Yeast cell cycle

Enoch, T and Nurse, P. (1990). Mutation of the fission yeast cell cycle control genes abolishes dependence of mitosis on DNA replication. Cell 60 665-673. 

Gautier, J., Norbury, C., Lohka, M., Nurse, P., and Mailer, J. (1988). Purified maturation-promoting factor contains the product of a Xenopus homologue of the fission yeast cell cycle control gene cdc2+. Cell 54 433-439. 

Friedman et al. (2000) tested this approach on a data set for yeast cell cycle expression patterns provided by Spellman and co-workers (1998), writing that This data set contains 76 gene expression measurements of the mRNA levels of 6177 S. cerevisiae ORFs. These experiments measure six... 

Murray and Hunt, 1993). Cyclins, kinases, and phosphatases that regulate the passage of the cell through the G] — S phase transition are all present in mammals, invertebrates, and plants (Solomon, 1993 Doonan and Fobart, 1997 Zavitz and Zipursky, 1997). However, multicellular eukaryotes contain multiple orthologs of yeast cell cycle proteins they initiate proliferation via growth factors, rather than, for example, yeast mating factors, and they possess additional checkpoint controls and repair pathways. 

McGrath, J. P., Varshavsky, A., and Byers, B. The yeast cell cycle gene CDG34 encodes a ubiquitin-conjugating enzyme. Science 1988,... 

If the cell cycle in amphibian embryonic cells appears to be driven by a limit cycle oscillator, the question arises as to the precise dynamical nature of more complex cell cycles in yeast and somatic cells. Novak et al. [144] constructed a detailed bifurcation diagram for the yeast cell cycle, piecing together the diagrams obtained as a function of increasing cell mass for the transitions between the successive phases of the cell cycle. In these studies, cell mass plays the role of control parameter a critical mass has to be reached for cell division to occur, provided that it coincides with a surge in cdkl activity which triggers the G2/M transition. 

Nasmyth, K. (1996). At the heart of the budding yeast cell cycle. Trends Genet 12, 405-12. 

Hayles, J., Beach, D., Durkacz, B., and Nurse, P. (1986). The fission yeast cell cycle control gene cdc2 isolation of a sequence sucl that suppresses cdc2 mutant function. Mol Gen Genet 202, 291-3. 

Jorgensen P, and Tyers M (1999) Altered states programmed proteolysis and the budding yeast cell cycle. Curr. Opin. Microbiol. 2 610-617. 

K. Nasmyth. Control of the yeast cell cycle by the Cdc28 protein kinase. Curr Opin Cell Biol, S, (2) 166-179, 1993. 

A. Amon, M. Tyers, B. Futcher, and K. Nasmyth. Mechanisms that help the yeast cell cycle clock tick G2 cyclins transcriptionally activate G2 cyclins and repress Gl cyclins. Cell, 74 (6), 993-1007, 1993. 

Roth AF, et al. Global analysis of protein palmitoylation in yeast. Cell Cycle 2006 125 1003-1013. 

The yeast cell cycle has also been analyzed at this high level of chemical detail [17]. The molecular mechanism of the cycle in the form of a series of chemical equations was described by a set of ten nonlinear ordinary differential kinetic rate equations for the concentrations of the cyclins and associated proteins and the cell mass, derived using the standard principles of biochemical kinetics. Numerical solution of these equations 3uelded the concentrations of molecules such as the cyclin, Cln2, which is required to activate the cell cycle, or the inhibitor, Sid, which helps to retain the cell in the resting Gi phase. The rate constants and concentrations ( 50 parameters) were estimated from published measurements and adjusted so that the solutions of the equations yielded appropriate variations, i.e., similar to those experimentally measured, of the concentrations of the constituents of the system and the cell mass. The model also provides a rationalization of the behavior of cells with mutant forms of various system constituents. 

