Network-dosage compensation topologies as recurrent network motifs in natural gene networks

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• 作者：Ruijie Song (1) (3)
  Ping Liu (2) (3)
  Murat Acar (2) (3)
  
  1. Interdepartmental Program in Computational Biology and Bioinformatics ; Yale University ; 300 George Street ; Suite 501 ; New Haven ; CT ; 06511 ; USA
  3. Systems Biology Institute ; Yale University ; 840 West Campus Drive ; West Haven ; CT ; 06516 ; USA
  2. Department of Molecular ; Cellular and Developmental Biology ; Yale University ; 219 Prospect Street ; P.O. Box 27391 ; New Haven ; CT ; 06511 ; USA
  
• 关键词：Network ; dosage compensation ; Network motifs ; Yeast galactose network ; Stochasticity ; Genetic interactions
• 刊名：BMC Systems Biology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：8
• 期：1
• 全文大小：864 KB
• 参考文献：1. Di Talia, S, Wang, H, Skotheim, JM, Rosebrock, AP, Futcher, B, Cross, FR (2009) Daughter-specific transcription factors regulate cell size control in budding yeast. PLoS Biol 7: pp. e1000221 CrossRef
  2. Zopf, CJ, Quinn, K, Zeidman, J, Maheshri, N (2013) Cell-cycle dependence of transcription dominates noise in gene expression. PLoS Comput Biol 9: pp. e1003161 CrossRef
  3. Galitski, T, Saldanha, AJ, Styles, CA, Lander, ES, Fink, GR (1999) Ploidy regulation of gene expression. Science 285: pp. 251-254 CrossRef
  4. Elowitz, MB, Levine, AJ, Siggia, ED, Swain, PS (2002) Stochastic gene expression in a single cell. Science 297: pp. 1183-1186 CrossRef
  5. Pedraza, JM, van Oudenaarden, A (2005) Noise propagation in gene networks. Science 307: pp. 1965-1969 CrossRef
  6. Lee, JA, Lupski, JR (2006) Genomic rearrangements and gene copy-number alterations as a cause of nervous system disorders. Neuron 52: pp. 103-121 CrossRef
  7. Malone, J, Cho, D-Y, Mattiuzzo, N, Artieri, C, Jiang, L, Dale, R, Smith, H, McDaniel, J, Munro, S, Salit, M, Andrews, J, Przytycka, T, Oliver, B (2012) Mediation of drosophila autosomal dosage effects and compensation by network interactions. Genome Biol 13: pp. R28 CrossRef
  8. Springer, M, Weissman, JS, Kirschner, MW (2010) A general lack of compensation for gene dosage in yeast. Mol Syst Biol 6: pp. 368 CrossRef
  9. Osley, MA, Hereford, LM (1981) Yeast histone genes show dosage compensation. Cell 24: pp. 377-384 CrossRef
  10. Acar, M, Pando, BF, Arnold, FH, Elowitz, MB, van Oudenaarden, A (2010) A general mechanism for network-dosage compensation in gene circuits. Science 329: pp. 1656-1660 CrossRef
  11. Blackwell, E, Halatek, IM, Kim, H-JN, Ellicott, AT, Obukhov, AA, Stone, DE (2003) Effect of the pheromone-responsive G伪 and phosphatase proteins of Saccharomyces cerevisiae on the subcellular localization of the Fus3 mitogen-activated protein kinase. Mol Cell Biol 23: pp. 1135-1150 CrossRef
  12. Mattison, CP, Ota, IM (2000) Two protein tyrosine phosphatases, Ptp2 and Ptp3, modulate the subcellular localization of the Hog1 MAP kinase in yeast. Gene Dev 14: pp. 1229-1235 CrossRef
  13. Siegmund, RF, Nasmyth, KA (1996) The Saccharomyces cerevisiae Start-specific transcription factor Swi4 interacts through the ankyrin repeats with the mitotic Clb2/Cdc28 kinase and through its conserved carboxy terminus with Swi6. Mol Cell Biol 16: pp. 2647-2655 CrossRef
  14. Cox, KH, Rai, R, Distler, M, Daugherty, JR, Coffman, JA, Cooper, TG (2000) Saccharomyces cerevisiae GATA sequences function as TATA elements during nitrogen catabolite repression and when Gln3p is excluded from the nucleus by overproduction of Ure2p. J Biol Chem 275: pp. 17611-17618 CrossRef
  15. Bardwell, L (2005) A walk-through of the yeast mating pheromone response pathway. Peptides 26: pp. 339-350 CrossRef
  16. Proft, M, Struhl, K (2002) Hog1 kinase converts the Sko1-Cyc8-Tup1 repressor complex into an activator that recruits SAGA and SWI/SNF in response to osmotic stress. Mol Cell 9: pp. 1307-1317 CrossRef
  17. Hu, F, Gan, Y, Aparicio, OM (2008) Identification of Clb2 residues required for Swe1 regulation of Clb2-Cdc28 in Saccharomyces cerevisiae. Genetics 179: pp. 863-874 CrossRef
