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Journal articles on the topic 'Budding yeast cell'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Breeden, Linda. "Cell cycle-regulated promoters in budding yeast." Trends in Genetics 4, no. 9 (September 1988): 249–53. http://dx.doi.org/10.1016/0168-9525(88)90031-5.

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12

Govindan, Brinda, and Peter Novick. "Development of cell polarity in budding yeast." Journal of Experimental Zoology 273, no. 5 (December 1, 1995): 401–24. http://dx.doi.org/10.1002/jez.1402730505.

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13

Winey, Mark, and Eileen T. O'Toole. "The spindle cycle in budding yeast." Nature Cell Biology 3, no. 1 (January 2001): E23—E27. http://dx.doi.org/10.1038/35050663.

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14

Weinberg, Jasper, and David G. Drubin. "Clathrin-mediated endocytosis in budding yeast." Trends in Cell Biology 22, no. 1 (January 2012): 1–13. http://dx.doi.org/10.1016/j.tcb.2011.09.001.

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15

Lord, Matthew, Ellen Laves, and Thomas D. Pollard. "Cytokinesis Depends on the Motor Domains of Myosin-II in Fission Yeast but Not in Budding Yeast." Molecular Biology of the Cell 16, no. 11 (November 2005): 5346–55. http://dx.doi.org/10.1091/mbc.e05-07-0601.

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Budding yeast possesses one myosin-II, Myo1p, whereas fission yeast has two, Myo2p and Myp2p, all of which contribute to cytokinesis. We find that chimeras consisting of Myo2p or Myp2p motor domains fused to the tail of Myo1p are fully functional in supporting budding yeast cytokinesis. Remarkably, the tail alone of budding yeast Myo1p localizes to the contractile ring, supporting both its constriction and cytokinesis. In contrast, fission yeast Myo2p and Myp2p require both the catalytic head domain as well as tail domains for function, with the tails providing distinct functions ( Bezanilla and Pollard, 2000 ). Myo1p is the first example of a myosin whose cellular function does not require a catalytic motor domain revealing a novel mechanism of action for budding yeast myosin-II independent of actin binding and ATPase activity.

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16

Boldogh, Istvan R., Hyeong-Cheol Yang, and Liza A. Pon. "Mitochondrial Inheritance in Budding Yeast." Traffic 2, no. 6 (June 2001): 368–74. http://dx.doi.org/10.1034/j.1600-0854.2001.002006368.x.

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17

Nurse, Paul. "Fission yeast cell cycle mutants and the logic of eukaryotic cell cycle control." Molecular Biology of the Cell 31, no. 26 (December 15, 2020): 2871–73. http://dx.doi.org/10.1091/mbc.e20-10-0623.

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Cell cycle mutants in the budding and fission yeasts have played critical roles in working out how the eukaryotic cell cycle operates and is controlled. The starting point was Lee Hartwell’s 1970s landmark papers describing the first cell division cycle (CDC) mutants in budding yeast. These mutants were blocked at different cell cycle stages and so were unable to complete the cell cycle, thus defining genes necessary for successful cell division. Inspired by Hartwell’s work, I isolated CDC mutants in the very distantly related fission yeast. This started a program of searches for mutants in fission yeast that revealed a range of phenotypes informative about eukaryotic cell cycle control. These included mutants defining genes that were rate-limiting for the onset of mitosis and of the S-phase, that were responsible for there being only one S-phase in each cell cycle, and that ensured that mitosis only took place when S-phase was properly completed. This is a brief account of the discovery of these mutants and how they led to the identification of cyclin-dependent kinases as core to these cell cycle controls.

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18

Yeong, Foong May, Hong Hwa Lim, C. G. Padmashree, and Uttam Surana. "Exit from Mitosis in Budding Yeast." Molecular Cell 5, no. 3 (March 2000): 501–11. http://dx.doi.org/10.1016/s1097-2765(00)80444-x.

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19

Wloka, Carsten, and Erfei Bi. "Mechanisms of cytokinesis in budding yeast." Cytoskeleton 69, no. 10 (July 31, 2012): 710–26. http://dx.doi.org/10.1002/cm.21046.

