[35]	Rebollo, A., Dumoutier, L., Renauld, J.C. et al. Bcl-3 expression promotes cell survival following interleukin-4 deprivation and is controlled by AP1 and AP1-like transcription factors Mol. Cell. Biol., 20 (2000),pp. 3407-3416
[36]	Robertson, G., Hirst, M., Bainbridge, M. et al. Genome-wide profiles of STAT1 DNA association using chromatin immunoprecipitation and massively parallel sequencing Nat. Methods, 4 (2007),pp. 651-657
[37]	Sark, M.W., Fischer, D.F., de Meijer, E. et al. AP-1 and ets transcription factors regulate the expression of the human SPRR1A keratinocyte terminal differentiation marker J. Biol. Chem., 273 (1998),pp. 24683-24692
[38]	Schreiber, M., Kolbus, A., Piu, F. et al. Control of cell cycle progression by c-Jun is p53 dependent Genes Dev., 13 (1999),pp. 607-619
[39]	Shaulian, E., Schreiber, M., Piu, F. et al. The mammalian UV response: c-Jun induction is required for exit from p53-imposed growth arrest Cell, 103 (2000),pp. 897-907
[40]	Sprowles, A., Robinson, D., Wu, Y.M. et al. c-Jun controls the efficiency of MAP kinase signaling by transcriptional repression of MAP kinase phosphatases Exp. Cell Res., 308 (2005),pp. 459-468
[41]	Szabowski, A., Maas-Szabowski, N., Andrecht, S. et al. C-Jun and JunB antagonistically control cytokine-regulated mesenchymal-epidermal interaction in skin Cell, 103 (2000),pp. 745-755
[42]	Takahashi, H., Asano, K., Kinouchi, M. et al. Structure and transcriptional regulation of the human cystatin A gene. The 12-O-tetradecanoylphorbol-13-acetate (TPA) responsive element-2 site (-272 to -278) on cystatin A gene is critical for TPA-dependent regulation J. Biol. Chem., 273 (1998),pp. 17375-17380
[43]	Takahashi, S., Harigae, H., Yokoyama, H. et al. Biochim. Biophys. Acta, 1522 (2001),pp. 207-211
[44]	Toft, D.J., Rosenberg, S.B., Bergers, G. et al. Reactivation of proliferin gene expression is associated with increased angiogenesis in a cell culture model of fibrosarcoma tumor progression Proc. Natl. Acad. Sci. USA, 98 (2001),pp. 13055-13059
[45]	Tseng, P.C., Hsu, H.C., Janmanchi, D. et al. Helioxanthin inhibits interleukin-1 beta-induced MIP-1 beta production by reduction of c-jun expression and binding of the c-jun/CREB1 complex to the AP-1/CRE site of the MIP-1 beta promoter in Huh7 cells Biochem. Pharmacol., 76 (2008),pp. 1121-1133
[46]	Ukon, K., Tanimoto, K., Shimokuni, T. et al. Activator protein accelerates dihydropyrimidine dehydrogenase gene transcription in cancer cells Cancer Res., 65 (2005),pp. 1055-1062
[47]	Valouev, A., Johnson, D.S., Sundquist, A. et al. Genome-wide analysis of transcription factor binding sites based on ChIP-Seq data Nat. Methods, 5 (2008),pp. 829-834
[48]	Wang, J.K., Li, T.X., Bai, Y.F. et al. Evaluating the binding affinities of NF-kappaB p50 homodimer to the wild-type and single-nucleotide mutant Ig-kappaB sites by the unimolecular dsDNA microarray Anal. Biochem., 316 (2003),pp. 192-201
[49]	Wederell, E.D., Bilenky, M., Cullum, R. et al. Nucleic Acids Res., 36 (2008),pp. 4549-4564
[50]	Whitfield, J., Neame, S.J., Paquet, L. et al. Dominant-negative c-Jun promotes neuronal survival by reducing BIM expression and inhibiting mitochondrial cytochrome c release Neuron, 29 (2001),pp. 629-643
[51]	Yang, A., Zhu, Z., Kapranov, P. et al. Relationships between p63 binding, DNA sequence, transcription activity, and biological function in human cells Mol. Cell, 24 (2006),pp. 593-602
[52]	Yu, X., Luo, A., Zhou, C. et al. Biochem. Biophys. Res. Commun., 342 (2006),pp. 286-292
[53]	Zenz, R., Scheuch, H., Martin, P. et al. C-Jun regulates eyelid closure and skin tumor development through EGFR signaling Dev. Cell, 4 (2003),pp. 879-889