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Dissertations / Theses on the topic 'Budding yeast cell'

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Published: 4 June 2021
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1

Huberman, Lori Bromer. "Studies on mating in the budding yeast." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11124.

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Budding yeast are capable of existing in both a haploid and diploid state. Haploid cells have two mating types, MATa and MATα. When cells from the two mating types come in contact they signal using reciprocal pheromones and pheromone receptors, starting a regulated pheromone response that includes transcription of pheromone-response genes, polarization in the direction of highest pheromone concentration, and cell cycle arrest. Once cells have chosen a mating partner, they must fuse their cell walls, plasma membranes, and nuclei to form a single diploid cell.
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2

Attner, Michelle Andrea. "Cell cycle regulation during gametogenesis in budding yeast." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/81031.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, June 2013.
"June 2013." Cataloged from PDF version of thesis.
Includes bibliographical references.
Sexual reproduction depends on meiosis, the specialized cell division that gives rise to gametes. During meiosis, two consecutive rounds of chromosome segregation follow one round of DNA replication to yield four haploid gametes from one diploid progenitor. In meiosis I, homologous chromosomes segregate and in meiosis 11, sister chromatids split. Much of the same cell cycle machinery controls mitosis and meiosis. However, segregation of homologous chromosomes in meiosis I and progression into meiosis 11 directly after meiosis I necessitate several modifications to the basic cell cycle machinery. In this thesis, I have investigated how cell cycle regulators function during gametogenesis. First, I show that the mitotic exit network, which is a signaling pathway essential for mitotic exit, is dispensable for the meiotic divisions, and in fact signals via a mechanism distinct from mitosis. Second, I present data that the Polo kinase Cdc5, which activates mitotic exit in budding yeast, has gained additional roles during meiosis 1. I show that CDC5 is required for the removal of cohesin from chromosome arms in meiosis I, which is a prerequisite for meiosis I segregation. Despite the central role of CDC5 in regulating meiosis I, CDC5 is dispensable during meiosis 11. In sum, understanding how cell cycle regulators control the specialized meiotic divisions has improved our understanding of how different cell division types are established.
by Michelle Andrea Attner.
Ph.D.
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3

Calzone, Laurence. "Mathematical Modeling of the Budding Yeast Cell Cycle." Thesis, Virginia Tech, 2000. http://hdl.handle.net/10919/31988.

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The cell cycle of the budding yeast, Saccharomyces cerevisiae, is regulated by a complex network of chemical reactions controlling the activity of the cyclin-dependent kinases (CDKs), a family of protein kinases that drive the major events of the cell cycle. A previous mathematical model by Chen et al. (2000) described a molecular mechanism for the Start transition (passage from G1 phase to S/M phase) in budding yeast. In this thesis, my main goal is to extend Chen's model to include new information about the mechanism controlling Finish (passage from S/M phase to G1 phase). Using laws of biochemical kinetics, I transcribed the hypothetical molecular mechanism into a set of differential equations. Simulations of the wild-type cell cycle and the phenotypes of more than 60 mutants provide a thorough understanding of how budding yeast cells exit mitosis.
Master of Science
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4

Vinton, Peter J., and Peter J. Vinton. "Cell Cycle Delay Stabilizes the Budding Yeast Genome." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/623021.

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When damaged DNA is detected during replication, a checkpoint delays the cell cycle to allow time for repair. Here I show that continually delaying the cell cycle in the G2/M phase of the cell cycle stabilizes the genome of Saccharomyces cerevisiae in both checkpoint proficient and deficient cells; a phenomenon I call slow cycle stabilization (SCS). SCS stabilizes the genome in cells defective for DNA damage response (DDR), spindle checkpoint, and telomere biology, as well as wild type (WT) cells. I verify SCS using genetic and chemical means and further substantiate SCS using three different Saccharomyces cerevisiae chromosome systems.
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5

Priya, Vattem Padma. "Genomic distribution of histone H1 in budding yeast (Saccharomyces cerevisiae) : yeast chromosome III." Master's thesis, University of Cape Town, 2002. http://hdl.handle.net/11427/4324.

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The linker histone HI binds to the nucleosome and is essential for the organization of nucleosomes into the 30-nm filament of the chromatin. This compaction of DNA has a well-characterized effect on DNA function. In Saccharomyces cerevisiae, HHO 1 encodes a putative linker histone with very significant homology to histone HI. In vitro chromatin assembly experiments with recombinant Hho 1 p have shown that it is able to complex with the dinucleosomes in a similar manner to histone HI. It has also been reported that disruption of HHOl has little affect on RNA levels. A longstanding issue concerns the location of Hho 1 p in the chromatin and studies have shown using immunoprecipitation technique with anti-HA antibody, that Hho 1 p shows a preferential binding to rDNA sequences. In this project we have tried to confirm the above results in wild type cells, using immunopurifi ed anti rHho 1 p antibody.
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6

Kiser, Gretchen Louise. "Cell cycle checkpoint control in budding yeast Saccharomyces cerevisiae." Diss., The University of Arizona, 1995. http://hdl.handle.net/10150/187074.

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Multiple checkpoint controls ensure that later cellular events are not initiated until previous cellular events have been successfully completed. Our laboratory studies the checkpoint at the G2/M boundary that ensures the integrity of chromosome transmission by blocking mitosis until DNA synthesis and repair is completed. The checkpoint-dependent cell division arrest is one of several prominent responses to DNA damage, which also includes transcriptional induction of damage-inducible genes and DNA repair. I undertook three projects that explore several aspects of the damage response: (1) I further characterized the checkpoint gene RAD24, in that I showed that RAD24 function has G2 phase-specificity after damage and that RAD24 contributes to genomic stability; (2) I evaluated the nature of the damage signal from UV-irradiation that elicits a checkpoint-dependent cell cycle arrest; and (3) I established a transcriptional role for some of the checkpoint genes. In addition, I characterized a gene that encodes a novel elongation factor-type GTPase. Upon examination of the checkpoint-dependent delay following UV-irradiation in a mutant defective for incision of pyrimidine dimers, I found that processing of DNA damage, i.e. dimer-incision, is necessary to generate an appropriate damage signal. Processing of damage may be a general property of the damage response and may involve the checkpoint proteins. I found that some checkpoint genes have an additional role in a complex transcriptional induction response to DNA damage. Primarily, I found: (i) mec1 and mec2 mutants are defective for DNA damage-induction of the RNR3 gene, whereas the other checkpoint mutants appear to play less of a role; (ii) all the checkpoint mutants are proficient for transcriptional induction UBI4; (iii) rad17 mutants, and to a lesser degree mec1 and mec2 mutants as well, are defective for damage-induction of DDR48; (v) transcription of the RAD17, RAD24, MEC1, and MEC2 (but not the RAD9) checkpoint genes is damage-inducible and MEC1 is required for the transcriptional induction of the MEC1 and MEC2 genes, but not the RAD17 or RAD24 genes. I suggest that their transcriptional function ties the checkpoint proteins to DNA repair, as damage-inducible transcriptional induction probably functions to augment repair.
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7

Gardner, Richard Donald 1967. "Defining response pathways of budding yeast checkpoint genes." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282722.

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Cell cycle events are ordered correctly; mitosis follows DNA replication. To ensure correct order, cells employ checkpoints that delay the cycle when DNA replication, repair, or spindle assembly have not been completed. In this dissertation, I have focused on the DNA damage checkpoint, which arrests the cell in G₂ in response to DNA damage (the G₂/M checkpoint). I have studied the roles of several checkpoint genes in the budding yeast Saccharomyces cerevisiae involved in the response to DNA damage, focusing on a key gene called MEC1. I have tested genetically where in several pathways checkpoint genes act: G₂/M checkpoint pathway. I found that after DNA damage, MEC1 signals G₂/M cell cycle arrest using two pathways, one involving RAD53 and DUN1, and the other involving PDS1. Both pathways must be functional for full checkpoint arrest; either pathway acting alone produces only a partial arrest. I speculate why there are two pathways for arrest. TEL1. I also tested the roles of TEL1, a putative MEC1 homolog. I showed that TEL1 has no normal checkpoint function. However, when overexpressed, TEL1 produces a constitutive G₂ delay, independent of DNA damage, a delay that requires the PDS1 pathway. This constitutive delay is responsible for the suppression by TEL1 of the UV sensitivity of mec1 mutants. When overexpressed, TEL1 also restores damage-inducible transcription to mec1 cells. I discuss TEL1's possible roles in checkpoint mediated responses. Essential function pathway. Previous results showed that MEC1 and RAD53 are also required for the transcriptional induction of repair genes and for an essential function. The nature of their essential function(s) remains unknown. My results, from a complex series of genetic tests, suggest that MEC1 and RAD53 share the same essential function, and that this function may in fact be related to the transcriptional function. I speculate on the nature of the essential function. I also present evidence that MEC1 and RAD53 may have a role in DNA replication. My results have led to refined models of pathways leading to checkpoint arrest, damage-inducible transcription, and an essential function(s).
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8

Talbot, Craig. "Start-specific transcriptional regulation of the budding yeast cell cycle." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391813.