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20

Houchens, Christopher R., Audrey Perreault, François Bachand, and Thomas J. Kelly. "Schizosaccharomyces pombe Noc3 Is Essential for Ribosome Biogenesis and Cell Division but Not DNA Replication." Eukaryotic Cell 7, no. 9 (July 7, 2008): 1433–40. http://dx.doi.org/10.1128/ec.00119-08.

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ABSTRACT The initiation of eukaryotic DNA replication is preceded by the assembly of prereplication complexes (pre-RCs) at chromosomal origins of DNA replication. Pre-RC assembly requires the essential DNA replication proteins ORC, Cdc6, and Cdt1 to load the MCM DNA helicase onto chromatin. Saccharomyces cerevisiae Noc3 (ScNoc3), an evolutionarily conserved protein originally implicated in 60S ribosomal subunit trafficking, has been proposed to be an essential regulator of DNA replication that plays a direct role during pre-RC formation in budding yeast. We have cloned Schizosaccharomyces pombe noc3 + (Spnoc3 +), the S. pombe homolog of the budding yeast ScNOC3 gene, and functionally characterized the requirement for the SpNoc3 protein during ribosome biogenesis, cell cycle progression, and DNA replication in fission yeast. We showed that fission yeast SpNoc3 is a functional homolog of budding yeast ScNoc3 that is essential for cell viability and ribosome biogenesis. We also showed that SpNoc3 is required for the normal completion of cell division in fission yeast. However, in contrast to the proposal that ScNoc3 plays an essential role during DNA replication in budding yeast, we demonstrated that fission yeast cells do enter and complete S phase in the absence of SpNoc3, suggesting that SpNoc3 is not essential for DNA replication in fission yeast.

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21

Escher, Dominik, Morana Bodmer-Glavas, Alcide Barberis, and Walter Schaffner. "Conservation of Glutamine-Rich Transactivation Function between Yeast and Humans." Molecular and Cellular Biology 20, no. 8 (April 15, 2000): 2774–82. http://dx.doi.org/10.1128/mcb.20.8.2774-2782.2000.

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ABSTRACT Several eukaryotic transcription factors such as Sp1 or Oct1 contain glutamine-rich domains that mediate transcriptional activation. In human cells, promoter-proximally bound glutamine-rich activation domains activate transcription poorly in the absence of acidic type activators bound at distal enhancers, but synergistically stimulate transcription with these remote activators. Glutamine-rich activation domains were previously reported to also function in the fission yeastSchizosaccharomyces pombe but not in the budding yeastSaccharomyces cerevisiae, suggesting that budding yeast lacks this pathway of transcriptional activation. The strong interaction of an Sp1 glutamine-rich domain with the general transcription factor TAFII110 (TAFII130), and the absence of any obvious TAFII110 homologue in the budding yeast genome, seemed to confirm this notion. We reinvestigated the phenomenon by reconstituting in the budding yeast an enhancer-promoter architecture that is prevalent in higher eukaryotes but less common in yeast. Under these conditions, we observed that glutamine-rich activation domains derived from both mammalian and yeast transcription factors activated only poorly on their own but strongly synergized with acidic activators bound at the remote enhancer position. The level of activation by the glutamine-rich activation domains of Sp1 and Oct1 in combination with a remote enhancer was similar in yeast and human cells. We also found that mutations in a glutamine-rich domain had similar phenotypes in budding yeast and human cells. Our results show that glutamine-rich activation domains behave very similarly in yeast and mammals and that their activity in budding yeast does not depend on the presence of a TAFII110 homologue.

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22

Waltermann, Christian, and Edda Klipp. "Signal integration in budding yeast." Biochemical Society Transactions 38, no. 5 (September 24, 2010): 1257–64. http://dx.doi.org/10.1042/bst0381257.

