Relevant bibliographies by topics / Budding yeast cell

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Budding yeast cell'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Budding yeast cell"

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Zhang, Dan, Yijia Wang, and Shiwu Zhang. "Asymmetric Cell Division in Polyploid Giant Cancer Cells and Low Eukaryotic Cells." BioMed Research International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/432652.

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Asymmetric cell division is critical for generating cell diversity in low eukaryotic organisms. We previously have reported that polyploid giant cancer cells (PGCCs) induced by cobalt chloride demonstrate the ability to use an evolutionarily conserved process for renewal and fast reproduction, which is normally confined to simpler organisms. The budding yeast,Saccharomyces cerevisiae, which reproduces by asymmetric cell division, has long been a model for asymmetric cell division studies. PGCCs produce daughter cells asymmetrically in a manner similar to yeast, in that both use budding for cell polarization and cytokinesis. Here, we review the results of recent studies and discuss the similarities in the budding process between yeast and PGCCs.
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Ohya, Yoshikazu, Yoshitaka Kimori, Hiroki Okada, and Shinsuke Ohnuki. "Single-cell phenomics in budding yeast." Molecular Biology of the Cell 26, no. 22 (November 5, 2015): 3920–25. http://dx.doi.org/10.1091/mbc.e15-07-0466.

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The demand for phenomics, a high-dimensional and high-throughput phenotyping method, has been increasing in many fields of biology. The budding yeast Saccharomyces cerevisiae, a unicellular model organism, provides an invaluable system for dissecting complex cellular processes using high-resolution phenotyping. Moreover, the addition of spatial and temporal attributes to subcellular structures based on microscopic images has rendered this cell phenotyping system more reliable and amenable to analysis. A well-designed experiment followed by appropriate multivariate analysis can yield a wealth of biological knowledge. Here we review recent advances in cell imaging and illustrate their broad applicability to eukaryotic cells by showing how these techniques have advanced our understanding of budding yeast.
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Ray, L. B. "Budding Yeast Kinome Revealed." Science Signaling 3, no. 123 (May 25, 2010): ec159-ec159. http://dx.doi.org/10.1126/scisignal.3123ec159.

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Toret, C. P., and D. G. Drubin. "The budding yeast endocytic pathway." Journal of Cell Science 119, no. 22 (October 24, 2006): 4585–87. http://dx.doi.org/10.1242/jcs.03251.

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Toret, C. P., and D. G. Drubin. "The budding yeast endocytic pathway." Journal of Cell Science 120, no. 8 (March 27, 2007): 1501. http://dx.doi.org/10.1242/jcs.03446.

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Schade, Babette, Gregor Jansen, Malcolm Whiteway, Karl D. Entian, and David Y. Thomas. "Cold Adaptation in Budding Yeast." Molecular Biology of the Cell 15, no. 12 (December 2004): 5492–502. http://dx.doi.org/10.1091/mbc.e04-03-0167.

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We have determined the transcriptional response of the budding yeast Saccharomyces cerevisiae to cold. Yeast cells were exposed to 10°C for different lengths of time, and DNA microarrays were used to characterize the changes in transcript abundance. Two distinct groups of transcriptionally modulated genes were identified and defined as the early cold response and the late cold response. A detailed comparison of the cold response with various environmental stress responses revealed a substantial overlap between environmental stress response genes and late cold response genes. In addition, the accumulation of the carbohydrate reserves trehalose and glycogen is induced during late cold response. These observations suggest that the environmental stress response (ESR) occurs during the late cold response. The transcriptional activators Msn2p and Msn4p are involved in the induction of genes common to many stress responses, and we show that they mediate the stress response pattern observed during the late cold response. In contrast, classical markers of the ESR were absent during the early cold response, and the transcriptional response of the early cold response genes was Msn2p/Msn4p independent. This implies that the cold-specific early response is mediated by a different and as yet uncharacterized regulatory mechanism.
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Henry-Stanley, Michelle J., and Carol L. Wells. "Viability and Versatility of the Yeast Cell." Microscopy Today 12, no. 3 (May 2004): 30–33. http://dx.doi.org/10.1017/s1551929500052135.

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Yeasts are single-celled eukaryotic microorganisms (generally about 5 to 10 microns in diameter) that divide by a budding process and are classified with the fungi. Yeast cells are ubiquitous in our environment and can be found on plants and in soil and water. Yeasts have considerable importance Ln industrial and agricultural settings,Saccharomyces cerevisiae(Figure 1) is also known as “bakers yeast” or “brewers yeast.” Specific strains of yeast are used to make pastries, bread, beer, ale, wine, distilled spirits, and industrial alcohol. In the paper industry,Candida utilisis used to break down die sugars from processed wood pulp. Yeast cells are also nutritious. In some societies, “cloudy” beer (containing yeast cells) provides essential B vitamins, minerals, and amino acids.
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Bi, Erfei, and Hay-Oak Park. "Cell Polarization and Cytokinesis in Budding Yeast." Genetics 191, no. 2 (June 2012): 347–87. http://dx.doi.org/10.1534/genetics.111.132886.