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9

McQueen, Jennifer. "Exploration of the budding yeast kinase Mck1 in cell cycle regulation." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42927.

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10

Fransson, Martin. "Identification of a Genetic Network in the Budding Yeast Cell Cycle." Thesis, Linköping University, Department of Electrical Engineering, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-2389.

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By using AR/ARX-models on data generated by a nonlinear differential equation system representing a model for the cell-cycle control system in budding yeast, the interactions among proteins and thereby also to some extent the genes, are sought. A method consisting of graphical analysis of differences between estimates from two local linear models seems to make it possible to separate a set of linear equations from the nonlinear system. By comparing the properties of the estimations in the linear equations a set of approximate equations corresponding well to the real ones are found.

A NARX model is tested on the same system to see whether it is possible to find the dependencies in one of the nonlinear differential equations. This approach did, for the choice of model, not work.

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11

Freire, P. S. D. S. "Mathematical modelling of mitotic exit control in budding yeast cell cycle." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:982b3244-328d-4b76-b333-50287a753bc0.

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The operating principles of complex regulatory networks are more easily understood with mathematical modelling than by intuitive reasoning. In this thesis, I study the dynamics of the mitotic exit control system in budding yeast. I present a comprehensive mathematical model, which provides a system’s-level understanding of the mitotic exit process. This model captures the dynamics of classic experimental situations reported in the literature, and overcomes a number of limitations present in previous models. Analysis of the model led to a number of breakthroughs in the understanding of mitotic exit control. Firstly, numerical analysis of the model quantified the dependence of mitotic exit on the proteolytic and non-proteolytic functions of separase. It was shown that the requirement for the non-proteolytic function of separase depends on cyclin-dependent kinase activity. Secondly, APC/Cdc20 is a critical node that controls the phosphatase (Cdc14) branch and both cyclin (Clb2 and Clb5) branches of the cell cycle regulatory network. Thirdly, the model proved to be a useful tool for the systematic analysis of the recently discovered phenomenon of Cdc14 endocycles. Most proteins belonging to the cell cycle control network are regulated at the level of synthesis, degradation and activity. Presumably, these multiple layers of regulation facilitate robust cell cycle behaviour in the face of genetic and environmental perturbations. To falsify this hypothesis, I subjected the model to global parameter perturbations and tested viability against pre-defined criteria. According to these analyses, the regulated transcription and degradation of proteins make different contributions to cell cycle control. Regulated degradation confers cell cycle oscillations with robustness against perturbations, while regulated transcription plays a major role in controlling the period of these oscillations. Both regulated transcription and degradation are part of important feedback loops, that combined promote robust behaviour in the face of parametric variations.
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12

Perley, Elizabeth (Elizabeth Bacher). "Budding yeast cell cycle analysis and morphological characterization by automated image analysis." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/66452.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2011.
Cataloged from PDF version of thesis.
Includes bibliographical references (p. 70-71).
Budding yeast Saccharomyces cerevisiae is a standard model system for analyzing cellular response as it is related to the cell cycle. The analysis of yeast cell cycle is typically done visually or by using flow cytometry. The first of these methods is slow, while the second offers a limited amount of information about the cell's state. This thesis develops methods for automatically analyzing yeast cell morphology and yeast cell cycle using high content screening with a high-capacity automated imaging system. The images obtained using this method can also provide information about fluorescently labelled proteins, unlike flow cytometry, which can only measure overall fluorescent intensity. The information about yeast cell cycle stage and protein amount and localization can then be connected in order to develop a model of yeast cellular response to DNA damage.
by Elizabeth Perley.
M.Eng.
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13

Nerusheva, Olga. "Dynamics and regulation of Shugoshin and other pericentromeric proteins in budding yeast." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/17907.

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Accurate distribution of genetic material is critical for the formation of functional cells and their proliferation. During cell division, sister chromatids separate from each other and segregate to opposite poles. To ensure accurate chromosome segregation all sister chromatids should be attached to microtubules from opposite spindle poles, known as bi-orientation. Cohesin is a protein complex that holds sister chromatids together from the time of its replication in S phase until anaphase onset, and it is required for proper chromosome segregation both in mitosis and in meiosis. It is distributed intermittently along the full length of chromosomes with significant enrichment in the region surrounding the centromere, known as the pericentromere. This chromosome domain was shown to be crucial for chromosome bi-orientation. In my PhD I studied how the establishment of tension between sister chromatids in the process of bi-orientation affects the distribution of different pericentromeric proteins on budding yeast chromosomes. It was known that levels of cohesin at the pericentromere are decreased in response to the establishment of tension. I demonstrate that other proteins, such as subunits of condensin, members of the Chromosome Passenger Complex (CPC) and others, exhibit similar dynamics, and suggest a model to explain this phenomenon. Out of all studied proteins, Shugoshin (Sgo1) was the only one that was completely removed from the pericentromere in response to spindle tension establishment. There is evidence that Sgo1 plays a role in sensing spindle tension and halting the cell cycle until this has been achieved but how it does so is not known. Therefore, removal of Shugoshin from the pericentromere might be a signal for the cell that bi-orientation occurred. I then found that spindle tension itself is not sufficient for Sgo1 re-localization from the pericentromere, and there are other factors that affect it. I showed that deletion of RTS1, a highly conserved regulatory subunit of Protein Phosphatase 2A (PP2A), results in substantial enrichment of Shugoshin at the pericentromere in the situation when spindle tension is absent. In addition, Bub1 kinase, a protein that is required for Sgo1 localization, was found to be removed from the centromere in response to spindle tension as well as Sgo1. The role of Bub1 the in localization of Shugoshin is to phosphorylate histone H2A, which then becomes a mark for Sgo1 loading. Therefore, we assume that Sgo1 dynamics and, potentially, its role in sensing bi-orientation, are regulated through the array of phosphorylation and de-phosphorylation events at the pericentromeric area. Finally, I have also found that budding yeast Sgo1 undergoes the posttranslational modification as sumoylation. I showed that sumoylation of Shugoshin is not required for its removal from the pericentromere during biorientation. However, it might be important for the regulation of Sgo1 degradation and its role in the metaphase to anaphase transition in mitosis.
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14

Calzone, Laurence. "Temporal organization of the budding yeast cell cycle: general principles and detailed simulations." Diss., Virginia Tech, 2003. http://hdl.handle.net/10919/11070.

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The budding yeast cell cycle has attracted attention from many experimentalists over the years for its simplicity and amenability to genetic manipulation. Moreover, the regulatory components described in budding yeast, Saccharomyces cerevisiae, are conserved in higher eukaryotes. The budding yeast cell cycle is governed by a complex network of chemical reactions controlling the activity of the cyclin-dependent kinases (CDKs), proteins that drive the major events of the cell cycle. The presence of these proteins is required for the transition from G1 to S phase (Start) whereas their absence permits the transition from S/M to G1 phase (Finish). The cell cycle of budding yeast is based on alternation between these two states. To test the accuracy of this theory against experiments, we built a hypothetical molecular mechanism of the budding yeast cell cycle and transcribed it into differential equations. With a proper choice of kinetic parameters, the differential equations reproduce the main events of the cell cycle such as: the synthesis of cyclins (Cln1,2; Cln3; Clb1,2; Clb5,6) by their transcription factors (SBF, Mcm1, MBF); their association with stoichiometric inhibitors (Sic1, Cdc6); their degradation by SCF and adaptors of the APC (Cdc20, Cdh1). The emphasis was put on mechanisms responsible for the release of Cdc14 from the RENT complex, Cdc14 being a major player in exit from mitosis. Simulations of the wild type strain and more than 100 mutants showed phenotypes in accordance with experimental observations. Some mutants defective in the Start and Finish transitions and the different ways to rescue them will be presented.
Ph. D.
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15

Shcheprova, Zhanna. "A mechanism for asymmetric segregation of age during cell division in budding yeast /." Zürich : ETH, 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17786.

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16

Noton, Elizabeth Anne. "The regulation of pre-replicative complex formation in the budding yeast cell cycle." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342284.

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17

Mendes, Pinto Inês. "Spatiotemporal mechanisms for actomyosin ring assembly and contraction in budding yeast cell division." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2012. http://hdl.handle.net/10362/8571.

