Phenotypic variability of bacterial cell cycle: mathematical model
Matematičeskaâ biologiâ i bioinformatika, Tome 11 (2016) no. 1, pp. 91-113.

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The results of the study of mechanisms of different cell phenotypes occurrence in a genetically homogenous population using the bacterial cell cycle model are presented. It was shown that phenotypic variability represents an internal, immanent property of bacteria. The basis of this phenomenon is universal non-linear properties of the conjugated transcription-translation system, that controls all cellular processes. Phenotypic variability occurs in a simple, deterministic, self-reproducing system under the uniform transmission of the structural components to the daughter cells during division and in the absence of any special control mechanisms of molecular-genetic processes and enzymatic reactions.
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V. A. Likhoshvai; T. M. Khlebodarova. Phenotypic variability of bacterial cell cycle: mathematical model. Matematičeskaâ biologiâ i bioinformatika, Tome 11 (2016) no. 1, pp. 91-113. http://geodesic.mathdoc.fr/item/MBB_2016_11_1_a6/

[1] Ferrell J. E. Jr., “Self-perpetuating states in signal transduction: positive feedback, double-negative feedback and bistability”, Curr. Opin. Cell. Biol., 14 (2002), 140–148 | DOI

[2] Angeli D., Ferrell J. E. Jr., Sontag E. D., “Detection of multistability, bifurcations, and hysteresis in a large class of biological positive-feedback systems”, Proc. Natl. Acad. Sci. USA, 101 (2004), 1822–1827 | DOI

[3] Ozbudak E. M., Thattai M., Lim H. N., Shraiman B. I., Van Oudenaarden A., “Multistability in the lactose utilization network of Escherichia coli”, Nature, 427:6976 (2004), 737–740 | DOI

[4] Smits W. K., Kuipers O. P., Veening J. W., “Phenotypic variation in bacteria: the role of feedback regulation”, Nat. Rev. Microbiol., 4:4 (2006), 259–271 | DOI

[5] Dubnau D., Losick R., “Bistability in bacteria”, Mol. Microbiol., 61 (2006), 564–572 | DOI

[6] Piggot P., “Epigenetic switching: bacteria hedge bets about staying or moving”, Curr. Biol., 20:11 (2010), R480–482 | DOI

[7] Avendaño M. S., Leidy C., Pedraza J. M., “Tuning the range and stability of multiple phenotypic states with coupled positive-negative feedback loops”, Nat. Commun., 4 (2013), 2605 | DOI

[8] Kaern M., Elston T. C., Blake W. J., Collins J. J., “Stochasticity in gene expression: from theories to phenotypes”, Nat. Rev. Genet., 6 (2005), 451–464 | DOI

[9] Sureka K., Ghosh B., Dasgupta A., Basu J., Kundu M., Bose I., “Positive feedback and noise activate the stringent response regulator rel in mycobacteria”, PLoS One, 3:3 (2008), e1771 | DOI

[10] To T. L., Maheshri N., “Noise can induce bimodality in positive transcriptional feedback loops without bistability”, Science, 327:5969 (2010), 1142–1145 | DOI

[11] Zheng X. D., Yang X. Q., Tao Y., “Bistability, probability transition rate and first-passage time in an autoactivating positive-feedback loop”, PLoS One, 6:3 (2011), e17104 | DOI

[12] Shu C. C., Chatterjee A., Dunny G., Hu W. S., Ramkrishna D., “Bistability versus bimodal distributions in gene regulatory processes from population balance”, PLoS Comput. Biol., 7:8 (2011), e1002140 | DOI | MR

[13] Ghosh S., Banerjee S., Bose I., “Emergent bistability: Effects of additive and multiplicative noise”, Eur. Phys. J. E Soft. Matter., 35:11 (2012) | DOI | Zbl

[14] Thomas P., Popović N., Grima R., “Phenotypic switching in gene regulatory networks”, Proc. Natl. Acad. Sci. USA, 111:19 (2014), 6994–6999 | DOI

[15] Casadesús J., Low D. A., “Programmed heterogeneity: epigenetic mechanisms in bacteria”, J. Biol. Chem., 288 (2013), 13929–13935 | DOI

[16] Stewart E. J., Madden R., Paul G., Taddei F., “Aging and death in an organism that reproduces by morphologically symmetric division”, PLoS Biol., 3:2 (2005), e45 | DOI

[17] Ghosh S., Sureka K., Ghosh B., Bose I., Basu J., Kundu M., “Phenotypic heterogeneity in mycobacterial stringent response”, BMC Syst. Biol., 5 (2011), 18 | DOI

[18] Kotte O., Volkmer B., Radzikowski J. L., Heinemann M., “Phenotypic bistability in Escherichia coli's central carbon metabolism”, Mol. Syst. Biol., 10 (2014), 736 | DOI

[19] Klapper I., Gilbert P., Ayati B. P., Dockery J., Stewart P. S., “Senescence can explain microbial persistence”, Microbiology, 153 (2007), 3623–3630 | DOI

[20] Balaban N. Q., Merrin J., Chait R., Kowalik L., Leibler S., “Bacterial persistence as a phenotypic switch”, Science, 305 (2004), 1622–1625 | DOI

[21] Verstraeten N., Knapen W., Fauvart M., Michiels J., “A Historical Perspective on Bacterial Persistence”, Methods Mol. Biol., 1333 (2016), 3–13 | DOI

[22] Dörr T., Vulić M., Lewis K., “Ciprofloxacin causes persister formation by inducing the TisB toxin in Escherichia coli”, PLoS Biol., 8:2 (2010), e1000317 | DOI