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Madden, Kevin, and Michael Snyder. "CELL POLARITY AND MORPHOGENESIS IN BUDDING YEAST." Annual Review of Microbiology 52, no. 1 (October 1998): 687–744. http://dx.doi.org/10.1146/annurev.micro.52.1.687.

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Drubin, David G. "Development of cell polarity in budding yeast." Cell 65, no. 7 (June 1991): 1093–96. http://dx.doi.org/10.1016/0092-8674(91)90001-f.

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Dissertations / Theses on the topic "Budding yeast cell"

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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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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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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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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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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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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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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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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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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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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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Books on the topic "Budding yeast cell"

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Randle, Eliot James. Analysis of CDC4 function during the cell cycle of budding yeast. Manchester: University of Manchester, 1995.

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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.

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Book chapters on the topic "Budding yeast cell"

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Tyson, John J., Katherine C. Chen, and Béla Novák. "Cell Cycle, Budding Yeast." In Encyclopedia of Systems Biology, 337–41. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_16.

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Pirincci Ercan, Deniz, and Frank Uhlmann. "Analysis of Cell Cycle Progression in the Budding Yeast S. cerevisiae." In Methods in Molecular Biology, 265–76. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1538-6_19.

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AbstractThe cell cycle is an ordered series of events by which cells grow and divide to give rise to two daughter cells. In eukaryotes, cyclin–cyclin-dependent kinase (cyclin–Cdk) complexes act as master regulators of the cell division cycle by phosphorylating numerous substrates. Their activity and expression profiles are regulated in time. The budding yeast S. cerevisiae was one of the pioneering model organisms to study the cell cycle. Its genetic amenability continues to make it a favorite model to decipher the principles of how changes in cyclin-Cdk activity translate into the intricate sequence of substrate phosphorylation events that govern the cell cycle. In this chapter, we introduce robust and straightforward methods to analyze cell cycle progression in S. cerevisiae. These techniques can be utilized to describe cell cycle events and to address the effects of perturbations on accurate and timely cell cycle progression.
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Moffat, Jason, Dongqing Huang, and Brenda Andrews. "Functions of Pho85 cyclin-dependent kinases in budding yeast." In Progress in Cell Cycle Research, 97–106. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4253-7_9.

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Teng, Xinchen, and J. Marie Hardwick. "Quantification of Genetically Controlled Cell Death in Budding Yeast." In Methods in Molecular Biology, 161–70. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-383-1_12.

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Leman, Adam R., Sara L. Bristow, and Steven B. Haase. "Analyzing Transcription Dynamics During the Budding Yeast Cell Cycle." In Methods in Molecular Biology, 295–312. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0888-2_14.

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Plevani, P., and G. Lucchini. "Function and Regulation of DNA Replication Genes in Budding Yeast." In DNA Replication and the Cell Cycle, 199–207. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77040-1_16.

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Lari, Azra, Farzin Farzam, Pierre Bensidoun, Marlene Oeffinger, Daniel Zenklusen, David Grunwald, and Ben Montpetit. "Live-Cell Imaging of mRNP–NPC Interactions in Budding Yeast." In Imaging Gene Expression, 131–50. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9674-2_9.

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Kim, Dong-Hwan, and Deanna M. Koepp. "Analyzing Cell Cycle-Dependent Degradation and Ubiquitination in Budding Yeast." In Methods in Molecular Biology, 343–56. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0888-2_17.

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Alberghina, L., M. Baroni, S. Livian, G. Frascotti, and E. Martegani. "Molecular Cloning and Physiological Analysis of the Start Gene cdc25 in Budding Yeast." In Cell Cycle and Oncogenes, 29–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71686-7_4.

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Levine, Kristi, Arthur H. Tinkelenberg, and Frederick Cross. "The CLN gene family: Central regulators of cell cycle Start in budding yeast." In Progress in Cell Cycle Research, 101–14. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1809-9_8.

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Conference papers on the topic "Budding yeast cell"

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Sun, Jiashu, Deyu Li, Chris Stowers, and Erik Boczko. "Measurement of the Volume Growth Rate of Single Budding Yeast." In ASME 2009 Second International Conference on Micro/Nanoscale Heat and Mass Transfer. ASMEDC, 2009. http://dx.doi.org/10.1115/mnhmt2009-18496.