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Dissertation presented to obtain the Ph.D degree in Molecular Medicine
Animal and yeast cells use a contractile ring that is attached to the plasma membrane to create a cleavage furrow that partitions a cell into two in the latest step of cell division. The contractile ring is a network of actin and myosin-II motor filaments embedded in a complex and compact protein core structure at the cell division site. In the absence of myosin-II, cells fail to assemble the contractile ring pursuing death or rapidly evolving divergent pathways to restore growth and cytokinesis, an event associated to aneuploidy, a common trait in cancer development and progression. The molecular mechanisms underlying myosin-II localization and function at the cell division site with actin ring assembly and contraction remain poorly understood. Based on analogy to the striated muscle, it has been classically proposed that contractile stress in the actomyosin ring is generated via a “sliding filament” mechanism in which bipolar myosin-II motor filaments walk along actin filaments, within organized sarcomere-like arrays. However, ultra-structural and genetic studies in different cellular systems have shown that contractile rings are more complex than striated muscles, and in some examples the motor activity can actually be dispensable for the contractibility of the cytokinetic ring.(...)
PhD fellowship awarded by the Rong Li laboratory and a previous awarded fellow of the GABBA PhD program at the Faculty of Medicine, University of Porto, Portugal and the Portuguese Foundation for Science and Technology, Portugal. Apoio financeiro da Fundação para a Ciência e Tecnologia e do Fundo Social Europeu no âmbito do Quadro Comunitário de Apoio, BD n°SFRH/BD/11760/2003.
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18

Ben, Meriem Zacchari. "Memory of stress response in the budding yeast Saccharomyces cerevisiae." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC311.

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La mémoire cellulaire est une capacité critique dont font preuve les micro-organismes pour s'adapter aux fluctuations environnementales potentiellement néfastes. Chez l'eucaryote unicellulaire S. cerevisiae, il a été montré à l’échelle d’une population que la mémoire cellulaire peut prendre la forme d'une réponse plus rapide ou moins prononcée suite à des stress répétés. Nous présentons ici une étude sur la façon dont les levures réagissent à des stress hyperosmotiques de courte durée à l’échelle de la cellule unique. Nous avons analysé le comportement dynamique du promoteur STL1, exprimé en condition de stress osmotique, et fusionné à un rapporteur fluorescent en faisant usage de microfluidique et de microscopie à fluorescence. Nous avons établi que pSTL1 présente une variabilité dynamique dans ses activations successives après deux stress courts. Malgré cette variabilité, la plupart des cellules présentent une mémoire des stress passés caractérisée par une diminution de l'activité de pSTL1. Nous avons montré que cette mémoire ne nécessite pas de nouvelle synthèse de protéines. L'emplacement génomique est important pour cette mémoire puisque le déplacement du promoteur vers un domaine chromatinien péricentromérique entraîne une diminution de sa force transcriptionnelle ainsi que la perte de la mémoire. Nos résultats indiquent aussi une implication non rapportée du complexe SIR sur l'activité de pSTL1 lorsqu'il est déplacé dans le domaine péricentromérique, dans nos conditions expérimentales. Cette étude fournit une description quantitative d'une mémoire cellulaire qui inclut la variabilité cellulaire et prend en compte la contribution de la structure de la chromatine sur la mémoire du stress. Nos travaux pourraient servir de base à des études plus larges sur le positionnement des gènes de réponse au stress en positions subtélomériques dans la levure, tant d'un point de vue génétique qu'évolutif
Cellular memory is a critical ability displayed by micro-organisms in order to adapt to potentially detrimental environmental fluctuations. In the unicellular eukaryote S. cerevisiae, it has been shown at the population level that cellular memory can take the form of a faster or a decreased response following repeated stresses. We here present a study on how yeasts respond to short, pulsed hyperosmotic stresses at the single-cell level. We analyzed the dynamical behavior of the stress responsive STL1 promoter fused to a fluorescent reporter using microfluidics and fluorescence time-lapse microscopy. We established that pSTL1 displays a dynamical variability in its successive activations following two short and repeated stresses. Despite this variability, most cells displayed a memory of past stresses through a decreased activity of pSTL1 upon repeated stresses. We showed that this memory does not require do novo protein synthesis. Rather, the genomic location is important for the memory since promoter displacement to a pericentromeric chromatin domain leads to its decreased transcriptional strength and to the loss of the memory. Interestingly, our results points towards an unreported involvement of the SIR complex on the activity of pSTL1 only when displaced to the pericentromeric domain in our experimental conditions. This study provides a quantitative description of a cellular memory that includes single-cell variability and points towards the contribution of the chromatin structure in stress memory. Our work could serve as a basis to broader studies on the positioning of stress response genes at subtelomeric positions in the budding yeast, from a genetic point of view as well as an evolutionary one
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19

Panning, Thomas D. "Deterministic Parallel Global Parameter Estimation for a Model of the Budding Yeast Cell Cycle." Thesis, Virginia Tech, 2006. http://hdl.handle.net/10919/33360.

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Two parallel deterministic direct search algorithms are combined to find improved parameters for a system of differential equations designed to simulate the cell cycle of budding yeast. Comparing the model simulation results to experimental data is difficult because most of the experimental data is qualitative rather than quantitative. An algorithm to convert simulation results to mutant phenotypes is presented. Vectors of the 143 parameters defining the differential equation model are rated by a discontinuous objective function. Parallel results on a 2200 processor supercomputer are presented for a global optimization algorithm, DIRECT, a local optimization algorithm, MADS, and a hybrid of the two. A second formulation is presented that uses a system of smooth inequalities to evaluate the phenotype of a mutant. Preliminary results of this formulation are given.
Master of Science
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20

Seaton, Daniel. "Mathematical modelling and systems analysis of intracellular signalling networks and the budding yeast cell cycle." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14631.

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Cellular signalling networks are responsible for coordinating a cell’s response to internal and external perturbations. In order to do this, these networks make use of a wide variety of molecular mechanisms, including allostery, gene regulation, and post-translational modifications. Mathematical modelling and systems approaches have been useful in understanding the signal processing capabilities and potential behaviours of such networks. In this thesis, a series of mathematical modelling and systems investigations are presented into the potential regulation of a variety of cellular systems. These systems range from ubiquitously seen mechanisms and motifs, common to a wide variety of signalling pathways across many organisms, to the study of a particular process in a particular cell type - the cell cycle in Saccharomyces cerevisiae. The first part of the thesis involves the analysis of ubiquitous signalling mechanisms and behaviours. The potential behaviours of these systems are examined, with particular attention paid to properties such as adaptive and switch-like signalling. This series of investigations is followed by a study of the dynamic regulation of cell cycle oscillators by external signalling pathways. A methodology is developed for the study of mathematical models of the cell cycle, based on linear sensitivity analysis, and this methodology is then applied to a range of models of the cell cycle in Saccharomyces cerevisiae. This allows the description of some interesting generic behaviours, such as nonmonotonic approach of cell cycle characteristics to their eventual values, as well as allowing identification of potential principles of dynamic regulation of the cell cycle.
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21

Shamrock, Vanessa J. "The functional significance of Hsp12p and trehalose in desiccation and oxidative stress in the budding yeast Saccharomyces cerevisiae." Master's thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/4331.

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The preservation of yeast viability and vitality during storage in the desiccated state is fundamental as several industrial processes utilise this technology. The significance of the stress response protein and putative hydrophilin, Hsp 12p, was therefore examined in vivo under desiccation conditions.
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22

Deniz, Ozgen. "Nucleosome Positioning in Budding Yeast = Posicionamiento de nucleosomas en Saccharomyces cerevisiae." Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/145763.