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A complex signalling network governs the response of Saccharomyces cerevisiae to an array of environmental stimuli and stresses. In the present article, we provide an overview of the main signalling system and discuss the mechanisms by which yeast integrates and separates signals from these sources. We apply our classification scheme to a simple semi-quantitative model of the HOG (high-osmolarity glycerol)/FG (filamentous growth)/PH (pheromone) MAPK (mitogen-activated protein kinase) signalling network by perturbing its signal integration mechanisms under combinatorial stimuli of osmotic stress, starvation and pheromone exposure in silico. Our findings include that the Hog1 MAPK might act as a timer for filamentous differentiation, not allowing morphological differentiation before osmo-adaptation is sufficiently completed. We also see that a mutually exclusive decision-making between pheromone and osmo-response might not be taken on the MAPK level and transcriptional regulation of MAPK targets. We conclude that signal integration mechanisms in a wider network including the cell cycle have to be taken into account for which our framework might provide focal points of study.

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23

Sebastian Franco, Jose Luis, Aranzazu Sanchis Otero, Jose Roldan Madronero, and Sagrario Munoz San Martin. "DIELECTRIC CHARACTERIZATION OF THE YEAST CELL BUDDING CYCLE." Progress In Electromagnetics Research 134 (2013): 1–22. http://dx.doi.org/10.2528/pier12100406.

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24

Irons, D. J. "Logical analysis of the budding yeast cell cycle." Journal of Theoretical Biology 257, no. 4 (April 2009): 543–59. http://dx.doi.org/10.1016/j.jtbi.2008.12.028.

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25

Asami, Koji, Eugen Gheorghiu, and Takeshi Yonezawa. "Dielectric behavior of budding yeast in cell separation." Biochimica et Biophysica Acta (BBA) - General Subjects 1381, no. 2 (July 1998): 234–40. http://dx.doi.org/10.1016/s0304-4165(98)00033-6.

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26

Lew, Daniel J., and Steven I. Reed. "Cell cycle control of morphogenesis in budding yeast." Current Opinion in Genetics & Development 5, no. 1 (February 1995): 17–23. http://dx.doi.org/10.1016/s0959-437x(95)90048-9.

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27

Kron, Stephen J., and Neil AR Gow. "Budding yeast morphogenesis: signalling, cytoskeleton and cell cycle." Current Opinion in Cell Biology 7, no. 6 (January 1995): 845–55. http://dx.doi.org/10.1016/0955-0674(95)80069-7.

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28

Short, Ben. "Budding yeast star in their own biofilm." Journal of Cell Biology 194, no. 5 (August 29, 2011): 659. http://dx.doi.org/10.1083/jcb.1945if.

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29

Short, Ben. "Budding yeast do the Cdc42 two-step." Journal of Cell Biology 206, no. 1 (July 7, 2014): 2. http://dx.doi.org/10.1083/jcb.2061iti1.

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30

Li, R., and A. W. Murray. "Feedback control of mitosis in budding yeast." Trends in Cell Biology 1, no. 5 (November 1991): 113. http://dx.doi.org/10.1016/0962-8924(91)90105-i.

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31

Côte, Pierre, Hervé Hogues, and Malcolm Whiteway. "Transcriptional Analysis of the Candida albicans Cell Cycle." Molecular Biology of the Cell 20, no. 14 (July 15, 2009): 3363–73. http://dx.doi.org/10.1091/mbc.e09-03-0210.

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We have examined the periodic expression of genes through the cell cycle in cultures of the human pathogenic fungus Candida albicans synchronized by mating pheromone treatment. Close to 500 genes show increased expression during the G1, S, G2, or M transitions of the C. albicans cell cycle. Comparisons of these C. albicans periodic genes with those already found in the budding and fission yeasts and in human cells reveal that of 2200 groups of homologous genes, close to 600 show periodicity in at least one organism, but only 11 are periodic in all four species. Overall, the C. albicans regulatory circuit most closely resembles that of Saccharomyces cerevisiae but contains a simplified structure. Although the majority of the C. albicans periodically regulated genes have homologues in the budding yeast, 20% (100 genes), most of which peak during the G1/S or M/G1 transitions, are unique to the pathogenic yeast.

