Relevant bibliographies by topics / Saccharomyces cerevisiae – Genetic aspects

Academic literature on the topic 'Saccharomyces cerevisiae – Genetic aspects'

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Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Saccharomyces cerevisiae – Genetic aspects"

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OBERNAUEROVÁ, M., and J. ŠUBÍK. "Biochemical-genetic aspects of saccharose utilization by yeast of Saccharomyces cerevisiae." Kvasny Prumysl 33, no. 4 (April 1, 1987): 108–10. http://dx.doi.org/10.18832/kp1987022.

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Dorer, Russell, Charles Boone, Tyler Kimbrough, Joshua Kim, and Leland H. Hartwell. "Genetic Analysis of Default Mating Behavior in Saccharomyces cerevisiae." Genetics 146, no. 1 (May 1, 1997): 39–55. http://dx.doi.org/10.1093/genetics/146.1.39.

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Haploid Saccharomyces cerevisiae cells find each other during conjugation by orienting their growth toward each other along pheromone gradients (chemotropism). However, when their receptors are saturated for pheromone binding, yeast cells must select a mate by executing a default pathway in which they choose a mating partner at random. We previously demonstrated that this default pathway requires the SPA2 gene. In this report we show that the default mating pathway also requires the AXL1, FUS1, FUS2, FUS3, PEAZ, RVS161, and BNI1 genes. These genes, including SPA2, are also important for efficient cell fusion during chemotropic mating. Cells containing null mutations in these genes display defects in cell fusion that subtly affect mating efficiency. In addition, we found that the defect in default mating caused by mutations in SPA2 is partially suppressed by multiple copies of two genes, FUS2 and MFA2. These findings uncover a molecular relationship between default mating and cell fusion. Moreover, because axl1 mutants secrete reduced levels of a-factor and are defective at both cell fusion and default mating, these results reveal an important role for a-factor in cell fusion and default mating. We suggest that default mating places a more stringent requirement on some aspects of cell fusion than does chemotropic mating.
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REED, LESTER J., KAREN S. BROWNING, XIAO-DA NIU, ROBERT H. BEHAL, and DAVID J. UHLINGER. "Biochemical and Molecular Genetic Aspects of Pyruvate Dehydrogenase Complex from Saccharomyces cerevisiae." Annals of the New York Academy of Sciences 573, no. 1 Alpha-Keto Ac (December 1989): 155–67. http://dx.doi.org/10.1111/j.1749-6632.1989.tb14993.x.

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Pâques, Frédéric, and James E. Haber. "Multiple Pathways of Recombination Induced by Double-Strand Breaks in Saccharomyces cerevisiae." Microbiology and Molecular Biology Reviews 63, no. 2 (June 1, 1999): 349–404. http://dx.doi.org/10.1128/mmbr.63.2.349-404.1999.

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SUMMARY The budding yeast Saccharomyces cerevisiae has been the principal organism used in experiments to examine genetic recombination in eukaryotes. Studies over the past decade have shown that meiotic recombination and probably most mitotic recombination arise from the repair of double-strand breaks (DSBs). There are multiple pathways by which such DSBs can be repaired, including several homologous recombination pathways and still other nonhomologous mechanisms. Our understanding has also been greatly enriched by the characterization of many proteins involved in recombination and by insights that link aspects of DNA repair to chromosome replication. New molecular models of DSB-induced gene conversion are presented. This review encompasses these different aspects of DSB-induced recombination in Saccharomyces and attempts to relate genetic, molecular biological, and biochemical studies of the processes of DNA repair and recombination.
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Babudri, Nora, Angela Lucaccioni, and Alessandro Achilli. "ADAPTIVE MUTAGENESIS IN THE YEAST SACCHAROMYCES CEREVISIAE." Ecological genetics 4, no. 3 (September 15, 2006): 20–28. http://dx.doi.org/10.17816/ecogen4320-28.