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The nucleosome is the fundamental structural unit of DNA compaction in eukaryotic cells and is formed by the wrapping of 147 bp double stranded DNA around a histone octamer. Nucleosome organization plays a major role in controlling DNA accessibility to regulatory proteins, hence affecting cellular processes such as transcription, DNA replication and repair. Our study focuses on genome-wide nucleosome positioning in S. cerevisiae to explore nucleosome determinants and plasticity throughout the cell cycle and their interplay with gene expression based on cell mRNA abundance. We pursued the contribution of DNA physical properties on nucleosome organization around key regulatory regions such as TSSs and TTSs by analyzing genome-wide MNase-digestion profile of genomic DNA. We also implemented a systematic approach to standardize MNase-Seq experiments by minimizing the noise generated by extrinsic factors to enable an accurate analysis of the underlying principles of nucleosome positioning and dynamics. Moreover, we carried out a large-scale study of nucleosome plasticity throughout the cell cycle and its interplay with transcription based on a comparative analysis among nucleosome maps, gene expression data and MNase sensitivity assays. We then focused on nucleosome organization around DNA replication origins and its possible effect on origin activation. Finally, we sought to characterize centromeric nucleosome composition and its oscillation along cell cycle. During the course of these studies, we found that key regulatory regions such as 5’ and 3’ nucleosome free regions (NFRs) contain unusual physical properties that are intrinsic to genomic DNA. We further demonstrated that DNA physical properties and transcription factors act synergistically to define NFRs, especially in genes with an open promoter structure. Once NFR is defined, the nucleosome positioning around TSSs can be predicted by a simple statistical model, supporting the energy barrier model for nucleosome positioning determination. However, we also observed that nucleosomes are quite dynamic at distal 5’ NFRs and do have distinct regulatory mechanisms. Our comparative analysis of nucleosome organization along cell cycle revealed that chromatin exhibits a distinct configuration due to DNA replication-dependent organization at S phase, showing higher sensitivity to MNase and displaying fuzzier nucleosomes along the genome. Moreover, we observed different features at M phase, where chromatin compaction is the highest and displays a slightly different pattern than in G1 and G2 phases. Interestingly, these changes in chromatin organization are sudden and acute and only affect some regions of the genome, whereas the majority of genes present conserved nucleosome patterns along cell cycle. Our individual gene analysis disclosed that the largest changes take place in cell cycle-dependent genes, indicating the interplay between chromatin and transcription. Moreover, a distinct nucleosome organization at high and low transcription rates further supports this relationship. The detailed analysis around replication origins shows that they display slightly wider NFRs at G1 phase due to pre-Replication complex binding. Once the replication origins are active, nucleosomes partially occupy NFRs up to a certain extent due to constitutive binding of ORC. Moreover, we provided further evidence that early firing origins tend to have more ordered nucleosome organization than late firing origins. Finally we illustrated that centromeric nucleosomes display a perfect positioning, confirming their strong centromeric sequence-dependent recruitment to DNA. The characterization of histone composition under physiological cell conditions suggested that the octameric nucleosome assembly model is favored in centromeres. Yet, our analysis along cell cycle showed centromeric nucleosome dynamics, proposing that its composition might oscillate along cell cycle. Taken together, our accurate study provides a dynamic picture of nucleosome positioning and its determinants; new insights into cell cycle-dependent chromatin organization on key regulatory regions and its interplay with gene expression; and adds a new dimension to the characterization of centromeric nucleosomes.
Nuestro estudio se centra en el posicionamiento de nucleosomas a nivel genómico en levadura, con tal de explorar los factores determinantes de nucleosomas y su plasticidad a lo largo del ciclo celular, así como su relación con la expresión génica basándonos en la cantidad de mARN celular. Encontramos que las regiones libres de nucleosomas (NFRs en inglés) en 5’ y 3’ contienen propiedades físicas inusuales, las cuales son intrínsecas del ADN genómico. Además, demostramos que estas propiedades físicas actúan sinérgicamente con factores de transcripción para definir las NFRs. Una vez la NFR está definida, el posicionamiento de nucleosomas en torno al inicio de transcripción (TSS en inglés) puede predecirse con modelos estadísticos simples. No obstante, también observamos que los nucleosomas son bastante dinámicos en las regiones distales a 5’NFRs y poseen distintos mecanismos reguladores. Nuestro análisis comparativo acerca de la organización de los nucleosomas reveló que la cromatina de hecho exhibe una configuración distinta debido al reordenamiento dependiente de la replicación en fase S, mostrando una mayor sensibilidad de corte por el enzima MNase y un mayor número de nucleosomas deslocalizados a lo largo del genoma. Adicionalmente, observamos características particulares en fase M, donde la cromatina sufre un mayor grado de compactación. Notablemente, estos cambios en la organización de la cromatina son repentinos y agudos y sólo afectan a algunas regiones del genoma, mientras que la mayoría de genes presentan una conservación del patrón de nucleosomas a lo largo del ciclo celular. El análisis detallado en torno a los orígenes de replicación muestra una NFR más ancha en fase G1, debido a la unión del complejo pre-replicatorio. Una vez se activa el origen, los nucleosomas sólo ocupan parcialmente la NFR, debido a la unión constitutiva del complejo de origen de replicación (ORC en inglés). También proporcionamos evidencias de que los orígenes tempranos tienden a tener una organización nucleosomal más ordenada que los tardíos. Finalmente, ilustramos que los nucleosomas centroméricos poseen un posicionamiento idóneo y asimismo, un ensamblaje distinto. Sin embargo, nuestro análisis también mostró la dinámica de los nucleosomas centroméricos a lo largo del ciclo celular, indicando que de hecho su composición puede oscilar a lo largo del ciclo celular. En conjunto, nuestro detallado estudio proporciona una imagen dinámica del posicionamiento de nucleosomas y sus factores determinantes; nuevos indicios respecto a la organización de la cromatina en regiones reguladoras clave en base al ciclo celular y su conexión con la expresión génica; y finalmente, añade una nueva dimensión a la caracterización de los nucleosomas centroméricos.
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23

Abd, El Rahim Metwally Galal Yahya. "Molecular retention mechanisms of the G1 cyclin/Cdk complex in budding yeast." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/368230.

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Budding yeast (Saccharomyces cerevisiae) cells coordinate cell growth and cell cycle progression essentially during G1, where they must reach a critical cell size to traverse Start and enter the cell cycle. The most upstream activator of Start is Cln3, a G1 cyclin that together with the cyclin-dependent kinase Cdc28 triggers a transcriptional wave that drives cell cycle entry. The Cln3 cyclin is a low abundant and very unstable protein whose levels respond very rapidly to nutritional changes. However, Cln3 expression is not sharply regulated through the cell cycle and it is already present in early G1 cells. Notably, most Cln3 is retained bound to the ER in early G1 with the assistance of Whi3, an RNA-binding protein that binds the CLN3 mRNA, and it is released in late G1 by Ydj1, a J-chaperone that might transmit growth capacity information to the cell cycle machinery. However, little is known on the molecular mechanisms that retain the Cdc28-C1n3 complex in the cytoplasm and how do these mechanisms transmit information of cell size to coordinate cell proliferation with cell growth. As Cdc28 is important for proper retention of Cln3 at the ER, we hypothesized that mutations weakening interactions to unknown ER retention factors would cause premature release of the Cdc28-C1n3 complex and, hence, a smaller cell size. This thesis describes the isolation and characterization of a CDC28 quintuple mutant, which we refer to as CDC28wee, that causes premature entry into the cell cycle and a small cell size. Next we used isobaric tags for relative and absolute quantitation (iTRAQ) to identify direct interactors with lower affinities for mutant Cdc28wee, aiming at the identification of proteins with key regulatory roles in the retention mechanism. Among the identified proteins we found Sr13, a protein of unknown function, here renamed as Whi7. Here we show that Whi7 acts as an inhibitor of Start, associates to the ER and contributes to efficient retention of the Cln3 cyclin, thus preventing its unscheduled accumulation in the nucleus. Our results demonstrate that Whi7 acts in a positive feedback loop to release the G1 Cdk¬cyclin complex and trigger Start once a critical size has been reached, thus uncovering a key nonlinear mechanism at the earliest known events of cell cycle entry. In addition to Whi7 we also identified Whi8, renamed here as Whi8, which is an RNA-binding protein present in both stress granules (SGs) and P bodies (PBs) with unknown biological function. We have found that Whi8 interacts with Cdc28 in vivo, binds and colocalizes with the CLN3 mRNA, and interacts with Whi3 in an RNA-dependent manner. Whi8-deficient cells showed a smaller budding cell size while, on the other hand, overexpression of Whi8 increased the budding volume. Cells lacking Whi8 were not capable of accumulating the CLN3 mRNA in SGs under stress conditions, and Cln3 synthesis remained high under glucose and nitrogen starvation, two environmental stress conditions that dramatically decrease Cln3 levels in the cell. Whi8 accumulation in SGs depended on an intrinsically disordered domain (IDD) identified at C-terminus of Whi8 and specific PKA phophosites. Our results suggest that Whi8 acts under stress as a safeguard that limits the influx of newly synthesized Cln3 (and likely other proteins) into the cell cycle machinery, by trapping the CLN3 mRNA in mRNA granules. Thus, we have found a unique target for signaling pathways that directly links stress response and cell cycle entry.
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24

Semple, Jeffrey. "Characterization of the role of Orc6 in the cell cycle of the budding yeast Saccharomyces cerevisiae." Thesis, University of Waterloo, 2006. http://hdl.handle.net/10012/2969.