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32

Lew, D. J., and S. I. Reed. "A cell cycle checkpoint monitors cell morphogenesis in budding yeast." Journal of Cell Biology 129, no. 3 (May 1, 1995): 739–49. http://dx.doi.org/10.1083/jcb.129.3.739.

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Checkpoint controls are regulatory pathways that inhibit cell cycle progression in cells that have not faithfully completed a prior step in the cell cycle. In the budding yeast Saccharomyces cerevisiae, DNA replication and spindle assembly are monitored by checkpoint controls that prevent nuclear division in cells that have failed to complete these processes. During the normal cell cycle, bud formation is temporally coincident with DNA replication and spindle assembly, and the nucleus divides along the mother-bud axis in mitosis. In this report, we show that inhibition of bud formation also causes a dramatic delay in nuclear division. This allows cells to recover from a transient disruption of cell polarity without becoming binucleate. The delay occurs after DNA replication and spindle assembly, and results from delayed activation of the master cell cycle regulatory kinase, Cdc28. Cdc28 activation is inhibited by phosphorylation of Cdc28 on tyrosine 19, and by delayed accumulation of the B-type cyclins Clb1 and Clb2. These results suggest the existence of a novel checkpoint that monitors cell morphogenesis in budding yeast.

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33

Todd, Robert G., and Tomáš Helikar. "Ergodic Sets as Cell Phenotype of Budding Yeast Cell Cycle." PLoS ONE 7, no. 10 (October 1, 2012): e45780. http://dx.doi.org/10.1371/journal.pone.0045780.

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34

Meitinger, Franz, and Saravanan Palani. "Actomyosin ring driven cytokinesis in budding yeast." Seminars in Cell & Developmental Biology 53 (May 2016): 19–27. http://dx.doi.org/10.1016/j.semcdb.2016.01.043.

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35

Shaw, Sidney L., Paul Maddox, Robert V. Skibbens, Elaine Yeh, E. D. Salmon, and Kerry Bloom. "Nuclear and Spindle Dynamics in Budding Yeast." Molecular Biology of the Cell 9, no. 7 (July 1998): 1627–31. http://dx.doi.org/10.1091/mbc.9.7.1627.

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36

Cheeseman, Iain M., David G. Drubin, and Georjana Barnes. "Simple centromere, complex kinetochore." Journal of Cell Biology 157, no. 2 (April 15, 2002): 199–203. http://dx.doi.org/10.1083/jcb.200201052.

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Although the budding yeast centromere is extremely short (125 bp) compared to those of other eukaryotes, the kinetochore that assembles on this DNA displays a rich molecular complexity. Here, we describe recent advances in our understanding of kinetochore function in budding yeast and present a model describing the attachment that is formed between spindle microtubules and centromeric DNA. This analysis may provide general principles for kinetochore function and regulation.

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37

Guacci, V., E. Hogan, and D. Koshland. "Chromosome condensation and sister chromatid pairing in budding yeast." Journal of Cell Biology 125, no. 3 (May 1, 1994): 517–30. http://dx.doi.org/10.1083/jcb.125.3.517.

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We have developed a fluorescent in situ hybridization (FISH) method to examine the structure of both natural chromosomes and small artificial chromosomes during the mitotic cycle of budding yeast. Our results suggest that the pairing of sister chromatids: (a) occurs near the centromere and at multiple places along the chromosome arm as has been observed in other eukaryotic cells; (b) is maintained in the absence of catenation between sister DNA molecules; and (c) is independent of large blocks of repetitive DNA commonly associated with heterochromatin. Condensation of a unique region of chromosome XVI and the highly repetitive ribosomal DNA (rDNA) cluster from chromosome XII were also examined in budding yeast. Interphase chromosomes were condensed 80-fold relative to B form DNA, similar to what has been observed in other eukaryotes, suggesting that the structure of interphase chromosomes may be conserved among eukaryotes. While additional condensation of budding yeast chromosomes were observed during mitosis, the level of condensation was less than that observed for human mitotic chromosomes. At most stages of the cell cycle, both unique and repetitive sequences were either condensed or decondensed. However, in cells arrested in late mitosis (M) by a cdc15 mutation, the unique DNA appeared decondensed while the repetitive rDNA region appeared condensed, suggesting that the condensation state of separate regions of the genome may be regulated differently. The ability to monitor the pairing and condensation of sister chromatids in budding yeast should facilitate the molecular analysis of these processes as well as provide two new landmarks for evaluating the function of important cell cycle regulators like p34 kinases and cyclins. Finally our FISH method provides a new tool to analyze centromeres, telomeres, and gene expression in budding yeast.