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The nature of mutation in microorganisms has been debated for a long time. Two theories have been at odds: random spontaneous mutagenesis vs. adaptive mutagenesis. "random mutagenesis" means that mutations occur in proliferating cells before they encountered the selective agent. "adaptive mutagenesis" means that advantageous mutations form in the environment where they have been selected, in non-replicating or poorly replicating cells even though other, non-selected, mutations occur at the same time. In the last 20 years it has been definitely shown that random as well as adaptive mutagenesis occur in bacteria and yeast. microorganisms in nature do not divide or divide poorly because of adverse environmental conditions; therefore adaptive mutations could provide cells with a selective advantage and allow evolution of populations. Here we will focus on some fundamental aspects of adaptive mutagenesis in the yeast Saccharomyces cerevisiae. We begin with a historical overview on the nature of mutation. We then focus on experimental systems aimed at proving or disproving adaptive mutagenesis. We have briefly summarized the results obtained in this field, with particular attention to genetic and molecular mechanisms.
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Heude, M., and F. Fabre. "a/alpha-control of DNA repair in the yeast Saccharomyces cerevisiae: genetic and physiological aspects." Genetics 133, no. 3 (March 1, 1993): 489–98. http://dx.doi.org/10.1093/genetics/133.3.489.

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Abstract It has long been known that diploid strains of yeast are more resistant to gamma-rays than haploid cells, and that this is in part due to heterozygosity at the mating type (MAT) locus. It is shown here that the genetic control exerted by the MAT genes on DNA repair involves the a1 and alpha 2 genes, in a RME1-independent way. In rad18 diploids, affected in the error-prone repair, the a/alpha effects are of a very large amplitude, after both UV and gamma-rays, and also depends on a1 and alpha 2. The coexpression of a and alpha in rad18 haploids suppresses the sensitivity of a subpopulation corresponding to the G2 phase cells. Related to this, the coexpression of a and alpha in RAD+ haploids depresses UV-induced mutagenesis in G2 cells. For srs2 null diploids, also affected in the error-prone repair pathway, we show that their G1 UV sensitivity, likely due to lethal recombination events, is partly suppressed by MAT homozygosity. Taken together, these results led to the proposal that a1-alpha 2 promotes a channeling of some DNA structures from the mutagenic into the recombinational repair process.
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Jacobus, Ana Paula, Jeferson Gross, John H. Evans, Sandra Regina Ceccato-Antonini, and Andreas Karoly Gombert. "Saccharomyces cerevisiae strains used industrially for bioethanol production." Essays in Biochemistry 65, no. 2 (July 2021): 147–61. http://dx.doi.org/10.1042/ebc20200160.

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Abstract Fuel ethanol is produced by the yeast Saccharomyces cerevisiae mainly from corn starch in the United States and from sugarcane sucrose in Brazil, which together manufacture ∼85% of a global yearly production of 109.8 million m3 (in 2019). While in North America genetically engineered (GE) strains account for ∼80% of the ethanol produced, including strains that express amylases and are engineered to produce higher ethanol yields; in South America, mostly (>90%) non-GE strains are used in ethanol production, primarily as starters in non-aseptic fermentation systems with cell recycling. In spite of intensive research exploring lignocellulosic ethanol (or second generation ethanol), this option still accounts for <1% of global ethanol production. In this mini-review, we describe the main aspects of fuel ethanol production, emphasizing bioprocesses operating in North America and Brazil. We list and describe the main properties of several commercial yeast products (i.e., yeast strains) that are available worldwide to bioethanol producers, including GE strains with their respective genetic modifications. We also discuss recent studies that have started to shed light on the genes and traits that are important for the persistence and dominance of yeast strains in the non-aseptic process in Brazil. While Brazilian bioethanol yeast strains originated from a historical process of domestication for sugarcane fermentation, leading to a unique group with significant economic applications, in U.S.A., guided selection, breeding and genetic engineering approaches have driven the generation of new yeast products for the market.
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Kartasheva, N. N., S. V. Kuchin, and S. V. Benevolensky. "Genetic aspects of carbon catabolite repression of the STA2 glucoamylase gene in Saccharomyces cerevisiae." Yeast 12, no. 13 (October 1996): 1297–300. http://dx.doi.org/10.1002/(sici)1097-0061(199610)12:13<1297::aid-yea13>3.0.co;2-u.