There are two main steady states in the cycle. One is Gi in which the cell is maintained by inhibitors such as Sicl. The other is at the S/M phase boundary to which the cell migrates due to an increase in cyclins, e.g., Cln2, and cyclin-dependent kinase activity. (These two states are controlled by the antagonism between the kinases and inhibitors.) Because of the complexity of the model, however, it is difficult to obtain an overall view of the location and character of all the steady states that might be accessible to the system. This approach has also been used to characterize the behavior of the morphogenesis checkpoint in budding yeast and also mutants [18] as well as to provide a more complete integrative analysis of the control of the yeast cell cycle [17]. 

B. Han, J. Wang, Quantifying robustness and dissipation cost of yeast cell cycle network the funneled energy landscape perspectives. Biophys. J. 92(11), 3755-3763 (2007)... 

K.C. Chen, A. Csikasz-Nagy, B. Gyorffy, J. Val, B. Novak, J.J. Tyson. Kinetic analysis of a molecular model of the budding yeast cell cycle. Mol Biol Cell 11(1), 369-391 (2000)... 

FIGURE 6.10 Cluster theme visualization with a heatmap. The OmniViz CoMet visualization provides a quick means to view how attributes are distributed across the dataset. In this example from the biomedical literature on yeast cell cycle regulation, CoMet has been configured to show how the major topics (columns) are distributed among the different clusters of documents (rows). The clusters represent over and under representation of co-occurrances between the major topics and documents. Note, the conversion to grayscale from color resulted in lost information in the figure as presented. 

Recently, Alter and coworkers and Holter and coworkers independently applied SVD analysis to previously described data on the yeast cell cycle (Alter et al., 2000 Holter et al., 2000). In those experiments mRNA levels as a function of cell cycle were determined by synchronizing... 

However, complementation of the recessive mutation by the wild-type allele carried by one of the plasmid clones In the library allows a transformed mutant cell to grow Into a colony the plasmids bearing the wild-type allele can then be recovered from those cells. Because many of the proteins that regulate the cell cycle are highly conserved, human cDNAs cloned into yeast expression vectors often can complement yeast cell-cycle mutants, leading to the rapid Isolation of human genes encoding cell-cycle control proteins. 

Cross, F.R. A.H. Tinkelenberg. 1991. A potential positive feedback loop controlling CLNl and CLN2 gene expression at the start of the yeast cell cycle. Ce 65 875-83. 

Iyer V R, Horak C E, Scafe C S, et al. (2001). Genomic binding sites of the yeast cell-cycle transcription factors SBF and MBF. Nature. 409 533-538. 

Other useful sites for yeast genome analysis include Saccharomyces cerevisiae Promoter Database, listing known regulatory elements and transcriptional factors in yeast TRansposon-Insertion Phenotypes, Localization, and Expression in Saccharomyces (TRIPLES) database, which tracks the expression of transposon-induced mutants and the cellular localization of transposon-tagged proteins, and the Saccharomyces Cell Cycle Expression Database, presenting the first results on changes in mRNA transcript levels dming the yeast cell cycle. 

Some tours deforce of these methods have been presented in several publications, (see [6,7] and references therein). The studies of Tyson and coworkers are focused on the kinetic analysis of the budding yeast cell cycle. The molecular mechanism of cell cycle control is known in more detail for budding yeast, Saccharomyces cerevisiae, than for any other eukaryotic organism. Many experiments have been done on this system over many years there are about 125 references cited in [6]. The biological details are second to stressing the enormity of this task. The model has nearly twenty variables and that many kinetic equations, and there are about fifty parameters (rate coefficients, binding constants, thresholds, relative efficiencies). A fair number of assumptions need to be made in the cases of absence of any substantiating experimental evidence, and a fair number of approximations need to be made to simplify the kinetic equations. The complexity of this system is indicated in fig. 13.3 and its caption. 

Li, C.J., Y.Z. Li, A.V. Pinto, and A.B. Pardee. 1999. Potent inhibition of tumor survival in vivo by beta-lapachone plus taxol Combining drugs imposes different artificial checkpoints. Proc. Natl. Acad. Sci. U.S.A. 96(23) 13369-13374. Menacho-Marquez, M., and J.R. Murguia. 2006. Beta-lapachone activates a Mrellp-Tellp Gl/S checkpoint in budding yeast. Cell Cycle 5(21) 2509-2516. 

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