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38

Molk, Jeffrey N., and Kerry Bloom. "Microtubule dynamics in the budding yeast mating pathway." Journal of Cell Science 119, no. 17 (August 24, 2006): 3485–90. http://dx.doi.org/10.1242/jcs.03193.

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39

Bergman, Zane J., Jonathan Wong, David G. Drubin, and Georjana Barnes. "Microtubule dynamics regulation reconstituted in budding yeast lysates." Journal of Cell Science 132, no. 4 (September 5, 2018): jcs219386. http://dx.doi.org/10.1242/jcs.219386.

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40

Rudner, Adam D., Kevin G. Hardwick, and Andrew W. Murray. "Cdc28 Activates Exit from Mitosis in Budding Yeast." Journal of Cell Biology 149, no. 7 (June 26, 2000): 1361–76. http://dx.doi.org/10.1083/jcb.149.7.1361.

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The activity of the cyclin-dependent kinase 1 (Cdk1), Cdc28, inhibits the transition from anaphase to G1 in budding yeast. CDC28-T18V, Y19F (CDC28-VF), a mutant that lacks inhibitory phosphorylation sites, delays the exit from mitosis and is hypersensitive to perturbations that arrest cells in mitosis. Surprisingly, this behavior is not due to a lack of inhibitory phosphorylation or increased kinase activity, but reflects reduced activity of the anaphase-promoting complex (APC), a defect shared with other mutants that lower Cdc28/Clb activity in mitosis. CDC28-VF has reduced Cdc20- dependent APC activity in mitosis, but normal Hct1- dependent APC activity in the G1 phase of the cell cycle. The defect in Cdc20-dependent APC activity in CDC28-VF correlates with reduced association of Cdc20 with the APC. The defects of CDC28-VF suggest that Cdc28 activity is required to induce the metaphase to anaphase transition and initiate the transition from anaphase to G1 in budding yeast.

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41

Pearson, Chad G., Paul S. Maddox, E. D. Salmon, and Kerry Bloom. "Budding Yeast Chromosome Structure and Dynamics during Mitosis." Journal of Cell Biology 152, no. 6 (March 19, 2001): 1255–66. http://dx.doi.org/10.1083/jcb.152.6.1255.

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Using green fluorescent protein probes and rapid acquisition of high-resolution fluorescence images, sister centromeres in budding yeast are found to be separated and oscillate between spindle poles before anaphase B spindle elongation. The rates of movement during these oscillations are similar to those of microtubule plus end dynamics. The degree of preanaphase separation varies widely, with infrequent centromere reassociations observed before anaphase. Centromeres are in a metaphase-like conformation, whereas chromosome arms are neither aligned nor separated before anaphase. Upon spindle elongation, centromere to pole movement (anaphase A) was synchronous for all centromeres and occurred coincident with or immediately after spindle pole separation (anaphase B). Chromatin proximal to the centromere is stretched poleward before and during anaphase onset. The stretched chromatin was observed to segregate to the spindle pole bodies at rates greater than centromere to pole movement, indicative of rapid elastic recoil between the chromosome arm and the centromere. These results indicate that the elastic properties of DNA play an as of yet undiscovered role in the poleward movement of chromosome arms.

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42

Oehlen, Bert, and Frederick R. Cross. "Signal transduction in the budding yeast Saccharomyces cerevisiae." Current Opinion in Cell Biology 6, no. 6 (December 1994): 836–41. http://dx.doi.org/10.1016/0955-0674(94)90053-1.