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The heterohexameric origin recognition complex (ORC) acts as a scaffold for the G1 phase assembly of pre-replicative complexes. Only the Orc1-5 subunits are required for origin binding in budding yeast, yet Orc6 is an essential protein for cell proliferation. In comparison to other eukaryotic Orc6 proteins, budding yeast Orc6 appears to be quite divergent. Two-hybrid analysis revealed that Orc6 only weakly interacts with other ORC subunits. In this assay Orc6 showed a strong ability to self-associate, although the significance of this dimerization or multimerization remains unclear. Imaging of Orc6-eYFP revealed a punctate sub-nuclear localization pattern throughout the cell cycle, representing the first visualization of replication foci in live budding yeast cells. Orc6 was not detected at the site of division between mother and daughter cells, in contrast to observations from metazoans. An essential role for Orc6 in DNA replication was identified by depleting the protein before and during G1 phase. Surprisingly, Orc6 was required for entry into S phase after pre-replicative complex formation, in contrast to what has been observed for other ORC subunits. When Orc6 was depleted in late G1, Mcm2 and Mcm10 were displaced from chromatin, the efficiency of replication origin firing was severely compromised, and cells failed to progress through S phase. Depletion of Orc6 late in the cell cycle indicated that it was not required for mitosis or cytokinesis. However, Orc6 was shown to be associated with proteins involved in regulating these processes, suggesting that it may act as a signal to mark the completion of DNA replication and allow mitosis to commence.
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25

Parsons, Michelle L. "The Role of SIR4 in the Establishment of Heterochromatin in the Budding Yeast Saccharomyces cerevisiae." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31028.

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Heterochromatin in the budding yeast Saccharomyces cerevisiae is composed of polymers of the SIR (Silent Information Regulator) complex bound to nucleosomal DNA. Assembly of heterochromatin requires all three proteins of the Sir complex: the histone deacetylase Sir2, and histone binding proteins Sir3 and Sir4. Heterochromatin establishment requires passage through at least one cell cycle, but is not dependent on replication. Inhibition of chromatin modifying enzymes may be a mechanism for how cells limit assembly. Dot1 dependent methylation of H3K79 is suggested to inhibit de novo assembly. Halving the levels of Sir4 in cells causes a loss of silencing, suggesting that Sir4 protein abundance regulates the assembly of heterochromatin. We examine de novo assembly using a single cell assay. Half the level of Sir4 affects establishment, but not the maintenance, of silencing at HM loci. Additional Sir4 accelerates the rate of assembly. Epistasis analysis suggests that Dot1 dependent chromatin modification may act upstream of Sir4 abundance. We hypothesize that dot1Δ mutants speed assembly by disrupting telomeric heterochromatin, which liberates Sir4 to act at the HM loci. Deletion of YKU70, which specifically disrupts telomeric silencing, also speeds de novo assembly, without altering the methylation of histone H3. Consistent with our model, we have shown that Sir4 abundance falls during pheromone and stationary phase arrests after which several cell cycles are required before silencing can be reestablished.
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26

Wu, Yehui [Verfasser]. "The proteins Boi1/2p link cell polarity establishment with exocytosis and actin organization in budding yeast Saccharomyces cerevisiae / Yehui Wu." Ulm : Universität Ulm. Fakultät für Naturwissenschaften, 2014. http://d-nb.info/1063637090/34.

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27

Rinonos, Serendipity Zapanta. "OVERT AND LATENT PATHWAYS OF POLARITY SPECIFICATION IN ZYGOTES: THE HAPLOID-TO-DIPLOID TRANSITION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1354902108.

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28

Laomettachit, Teeraphan. "Mathematical modeling approaches for dynamical analysis of protein regulatory networks with applications to the budding yeast cell cycle and the circadian rhythm in cyanobacteria." Diss., Virginia Tech, 2011. http://hdl.handle.net/10919/29492.

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Mathematical modeling has become increasingly popular as a tool to study regulatory interactions within gene-protein networks. From the modelerâ s perspective, two challenges arise in the process of building a mathematical model. First, the same regulatory network can be translated into different types of models at different levels of detail, and the modeler must choose an appropriate level to describe the network. Second, realistic regulatory networks are complicated due to the large number of biochemical species and interactions that govern any physiological process. Constructing and validating a realistic mathematical model of such a network can be a difficult and lengthy task. To confront the first challenge, we develop a new modeling approach that classifies components in the networks into three classes of variables, which are described by different rate laws. These three classes serve as â building blocksâ that can be connected to build a complex regulatory network. We show that our approach combines the best features of different types of models, and we demonstrate its utility by applying it to the budding yeast cell cycle. To confront the second challenge, modelers have developed rule-based modeling as a framework to build complex mathematical models. In this approach, the modeler describes a set of rules that instructs the computer to automatically generate all possible chemical reactions in the network. Building a mathematical model using rule-based modeling is not only less time-consuming and error-prone, but also allows modelers to account comprehensively for many different mechanistic details of a molecular regulatory system. We demonstrate the potential of rule-based modeling by applying it to the generation of circadian rhythms in cyanobacteria.
Ph. D.
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29

Mapa, Claudine E. "Identification of Deubiquitinating Enzymes that Control the Cell Cycle in Saccharomyces cerevisiae." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/1004.

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A large fraction of the proteome displays cell cycle-dependent expression, which is important for cells to accurately grow and divide. Cyclical protein expression requires protein degradation via the ubiquitin proteasome system (UPS), and several ubiquitin ligases (E3) have established roles in this regulation. Less is understood about the roles of deubiquitinating enzymes (DUB), which antagonize E3 activity. A few DUBs have been shown to interact with and deubiquitinate cell cycle-regulatory E3s and their protein substrates, suggesting DUBs play key roles in cell cycle control. However, in vitro studies and characterization of individual DUB deletion strains in yeast suggest that these enzymes are highly redundant, making it difficult to identify their in vivo substrates and therefore fully understand their functions in the cell. To determine if DUBs play a role in the cell cycle, I performed a screen to identify specific DUB targets in vivo and then explored how these interactions contribute to cell cycle control. I conducted an in vivo overexpression screen to identify specific substrates of DUBs from a sample of UPS-regulated proteins and I determined that DUBs regulate different subsets of targets, confirming they display specificity in vivo. Five DUBs regulated the largest number of substrates, with Ubp10 stabilizing 40% of the proteins tested. Deletion of Ubp10 delayed the G1-S transition and reduced expression of Dbf4, a regulatory subunit of Cdc7 kinase, demonstrating Ubp10 is important for progression into S-phase. We hypothesized that compound deletion strains of these five DUBs would be deficient in key cellular processes because they regulated the largest number of cell cycle proteins from our screen. I performed genetic analysis to determine if redundancies exist between these DUBs. Our results indicate that most individual and combination deletion strains do not have impaired proliferation, with the exception of cells lacking UBP10. However, I observed negative interactions in some combinations when cells were challenged by different stressors. This implies the DUB network may activate redundant pathways only upon certain environmental conditions. While deletion of UBP10 impaired proliferation under standard growth conditions, I discovered that deletion of the proteasome-regulatory DUBs Ubp6 or Ubp14 rescues the cell cycle defect inubp10∆ cells. This suggests in the absence of Ubp10 substrates such as Dbf4 are rapidly degraded by the proteasome, but deletion of proteasome-associated DUBs restores cell cycle progression. Our work demonstrates that in unperturbed cells DUBs display specificity for their substrates in vivo and that a coordination of DUB activities promotes cell cycle progression.
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30

Park, Changwon. "Characterization of four septin genes, and detection of genetic interactions between WdCDC10 and chitin synthase genes during yeast budding in the polymorphic mold, Wangiella ( Exophiala) dermatitidis." Thesis, The University of Texas at Austin, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=3684368.

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Septins are a highly conserved family of eukaryotic proteins having significant homology within and among species. In the budding yeast, Saccharomyces cerevisiae, a septin-based hierarchy of proteins is required to localize chitin in the bud neck prior to septum formation. However, this process has not been clarified in a filamentous, conidiogenous fungus capable of yeast growth, such as Wangiella dermatitidis, a polymorphic agent of human phaeohyphomycosis. Prior studies of this melanized mold showed that some chitin synthase mutants (wdchsa??) have defects in yeast septum formation, suggesting that the septins of W. dermatitidis might functionally associate with some of its chitin synthases (WdChsp). To test this hypothesis, four vegetative septin homologs of S. cerevisiae were cloned from W. dermatitidis and designated WdCDC3, WdCDC10, WdCDC11, and WdCDC12. Of the four, only WdCDC3 functionally complemented completely a strain of S. cerevisiae with a ts mutation in the corresponding gene, although WdCDC12 did so partially. Functional characterizations by mutagenesis of the four W. dermatitidis septin genes revealed that resulting mutants (wdcdca??) each had unique defects in yeast growth and morphology, indicating that each septin carried out a distinct function. Furthermore, when a wdcdc10a?? mutation was introduced into five different wdchsa?? strains, weak genetic interactions were detected between WdCDC10 and WdCHS3 and WdCHS4, and a strong interaction between WdCDC10 and WdCHS5. Cytological studies showed that WdChs5p was mislocalized in some septin mutants, including wdcdc10a??. These results confirmed that in W. dermatitidis septins are important for proper cellular morphogenesis, cytokinesis, and especially septum formation through associations with some chitin synthases.

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31

Fauré, Adrien. "Modélisation logique du réseau de régulation contrôlant le cycle cellulaire chez les eucaryotes." Aix-Marseille 2, 2009. http://theses.univ-amu.fr.lama.univ-amu.fr/2009AIX22066.pdf.