  18. Valenzuela, L, Aranda, C, Gonz谩lez, A (2001) TOR modulates GCN4-dependent expression of genes turned on by nitrogen limitation. J Bacteriol 183: pp. 2331-2334 CrossRef
  19. Hern谩ndez, H, Aranda, C, Riego, L, Gonz谩lez, A (2011) Gln3鈥揋cn4 hybrid transcriptional activator determines catabolic and biosynthetic gene expression in the yeast Saccharomyces cerevisiae. Biochem Biophys Res Comm 404: pp. 859-864 CrossRef
  20. Timson, DJ, Ross, HC, Reece, RJ (2002) Gal3p and Gal1p interact with the transcriptional repressor Gal80p to form a complex of 1:1 stoichiometry. Biochem J 363: pp. 515-520 CrossRef
  21. Zhan, X-L, Guan, K-L (1999) A specific protein鈥損rotein interaction accounts for the in vivo substrate selectivity of Ptp3 towards the Fus3 MAP kinase. Gene Dev 13: pp. 2811-2827 CrossRef
  22. Metodiev, MV, Matheos, D, Rose, MD, Stone, DE (2002) Regulation of MAPK function by direct interaction with the mating-specific G伪 in yeast. Science 296: pp. 1483-1486 CrossRef
  23. Thual, C, Bousset, L, Komar, AA, Walter, S, Buchner, J, Cullin, C, Melki, R (2001) Stability, folding, dimerization, and assembly properties of the yeast prion Ure2p鈥? Biochemistry 40: pp. 1764-1773 CrossRef
  24. Umland, TC, Taylor, KL, Rhee, S, Wickner, RB, Davies, DR (2001) The crystal structure of the nitrogen regulation fragment of the yeast prion protein Ure2p. Proc Natl Acad Sci 98: pp. 1459-1464 CrossRef
  25. Carvalho, J, Zheng, XFS (2003) Domains of Gln3p Interacting with karyopherins, Ure2p, and the target of rapamycin protein. J Biol Chem 278: pp. 16878-16886 CrossRef
  26. Holland, AJ, Cleveland, DW (2012) Losing balance: the origin and impact of aneuploidy in cancer. EMBO reports 13: pp. 501-514 CrossRef
  27. Dixon, SJ, Costanzo, M, Baryshnikova, A, Andrews, B, Boone, C (2009) Systematic mapping of genetic interaction networks. Annu Rev Genet 43: pp. 601-625 CrossRef
  28. Young, MW, Kay, SA (2001) Time zones: a comparative genetics of circadian clocks. Nat Rev Genet 2: pp. 702-715 CrossRef
  29. Buchler, NE, Louis, M (2008) Molecular titration and ultrasensitivity in regulatory networks. J Mol Biol 384: pp. 1106-1119 CrossRef
  30. Cherry, JM, Hong, EL, Amundsen, C, Balakrishnan, R, Binkley, G, Chan, ET, Christie, KR, Costanzo, MC, Dwight, SS, Engel, SR, Fisk, DG, Hirschman, JE, Hitz, BC, Karra, K, Krieger, CJ, Miyasato, SR, Nash, RS, Park, J, Skrzypek, MS, Simison, M, Weng, S, Wong, ED (2012) Saccharomyces genome database: the genomics resource of budding yeast. Nucleic Acids Res 40: pp. D700-D705 CrossRef
  31. Abdulrehman, D, Monteiro, PT, Teixeira, MC, Mira, NP, Lourenco, AB, dos Santos, SC, Cabrito, TR, Francisco, AP, Madeira, SC, Aires, RS, Oliveira, AL, Sa-Correia, I, Freitas, AT (2011) YEASTRACT: providing a programmatic access to curated transcriptional regulatory associations in Saccharomyces cerevisiae through a web services interface. Nucleic Acids Res 39: pp. D136-D140 CrossRef
  32. Monteiro, PT, Mendes, ND, Teixeira, MC, d鈥橭rey, S, Tenreiro, S, Mira, NP, Pais, H, Francisco, AP, Carvalho, AM, Louren莽o, AB, S谩-Correia, I, Oliveira, AL, Freitas, AT (2008) YEASTRACT-DISCOVERER: new tools to improve the analysis of transcriptional regulatory associations in Saccharomyces cerevisiae. Nucleic Acids Res 36: pp. D132-D136 CrossRef
  33. Teixeira, MC, Monteiro, P, Jain, P, Tenreiro, S, Fernandes, AR, Mira, NP, Alenquer, M, Freitas, AT, Oliveira, AL, S谩-Correia, I (2006) The YEASTRACT database: a tool for the analysis of transcription regulatory associations in Saccharomyces cerevisiae. Nucleic Acids Res 34: pp. D446-D451 CrossRef
  34. MacIsaac, K, Wang, T, Gordon, DB, Gifford, D, Stormo, G, Fraenkel, E (2006) An improved map of conserved regulatory sites for Saccharomyces cerevisiae. BMC Bioinformatics 7: pp. 113 CrossRef
  35. Stark, C, Breitkreutz, B-J, Reguly, T, Boucher, L, Breitkreutz, A, Tyers, M (2006) BioGRID: a general repository for interaction datasets. Nucleic Acids Res 34: pp. D535-D539 CrossRef
  