[23] Fasani R. A., Savageau M. A., “Molecular mechanisms of multiple toxin-antitoxin systems are coordinated to govern the persister phenotype”, Proc. Natl. Acad. Sci. USA, 110 (2013), E2528–2537 | DOI

[24] Gelens L., Hill L., Vandervelde A., Danckaert J., Loris R., “A general model for toxin-antitoxin module dynamics can explain persister cell formation in E. coli”, PLoS Comput. Biol., 9 (2013), e1003190 | DOI

[25] Likhoshvai V. A., Khlebodarova T. M., “Soglasovanie tempov rosta ob'ema kletki i replikatsii DNK: matematicheskaya model”, Matem. biologiya i bioinform., 8:1 (2013), 66–92 | DOI

[26] Likhoshvai V. A., Khlebodarova T. M., “Mathematical modeling of bacterial cell cycle: The problem of coordinating genome replication with cell growth”, J. Bioinform. Comput. Biol., 12:3 (2014), 1450009 | DOI

[27] Donachie W. D., “Relationship between cell size and time of initiation of DNA replication”, Nature, 219 (1968), 1077–1079 | DOI

[28] Cooper S., Helmstetter C. E., “Chromosome replication and the division cycle of Escherichia coli B/r”, J. Mol. Biol., 31 (1968), 619–644 | DOI

[29] Neidhardt F. C. (ed.), Escherichia coli and Salmonella typhimurium: Cellular and Molecular Biology, American Society for Microbiology, Washington D. C., 1987, 1654 pp.

[30] Kennell D., Riezman H., “Transcription and translation initiation frequencies of the Escherichia coli lac operon”, J. Mol. Biol., 114 (1977), 1–21 | DOI

[31] Zaritsky A., Woldringh C. L., “Chromosome replication rate and cell shape in Escherichia coli: lack of coupling”, J. Bacteriol., 135:2 (1978), 581–587

[32] Pedersen S., Reeh S., Friesen D. J., “Functional mRNA half-lives in E. coli”, Mol. Gen. Genet., 166 (1978), 329–336

[33] Mosteller R. D., Goldstein R. V., Nishimoto K. R., “Metabolism of individual proteins in exponentially growing Escherichia coli”, J. Biol. Chem., 255:6 (1980), 2524–2532

[34] Selinger D. W., Saxena R. M., Cheung K. J., Church G. M., Rosenow C., “Global RNA half-life analysis in Escherichia coli reveals positional patterns of transcript degradation”, Genome Res., 13:2 (2003), 216–223 | DOI

[35] Bernstein J. A., Lin P. H., Cohen S. N., Lin-Chao S., “Global analysis of Escherichia coli RNA degradosome function using DNA microarrays”, Proc. Natl. Acad. Sci. USA, 101:9 (2004), 2758–2763 | DOI

[36] Jayapal K. P., Sui S., Philp R. J., Kok Y. J., Yap M. G., Griffin T. J., Hu W. S., “Multitagging proteomic strategy to estimate protein turnover rates in dynamic systems”, J. Proteome Res., 9:5 (2010), 2087–2097 | DOI

[37] Taniguchi Y., Choi P. J., Li G. W., Chen H., Babu M., Hearn J., Emili A., Xie X. S., “Quantifying E. coli proteome and transcriptome with single-molecule sensitivity in single cells”, Science, 329:5991 (2010), 533–538 | DOI

[38] Inouye M., Shaw J., Shen C., “The assembly of a structural lipoprotein in the envelope of Escherichia coli”, J. Biol. Chem., 247:24 (1972), 8154–8159

[39] Schaechter M., Maaloe O., Kjeldgaard N. O., “Dependency on medium and temperature of cell size and chemical composition during balanced grown of Salmonella typhimurium”, J. Gen. Microbiol., 19 (1958), 592–606 | DOI

[40] Schaechter M., Williamson J. P., Hood J. R. Jr., Koch A. L., “Growth, cell and nuclear divisions in some bacteria”, J. Gen. Microbiol., 29 (1962), 421–434 | DOI

[41] Yoshikawa H., O'Sullivan A., Sueoka N., “Sequential replication of the Bacillus subtilis chromosome. III. Regulation of initiation”, Proc. Natl. Acad. Sci. USA, 52 (1964), 973–980 | DOI

[42] Zaritsky A., Vischer N., Rabinovitch A., “Changes of initiation mass and cell dimensions by the 'eclipse'”, Mol. Microbiol., 63 (2007), 15–21 | DOI

[43] Zaritsky A., Wang P., Vischer N. O., “Instructive simulation of the bacterial cell division cycle”, Microbiology, 157 (2011), 1876–1885 | DOI

[44] Grant M. A., Saggioro C., Ferrari U., Bassetti B., Sclavi B., Cosentino Lagomarsino M., “DnaA and the timing of chromosome replication in Escherichia coli as a function of growth rate”, BMC Syst. Biol., 5 (2011), 201 | DOI

[45] Soo V. W., Cheng H. Y., Kwan B. W., Wood T. K., “De novo synthesis of a bacterial toxin/antitoxin system”, Sci. Rep., 4 (2014), 4807 | DOI

[46] Keren I., Shah D., Spoering A., Kaldalu N., Lewis K., “Specialized persister cells and the mechanism of multidrug tolerance in Escherichia coli”, J. Bacteriol., 186 (2004), 8172–8180 | DOI

[47] Shah D., Zhang Z., Khodursky A., Kaldalu N., Kurg K., Lewis K., “Persisters: a distinct physiological state of E. coli”, BMC Microbiol., 6 (2006), 53 | DOI