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La dérégulation du cycle cellulaire peut entraîner d'importants dommages pour la cellule elle-même, ainsi que pour tout l'organisme : il s'agit en effet d'un des signes avant-coureurs du cancer. Par ailleurs, la souplesse des mécanismes de contrôle permet à la cellule de s'adapter à des signaux internes et externes variés. La réponse à ces signaux peut aller de l'arrêt du cycle à la possibilité de "sauter" une phase du cycle canonique, comme dans le cas des endocycles, des cycles syncytiaux ou de la méiose. Les données qualitatives étant les plus nombreuses, nous avons choisi le formalisme logique pour étudier le cycle cellulaire d'un point de vue théorique. La relative simplicité de ce formalisme nous permet de construire rapidement des modèles impliquant des dizaines de composants. De plus, des outils analytiques spécifiques permettent d'identifier les états stables ou d'analyser le rôle dynamique des circuits de régulation. Après une introduction au cycle cellulaire et au formalisme logique, je présente les résultats obtenus au cours de mon doctorat, articulés autour des articles auxquels j'ai collaboré. La première partie traite d'un modèle schématique du cycle cellulaire chez les mammifères et du système de priorités développé à cette occasion. La seconde partie traite de la levure bourgeonnante, et de l'approche modulaire utilisée pour étendre le modèle avec des modules de régulation supplémentaires. Pour finir, la troisième partie présente ma contribution à la dernière version publique du logiciel de modélisation logique GINsim. Au cours de la discussion, j'analyse la conservation de la fonctionnalité des circuits de régulation dans des modèles du cycle cellulaire de différents organismes. Ensuite, je discute les perspectives de développement des modèles levure et mammifères ouvertes par l'approche modulaire. Enfin, j'aborde les questions de modularité, de fonctionnalité des circuits et de robustesse
Deregulation of the cell cycle can lead to important damage to the cell itself, or to the whole organism. Indeed, unrestricted proliferation is one of the hallmarks of cancer. Moreover, cell cycle control is very flexible, allowing the cell to adapt to many different external and internal signals. Response to these signals may involve profound modifications, including cell cycle arrest, or yet the possibility to “skip” one phase of the canonical cycle, as in endocycles, syncytial cycles or meiosis. In regard to the scarcity of quantitative data, we chose the logical formalism to study the cell cycle from a theoretical point of view. Moreover, the relative simplicity of this formalism allows us to rapidly build large models involving tens of components. Last but not least, this formalism comes with specific analytical tools, including the possibility to identify stable states and analyse the dynamical role of specific regulatory circuits. After an introduction to both the cell cycle and the logical formalism, I present the results obtained during my Ph. D, articulated around the articles I co-authored. The first part of my work deals with a schematic logical model of the mammalian cell cycle and the prioritisation system developed in this context. The second part deals with budding yeast and a modular approach used to extend and update a model of the core cell cycle engine with regulatory modules developed separately. Finally, the third part presents my contribution to the latest public version of the logical modelling software GINsim. In the discussion, I analyse the conservation of functional regulatory circuits in various logical models of the cell cycle in different organisms. Next I discuss perspectives of extension of the budding yeast and mammalian models open by the modular approach. Finally I consider the questions raised by my work in terms of modularity, circuit functionality and robustness
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32

Wang, Yanli. "Mathematical models of budding yeast colony formation and damage segregation in stem cells." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1500544727569612.

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33

Brümmer, Anneke. "Mathematical modelling of DNA replication." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16212.

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Bevor sich eine Zelle teilt muss sie ihr gesamtes genetisches Material verdoppeln. Eukaryotische Genome werden von einer Vielzahl von Replikationsstartpunkten, den sogenannten Origins, aus repliziert, die über das gesamte Genome verteilt sind. In dieser Arbeit wird der zugrundeliegende molekulare Mechanismus quantitativ analysiert, der für die nahezu simultane Initiierung der Origins exakt ein Mal pro Zellzyklus verantwortlich ist. Basierend auf umfangreichen experimentellen Studien, wird zunächst ein molekulares regulatorisches Netzwerk rekonstruiert, welches das Binden von Molekülen an die Origins beschreibt, an denen sich schließlich komplette Replikationskomplexe (RKs) bilden. Die molekularen Reaktionen werden dann in ein Differentialgleichungssystem übersetzt. Um dieses mathematische Modell zu parametrisieren, werden gemessene Proteinkonzentrationen als Anfangswerte verwendet, während kinetische Parametersätze in einen Optimierungsverfahren erzeugt werden, in welchem die Dauer, in der sich eine Mindestanzahl von RKs gebildet hat, minimiert wird. Das Modell identifiziert einen Konflikt zwischen einer schnellen Initiierung der Origins und einer effizienten Verhinderung der DNA Rereplikation. Modellanalysen deuten darauf hin, dass eine zeitlich verzögerte Origininitiierung verursacht durch die multiple Phosphorylierung der Proteine Sic1 und Sld2 durch Cyclin-abhängige Kinasen, G1-Cdk bzw. S-Cdk, essentiell für die Lösung dieses Konfliktes ist. Insbesondere verschafft die Mehrfach-Phosphorylierung von Sld2 durch S-Cdk eine zeitliche Verzögerung, die robust gegenüber Veränderungen in der S-Cdk Aktivierungskinetik ist und außerdem eine nahezu simultane Aktivierung der Origins ermöglicht. Die berechnete Verteilung der Fertigstellungszeiten der RKs, oder die Verteilung der Originaktivierungszeiten, wird auch genutzt, um die Konsequenzen bestimmter Mutationen im Assemblierungsprozess auf das Kopieren des genetischen Materials in der S Phase des Zellzyklus zu simulieren.
Before a cell divides it has to duplicate its entire genetic material. Eukaryotic genomes are replicated from multiple replication origins across the genome. This work is focused on the quantitative analysis of the underlying molecular mechanism that allows these origins to initiate DNA replication almost simultaneously and exactly once per cell cycle. Based on a vast amount of experimental findings, a molecular regulatory network is constructed that describes the assembly of the molecules at the replication origins that finally form complete replication complexes. Using mass–action kinetics, the molecular reactions are translated into a system of differential equations. To parameterize the mathematical model, the initial protein concentrations are taken from experimental data, while kinetic parameter sets are determined using an optimization approach, in particular a minimization of the duration, in which a minimum number of replication complexes has formed. The model identifies a conflict between the rapid initiation of replication origins and the efficient inhibition of DNA rereplication. Analyses of the model suggest that a time delay before the initiation of DNA replication provided by the multiple phosphorylations of the proteins Sic1 and Sld2 by cyclin-dependent kinases in G1 and S phase, G1-Cdk and S-Cdk, respectively, may be essential to solve this conflict. In particular, multisite phosphorylation of Sld2 by S-Cdk creates a time delay that is robust to changes in the S-Cdk activation kinetics and additionally allows the near-simultaneous activation of multiple replication origins. The calculated distribution of the assembly times of replication complexes, that is also the distribution of origin activation times, is then used to simulate the consequences of certain mutations in the assembly process on the copying of the genetic material in S phase of the cell cycle.
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34

Howell, Audrey. "Cell Polarity Establishment in the Budding Yeast Saccharomyces Cerevisiae." Diss., 2009. http://hdl.handle.net/10161/1145.

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Establishing an axis of cell polarity is central to cell motility, tissue morphogenesis, and cell proliferation. A highly conserved group of polarity regulators is responsible for organizing a wide variety of polarized morphologies. One of the most widely expressed polarity regulators is the Rho-type GTPase Cdc42. In response to cell cycle cues the budding yeast Saccharomyces cerevisiae polarizes Cdc42p to a discrete site on the cell periphery. GTP-Cdc42p recruits a number of effectors that aid in the organization of a polarized actin cytoskeleton. The polarized actin cytoskeleton acts as tracks to facilitate the delivery of the secretory vesicles that will grow the bud, an essential process for an organism that proliferates by budding. We have employed treatment with the actin depolymerizing drugs Latrunculin A and B as well as high-speed timelapse microscopy of fluorescently labeled polarity proteins to characterize the assembly of the incipient bud site.

Often, ensuring that only a single axis of polarity is established is as important as generating asymmetry in the cell. Even in the absence of positional cues dictating the direction of polarization, many cells are still able to self-organize and establish one, and only one, polarity axis through a process termed symmetry breaking. Symmetry breaking is thought to employ positive feedback to amplify stochastic fluctuations in protein concentration into a larger asymmetry. To test whether singularity could be guaranteed by the amplification mechanism we re-wired yeast to employ a synthetic positive feedback mechanism. The re-wired cells could establish polarity, however they occasionally made two buds simultaneously, suggesting that singularity is guaranteed by the amplification mechanism.