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We report on measurements of the growth rate of single budding yeasts with two microfluidic devices. One device is a MOSFET-based microfluidic Coulter-type sensor, which amplifies nonlinearly the resistance modulation from the translocation of budding yeast through the sensing microchannel. By moving a budding yeast cell back and forth through the sensing channel and measuring the induced resistance pulse from the translocation of the budding yeast, the volume growth rate of a budding yeast cell can be measured over its whole cell cycle. The other microfluidic device is based on comparing the resistance of the sensing microchannel with that of a reference microchannel, which eliminates the signal drift from the electrical conductivity change of the culture media. The reference channel-based sensing scheme enables real-time measurements of the volume growth rate of a budding yeast cell sitting in the sensing microchannel over a whole cell cycle. Measurement results from both devices show that the volume growth of single budding yeast is of sigmoid shape with a slow growth rate both before the bud emergence and at the end of the cell cycle. The device could be used for other important applications such as sensing the response of kidney cells to their micro-environments.
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Sun, Jiashu, Deyu Li, Chris Stowers, and Erik Boczko. "Measurement of Budding Yeast Growth Rate With MOSFET-Based Microfluidic Coulter Counters." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-68098.

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Many bioassays are performed on an ensemble of cells and assay results depend crucially on the state of cells relative to one another. If the cells in the ensemble are disordered with respect to one variable, then the measurements that depend on that variable are confounded by averaging. One solution to this is to maintain the cell cycle synchrony for the cells in the ensemble. To do this, it is extremely important to accurately measure the cell growth rate. For example, the volume growth rate of budding yeast is closely linked to many aspects of the cell cycle. Therefore, investigation of the volume growth rate of budding yeast has become an appealing research topic because of its important implications in achieving cell cycle synchrony. In this paper, we report on applications of novel microfluidic sensing technique to measure the volume growth rate of individual budding yeast. We apply our recently developed MOSFET-based microfluidic Coulter counters to detect the volume of budding yeast when it is translocated through the sensing aperture forth and back, controlled by adjusting the direction of electroosmotic flow inside the microfluidic device. Our results indicate that because of the enhanced sensitivity of the MOSFET-based microfluidic Coulter counter, it is possible to measure the volume growth rate of individual budding yeast over its whole cell cycle. The measurement results clearly showed the volume growth of the individual budding yeast.
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Ahn, Tae-Hyuk, and Adrian Sandu. "Parallel stochastic simulations of budding yeast cell cycle." In the First ACM International Conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1854776.1854811.

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Hashimoto, Ronaldo Fumio, Henrique Stagni, and Carlos Henrique Aguena Higa. "Budding yeast cell cycle modeled by context-sensitive probabilistic Boolean network." In 2009 IEEE International Workshop on Genomic Signal Processing and Statistics (GENSIPS). IEEE, 2009. http://dx.doi.org/10.1109/gensips.2009.5174356.

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Wegerhoff, S., T. C. Neymann, and S. Engell. "Synchronization of a budding yeast cell culture by manipulating inner cell cycle concentrations." In 2012 IEEE 51st Annual Conference on Decision and Control (CDC). IEEE, 2012. http://dx.doi.org/10.1109/cdc.2012.6426766.

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Ruz, Gonzalo A., Tania Timmermann, and Eric Goles. "Building Synthetic Networks of the Budding Yeast Cell-Cycle Using Swarm Intelligence." In 2012 Eleventh International Conference on Machine Learning and Applications (ICMLA). IEEE, 2012. http://dx.doi.org/10.1109/icmla.2012.29.

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Ahmadian, Mansooreh, John Tyson, and Yang Cao. "A Stochastic Model of Size Control in the Budding Yeast Cell Cycle." In BCB '18: 9th ACM International Conference on Bioinformatics, Computational Biology and Health Informatics. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3233547.3233685.

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Wang, Shuo, Mansooreh Ahmadian, Minghan Chen, John Tyson, and Young Cao. "A Hybrid Stochastic Model of the Budding Yeast Cell Cycle Control Mechanism." In BCB '16: ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2975167.2975194.

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"CODING BIOLOGICAL SYSTEMS IN A STOCHASTIC FRAMEWORK - The Case Study of Budding Yeast Cell Cycle." In International Conference on Bioinformatics. SciTePress - Science and and Technology Publications, 2010. http://dx.doi.org/10.5220/0002739601530159.

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Ahmadian, Mansooreh, Shuo Wang, John Tyson, and Young Cao. "Hybrid ODE/SSA Model of the Budding Yeast Cell Cycle Control Mechanism with Mutant Case Study." In BCB '17: 8th ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3107411.3107437.

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