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43

Geymonat, Marco, Ad Spanos, Susan J. M. Smith, Edward Wheatley, Katrin Rittinger, Leland H. Johnston, and Steven G. Sedgwick. "Control of Mitotic Exit in Budding Yeast." Journal of Biological Chemistry 277, no. 32 (June 4, 2002): 28439–45. http://dx.doi.org/10.1074/jbc.m202540200.

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44

Styles, Erin, Ji-Young Youn, Mojca Mattiazzi Usaj, and Brenda Andrews. "Functional genomics in the study of yeast cell polarity: moving in the right direction." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1629 (November 5, 2013): 20130118. http://dx.doi.org/10.1098/rstb.2013.0118.

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The budding yeast Saccharomyces cerevisiae has been used extensively for the study of cell polarity, owing to both its experimental tractability and the high conservation of cell polarity and other basic biological processes among eukaryotes. The budding yeast has also served as a pioneer model organism for virtually all genome-scale approaches, including functional genomics, which aims to define gene function and biological pathways systematically through the analysis of high-throughput experimental data. Here, we outline the contributions of functional genomics and high-throughput methodologies to the study of cell polarity in the budding yeast. We integrate data from published genetic screens that use a variety of functional genomics approaches to query different aspects of polarity. Our integrated dataset is enriched for polarity processes, as well as some processes that are not intrinsically linked to cell polarity, and may provide new areas for future study.

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45

Strich, Randy. "Programmed Cell Death Initiation and Execution in Budding Yeast." Genetics 200, no. 4 (August 2015): 1003–14. http://dx.doi.org/10.1534/genetics.115.179150.

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46

Vinton, Peter J., and Ted Weinert. "A Slowed Cell Cycle Stabilizes the Budding Yeast Genome." Genetics 206, no. 2 (May 3, 2017): 811–28. http://dx.doi.org/10.1534/genetics.116.197590.

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47

Casamayor, A. "Bud-site selection and cell polarity in budding yeast." Current Opinion in Microbiology 5, no. 2 (April 1, 2002): 179–86. http://dx.doi.org/10.1016/s1369-5274(02)00300-4.

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48

Fauré, Adrien, Aurélien Naldi, Fabrice Lopez, Claudine Chaouiya, Andrea Ciliberto, and Denis Thieffry. "Modular logical modelling of the budding yeast cell cycle." Molecular BioSystems 5, no. 12 (2009): 1787. http://dx.doi.org/10.1039/b910101m.

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49

Soifer, Ilya, and Naama Barkai. "Systematic identification of cell size regulators in budding yeast." Molecular Systems Biology 10, no. 11 (November 2014): 761. http://dx.doi.org/10.15252/msb.20145345.

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Chen, Katherine C., Laurence Calzone, Attila Csikasz-Nagy, Frederick R. Cross, Bela Novak, and John J. Tyson. "Integrative Analysis of Cell Cycle Control in Budding Yeast." Molecular Biology of the Cell 15, no. 8 (August 2004): 3841–62. http://dx.doi.org/10.1091/mbc.e03-11-0794.

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Abstract:

The adaptive responses of a living cell to internal and external signals are controlled by networks of proteins whose interactions are so complex that the functional integration of the network cannot be comprehended by intuitive reasoning alone. Mathematical modeling, based on biochemical rate equations, provides a rigorous and reliable tool for unraveling the complexities of molecular regulatory networks. The budding yeast cell cycle is a challenging test case for this approach, because the control system is known in exquisite detail and its function is constrained by the phenotypic properties of >100 genetically engineered strains. We show that a mathematical model built on a consensus picture of this control system is largely successful in explaining the phenotypes of mutants described so far. A few inconsistencies between the model and experiments indicate aspects of the mechanism that require revision. In addition, the model allows one to frame and critique hypotheses about how the division cycle is regulated in wild-type and mutant cells, to predict the phenotypes of new mutant combinations, and to estimate the effective values of biochemical rate constants that are difficult to measure directly in vivo.

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