Dissertation
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35

Walton, Olivia A. "An analysis of Golgi structure and inheritance in budding yeast /." 2000. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:9990606.

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36

Lee, Wen-Bin, and 李文斌. "Study of robustness of cell-cycle regulatory network in budding yeast." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/51622471312981654410.

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碩士
中華大學
資訊工程學系(所)
96
Robustness of cell cycle network against external perturbations is a fundamental and universal property in biological systems. We proposed a stochastic Boolean network dynamics to investigate the robustness of yeast cell-cycle network under gene noise perturbations. We found that the dynamic trajectory, i.e. gene expression from cell size check point starting signal to steady state, is the global maximal flux trajectory which dominated over all other trajectories. Robustness of cell-cycle network means not only maintenance of its steady state, but also the dynamic gene expression from starting input signal to steady state. A network is said to be a robust network if its signal input trajectory is maximal flux trajectory. As gene noise strengthens to a critical value ρc, the signal input trajectory begins to deviate from maximal flux trajectory. This critical noise could offer us a robustness measure of cell cycle network. We then altered the network topology and found that there were many networks that are robust against noise.
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37

Taheri, Talesh Naimeh. "Regulation of Cell Polarity in the Budding Yeast Saccharomyces cerevisiae." Doctoral thesis, 2002. http://hdl.handle.net/11858/00-1735-0000-0006-AB94-E.

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38

Cook, Michael Alexander. "Systematic Analysis of Cell Size Control in the Budding Yeast Saccharomyces cerevisiae." Thesis, 2012. http://hdl.handle.net/1807/65466.

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The budding yeast Saccharomyces cerevisiae exhibits exquisite control of cellular size in response to the nutritional composition of its environment. Size control is mediated at the G1/S phase transition, termed Start: passage through Start represents an irreversible commitment to cell division and is contingent on achieving a critical size. When nutrients are plentiful, yeast increase their critical size set-point resulting in larger cells; in contrast, in poor nutrients, yeast pass Start at a smaller size. The genetic basis for nutrient-dependent size control and the means by which yeast sense their size remain elusive. One measure of growth potential is ribosome biogenesis, the rate of which correlates with cell size. I characterized a G-patch domain containing protein, Pfa1, which has been shown to activate the helicase activity of the pre-rRNA processing factor Prp43. Intriguingly, Pfa1 is multiply phosphorylated in response to inhibition of the TOR kinase, the central player in growth regulation. This phosphorylation occurs in a region required for Pfa1 function in ribosome biogenesis, independent of its role as a helicase activator. Consistently, phosphorylation correlates with loss of physical interactions with ribosome biogenesis and altered interactions with the ribosome. Mutation of these phosphorylation sites eliminates TOR-dependent phospho-regulation, and confers sensitivity to TOR inhibition. I propose a model wherein Pfa1 is phosphorylated in response to nutrient stress, leading to relocalization of essential processing factors, and inhibition of both ribosome biogenesis and tRNA maturation. Further, I constructed and verified a non-covalent short oligonucleotide barcode microarray platform, and applied it to genome-scale parallel analyses of both the DNA damage response and cell size control in S. cerevisiae. Through these studies, I uncovered novel connections between size control and numerous cellular processes including: the large subunit of the ribosome; the mitochondrial pH gradient; and proteins involved in oxidant-induced cell cycle arrest.
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39

Taheri, Talesh Naimeh [Verfasser]. "Regulation of cell polarity in the budding yeast Saccharomyces cerevisiae / vorgelegt von Naimeh Taheri Talesh." 2002. http://d-nb.info/96709013X/34.

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Gandhi, Meghal Kanaiyalal Chan Clarence S. M. "Genetic interactors of the Cdc42 GTPase effectors Gic1 and Gic2 their identification and functions in budding yeast cell polarity /." 2004. http://wwwlib.umi.com/cr/utexas/fullcit?p3142724.

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Gandhi, Meghal Kanaiyalal. "Genetic interactors of the Cdc42 GTPase effectors Gic1 and Gic2: their identification and functions in budding yeast cell polarity." Thesis, 2004. http://hdl.handle.net/2152/1225.

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Chee, Mark Kuan Leng. "B-cyclin/CDK Regulation of Mitotic Spindle Assembly through Phosphorylation of Kinesin-5 Motors in the Budding Yeast, Saccharomyces cerevisiae." Diss., 2012. http://hdl.handle.net/10161/5419.

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Although it has been known for many years that B-cyclin/CDK complexes regulate the assembly of the mitotic spindle and entry into mitosis, the full complement of relevant CDK targets has not been identified. It has previously been shown in a variety of model systems that B-type cyclin/CDK complexes, kinesin-5 motors, and the SCFCdc4 ubiquitin ligase are required for the separation of spindle poles and assembly of a bipolar spindle. It has been suggested that in the budding yeast, Saccharomyces cerevisiae, B-type cyclin/CDK (Clb/Cdc28) complexes promote spindle pole separation by inhibiting the degradation of the kinesins-5 Kip1 and Cin8 by the anaphase-promoting complex (APCCdh1). I have determined, however, that the Kip1 and Cin8 proteins are actually present at wild-type levels in yeast in the absence of Clb/Cdc28 kinase activity. Here, I show that Kip1 and Cin8 are in vitro targets of Clb2/Cdc28, and that the mutation of conserved CDK phosphorylation sites on Kip1 inhibits spindle pole separation without affecting the protein's in vivo localization or abundance. Mass spectrometry analysis confirms that two CDK sites in the tail domain of Kip1 are phosphorylated in vivo. In addition, I have determined that Sic1, a Clb/Cdc28-specific inhibitor, is the SCFCdc4 target that inhibits spindle pole separation in cells lacking functional Cdc4. Based on these findings, I propose that Clb/Cdc28 drives spindle pole separation by direct phosphorylation of kinesin-5 motors.

In addition to the positive regulation of kinesin-5 function in spindle assembly, I have also found evidence that suggests CDK phosphorylation of kinesin-5 motors at different sites negatively regulates kinesin-5 activity to prevent premature spindle pole separation. I have also begun to characterize a novel putative role for the kinesins-5 in mitochondrial genome inheritance in S. cerevisiae that may also be regulated by CDK phosphorylation.

In the course of my dissertation research, I encountered problems with several established molecular biology tools used by yeast researchers that I have tried to address. I have constructed a set of 42 plasmid shuttle vectors based on the widely used pRS series for use in S. cerevisiae that can be propagated in the bacterium Escherichia coli. This set of pRSII plasmids includes new shuttle vectors that can be used with histidine and adenine auxotrophic laboratory yeast strains carrying mutations in the genes HIS2 and ADE1, respectively. My new pRSII plasmids also include updated versions of commonly used pRS plasmids from which common restriction sites that occur within their yeast-selectable biosynthetic marker genes have been removed in order to increase the availability of unique restriction sites within their polylinker regions. Hence, my pRSII plasmids are a complete set of integrating, centromere and 2 episomal plasmids with the biosynthetic marker genes ADE2, HIS3, TRP1, LEU2, URA3, HIS2 and ADE1 and a standardized selection of at least 16 unique restriction sites in their polylinkers. Additionally, I have expanded the range of drug selection options that can be used for PCR-mediated homologous replacement using pRS plasmid templates by replacing the G418-resistance kanMX4 cassette of pRS400 with MX4 cassettes encoding resistance to phleomycin, hygromycin B, nourseothricin and bialaphos. Finally, in the process of generating the new plasmids, I have determined several errors in existing publicly available sequences for several commonly used yeast plasmids. Using updated plasmid sequences, I constructed pRS plasmid backbones with a unique restriction site for inserting new markers in order to facilitate future expansion of the pRS/pRSII series.


Dissertation
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Jorgensen, Paul Conrad. "Systematic identification of regulators of cell cycle commitment and a dynamic transcriptional network that communicates growth potential to ribosome synthesis and critical cell size in budding yeast." 2004. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=94750&T=F.

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Sharom, Jeffrey Roslan. "A Global Kinase and Phosphatase Interaction Network in the Budding Yeast Reveals Novel Effectors of the Target of Rapamycin (TOR) Pathway." Thesis, 2011. http://hdl.handle.net/1807/29864.