• 刊物主题：Bioinformatics; Systems Biology; Simulation and Modeling; Computational Biology/Bioinformatics; Physiological, Cellular and Medical Topics; Algorithms;
• 出版者：BioMed Central
• ISSN：1752-0509

文摘

Background Global noise in gene expression and chromosome duplication during cell-cycle progression cause inevitable fluctuations in the effective number of copies of gene networks in cells. These indirect and direct alterations of network copy numbers have the potential to change the output or activity of a gene network. For networks whose specific activity levels are crucial for optimally maintaining cellular functions, cells need to implement mechanisms to robustly compensate the effects of network dosage fluctuations. Results Here, we determine the necessary conditions for generalized N-component gene networks to be network-dosage compensated and show that the compensation mechanism can robustly operate over large ranges of gene expression levels. Furthermore, we show that the conditions that are necessary for network-dosage compensation are also sufficient. Finally, using genome-wide protein-DNA and protein-protein interaction data, we search the yeast genome for the abundance of specific dosage-compensation motifs and show that a substantial percentage of the natural networks identified contain at least one dosage-compensation motif. Conclusions Our results strengthen the hypothesis that the special network topologies that are necessary for network-dosage compensation may be recurrent network motifs in eukaryotic genomes and therefore may be an important design principle in gene network assembly in cells.