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In the budding yeast Saccharomyces cerevisiae, the evolutionarily conserved Target of Rapamycin (TOR) signaling network regulates cell growth in accordance with nutrient and stress conditions. In this work, I present evidence that the TOR complex 1 (TORC1)-interacting proteins Nnk1, Fmp48, Mks1, and Sch9 link TOR to various facets of nitrogen metabolism and mitochondrial function. The Nnk1 kinase controlled nitrogen catabolite repression-sensitive gene expression via Ure2 and Gln3, and physically interacted with the NAD+-linked glutamate dehydrogenase Gdh2 that catalyzes deamination of glutamate to alpha-ketoglutarate and ammonia. In turn, Gdh2 modulated rapamycin sensitivity, was phosphorylated in Nnk1 immune complexes in vitro, and was relocalized to a discrete cytoplasmic focus in response to NNK1 overexpression or respiratory growth. The Fmp48 kinase regulated respiratory function and mitochondrial morphology, while Mks1 linked TORC1 to the mitochondria-to-nucleus retrograde signaling pathway. The Sch9 kinase appeared to act as both an upstream regulator and downstream sensor of mitochondrial function. Loss of Sch9 conferred a respiratory growth defect, a defect in mitochondrial DNA transmission, lower mitochondrial membrane potential, and decreased levels of reactive oxygen species. Conversely, loss of mitochondrial DNA caused loss of Sch9 enrichment at the vacuolar membrane, loss of Sch9 phospho-isoforms, and small cell size suggestive of reduced Sch9 activity. Sch9 also exhibited dynamic relocalization in response to stress, including enrichment at mitochondria under conditions that have previously been shown to induce apoptosis in yeast. Taken together, this work reveals intimate connections between TORC1, nitrogen metabolism, and mitochondrial function, and has implications for the role of TOR in regulating aging, cancer, and other human diseases.
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Krappmann, Anne-Brit. "Structure-Function Analysis of the Cell Polarity Determinants Bud8p and Bud9p in Saccharomyces cerevisiae." Doctoral thesis, 2007. http://hdl.handle.net/11858/00-1735-0000-0006-AC58-E.

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46

Gupta, Ritu. "Functional Characterization of Saccharomyces Cerevisiae SUB1 in Starvation Induced Sporulation Response." Thesis, 2014. http://hdl.handle.net/2005/2905.

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Among the various external signals perceived by yeast cells, nutrient availability is a condition to which these cells show a highly diverse biological response. Diploid cells in response to different nutritional stress conditions shows different developmental outcomes. On nitrogen starvation, cells undergo dimorphic transition whereby a unicellular yeast form transforms to a multicellular pseudohyphal form. While in the complete absence of a nitrogen source and a fermentable carbon source, yeast cells enter into a complex developmental program termed sporulation which culminates in haploid spores. The main objective of this work was to understand the role played by S. cerevisiaeSUB1 in starvation-induced meiotic program of diploid cells, decipher its target in sporulation specific gene expression cascade, study the domain architecture of Sub1 and examine its functional homology to mammalian PC4. Role of Sub1 in induction of sporulation and other stress responses in S. cerevisiae In a previous whole-genome screen for mutants with altered sporulation efficiency in the Saccharomyces cerevisiae S288c strain, SUB1 locus was identified as a negative regulator of sporulation (Deutschbaueret al., 2002). Moreover, genome-wide gene expression analysis in SK1 strain had shown that SUB1 transcript levels are repressed during sporulation (Chu et al., 1998). Many studies in different yeast strain backgrounds implicate more than 1,000 genesout of 6,200 genes in yeast genome as being differentially expressed during the sporulation process (Chu et al., 1998; Primiget al., 2000; Deutschbaueret al., 2002). Interestingly, these studies show the number of regulatory genes that negatively affect sporulation is far lower than those that are activators of sporulation and moreover their mechanism of action is poorly studied. S. cerevisiae.SUB1 is one among negative regulators of sporulation(Deutschbaueret al., 2002). Global transcriptome of diploid yeast cells undergoing sporulation showed SUB1 transcripts are greatly reduced with time progression (Chu et al., 1998). To understand the role of SUB1 in sporulation, we generated deletion of both SUB1 alleles in the diploid S288c strain background and compared the kinetics of asci formation in this strain with that of the wild-type. We observed that cells lacking SUB1 exhibit ~5-fold increase in tetrad asci. Based on Eosin Y and Calcoflour White staining assays, we find no change in spore morphology in the mutant. Thus the increase in sporulation efficiency in sub1/sub1diploids is not accompanied by formation of defective spores. We validated the reduction in SUB1 transcript levels during sporulation in wild-type SK1 strain background. We also examined the Sub1 protein levels by epitope-tagging of the chromosomal SUB1 open reading frame and determining protein levels in this strain. We find that consistent with the data on transcript levels, Sub1-TAP tagged protein levels too decreased gradually on shift to sporulation medium. We created sub1alleles in diploids in the SK1 strain background and using this strain background we investigated Sub1 target genes and chose IME2 (early), SMK1, SPS2 (middle), DIT1, DIT2 (mid-late) and SPS100 (late) genes as representative sporulation genes. We observed that sub1∆/sub1∆cells have a significantly elevated expression of middle genes (SPS2 and SMK1) that followed normal induction kinetics i.e., 5 hours post transfer to sporulation medium. However, the expression levels or timing for other class of sporulation genes did not change in sub1∆strain as compared with the wild-type. In order to confirm these observations, we also studied the effects of over-expression of SUB1 from the GAL1 promoter by transforming the high copy plasmid. This was done in wild-type SK1 cells and the expression of sporulation genes were analyzed. We observed that expression of SMK1 and SPS2middle sporulation genes was reduced on over-expression of SUB1.We used the Sub1-TAP protein to assess if Sub1 directly regulates these genes by Chromatin immunoprecipitation assays. For these studies, we examined the recruitment of Sub1 to these loci through the time course of sporulation. In wild-type SK1 cells, Sub1 was to bound to middle sporulation genes and this was striking in cells at 5th hour post-induction of sporulation. These data establish that Sub1 directly associates with chromatin at these loci co-incident with the time points where expression levels of these changes is altered in cells lacking Sub1. Furthermore, to assess the role of Sub1 in other stress responses, such as pseudohyphae formation in response to nitrogen starvation, pheromone-induced agar invasion and secretory stress, we employed a genetic approach. Genetic interaction studies of SUB1 with RPB4, a subunit of RNA polymerase with functions in stress response and HOS2, a subunit of Set3 complex and a close homolog of mammalian HDAC3, reported to be involved in sporulation and secretory stress, were performed. Based on sporulation frequency and pseudohyphal formation in the double mutants we conclude that SUB1 is downstream of both these genes. Moreover, our results from assays of schmoo formation and pheromone-induced agar invasion suggest that SUB1 functionally interacts with HOS2. Study of domain architecture of Sub1 and homology to human PC4 Comparison of the S. cerevisiae Sub1 protein with its higher eukaryotic homologs showed that the N-terminal region of yeast Sub1 (32-105 aa) is highly conserved (Knauset al., 1996; Henry et al., 1996) with the 106-292 C -terminal amino acids being yeast-specific. We employed deletion analysis to generate partial Sub1 proteins and used them to understand the roles played by these domains in different phenotypes associated with Sub1. Our analysis of the localization of various Sub1-GFP fusion proteins shows that 146-172 aa in the C-terminal domain of Sub1 confers nuclear localization. Sporulation frequency analysis of the different domains of Sub1 suggests that both the N and C terminal domains are necessary for sporulation function of Sub1. The N terminal domain of yeast Sub1 shares homology with human PC4 and not surprisingly possesses ssDNA binding ability first attributed to human PC4 (Kaiser et al., 1995). In order to investigate whether the effects of SUB1 on kinetics of sporulation require its ssDNA binding function, we generated the sub1(Y66A) ssDNA binding mutant (Sikorskiet al., 2011) and over-expressed it in the S288c genetic background. We assessed sporulation efficiency of sub1∆/sub1∆cells over-expressing sub1(Y66A) mutant allele as compared to cells over-expressing wild-type SUB1. Interestingly, cells with over-expression of sub1(Y66A) have reduced sporulation efficiency that is equivalent to the levels achieved on over-expression of wild type SUB1. This data suggests that the ssDNA-binding ability of Sub1 is not important for its role in sporulation. Furthermore, we examined the ability of human PC4 to contribute to yeast sporulation process by complementation analysis. We observed that over-expression of PC4 complemented the phenotypes of sub1∆strain, suggesting that the function of Sub1/PC4 family is evolutionarily conserved. Studies on biochemical interactions of Sub1 with histone proteins Human PC4 is a chromatin-associated protein, present on metaphase chromosomes (Das et al., 2006). The short C-terminal domain of PC4(62-87 aa) interacts with core histones H3 and H2B in vitro and in vivo and this interaction mediates chromatin condensation. The homology between S. cerevisiaeSub1 (32-105 aa) and human PC4 (62-127 aa)is in the domain required for their DNA binding properties and coactivator functions, suggesting possible conservation in their interactions. We tested the interactions of yeast Sub1 with histone proteins by adopting both in vitro and in vivo interaction assays. We find recombinant Sub1 had strong interactions with rat and yeast histone H3in vitro. Moreover,Sub1 was found to interact with histone H2B, but not with H2A, in vivo, a binding specificity also shown by human PC4.Thus, we demonstrate conservation in the interaction of Sub1 with histone proteins.
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