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Kunz, Bernard A., Karthikeyan Ramachandran, and Edward J. Vonarx. "DNA Sequence Analysis of Spontaneous Mutagenesis in Saccharomyces cerevisiae." Genetics 148, no. 4 (April 1, 1998): 1491–505. http://dx.doi.org/10.1093/genetics/148.4.1491.

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Abstract To help elucidate the mechanisms involved in spontaneous mutagenesis, DNA sequencing has been applied to characterize the types of mutation whose rates are increased or decreased in mutator or antimutator strains, respectively. Increased spontaneous mutation rates point to malfunctions in genes that normally act to reduce spontaneous mutation, whereas decreased rates are associated with defects in genes whose products are necessary for spontaneous mutagenesis. In this article, we survey and discuss the mutational specificities conferred by mutator and antimutator genes in the budding yeast Saccharomyces cerevisiae. The implications of selected aspects of the data are considered with respect to the mechanisms of spontaneous mutagenesis.
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Spencer, F., S. L. Gerring, C. Connelly, and P. Hieter. "Mitotic chromosome transmission fidelity mutants in Saccharomyces cerevisiae." Genetics 124, no. 2 (February 1, 1990): 237–49. http://dx.doi.org/10.1093/genetics/124.2.237.

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Abstract We have isolated 136 independent mutations in haploid yeast strains that exhibit decreased chromosome transmission fidelity in mitosis. Eighty-five percent of the mutations are recessive and 15% are partially dominant. Complementation analysis between MATa and MAT alpha isolates identifies 11 chromosome transmission fidelity (CTF) complementation groups, the largest of which is identical to CHL1. For 49 independent mutations, no corresponding allele has been recovered in the opposite mating type. The initial screen monitored the stability of a centromere-linked color marker on a nonessential yeast chromosome fragment; the mitotic inheritance of natural yeast chromosome III is also affected by the ctf mutations. Of the 136 isolates identified, seven were inviable at 37 degrees and five were inviable at 11 degrees. In all cases tested, these temperature conditional lethalities cosegregated with the chromosome instability phenotype. Five additional complementation groups (ctf12 through ctf16) have been defined by complementation analysis of the mutations causing inviability at 37 degrees. Twenty-three of the 136 isolates exhibited growth defects at concentrations of benomyl permissive for the parent strain, and nine appeared to be tolerant of inhibitory levels of benomyl. All of the mutant strains showed normal sensitivity to ultraviolet and gamma-irradiation. Further characterization of these mutant strains will describe the functions of gene products crucial to the successful execution of processes required for aspects of the chromosome cycle that are important for chromosome transmission fidelity in mitosis.
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Dissertations / Theses on the topic "Saccharomyces cerevisiae – Genetic aspects"

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Reodica, Mayfebelle Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Transcriptional repression mechanisms of sporulation-specific genes in saccharomyces cerevisiae." Awarded by:University of New South Wales. School of Biotechnology and Biomolecular Sciences, 2006. http://handle.unsw.edu.au/1959.4/32731.

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For organisms undergoing a developmental process it is ideal that specific genes are induced and repressed at the correct time and to the correct level in a coordinated manner. The process of meiosis and spore formation (collectively known as sporulation) in Saccharomyces cerevisiae provides a convenient system to elucidate transcriptional mechanisms of gene repression and the contribution such repression mechanisms offer to cells capable of undergoing a developmental process. This thesis focuses on transcriptional repression of sporulation-specific genes during both vegetative/mitotic conditions and sporulation. The fitness contribution of transcriptional repressors that regulate sporulationspecific genes during vegetative growth were investigated considering the similarities between meiosis and mitosis such as DNA replication, chromosome segregation and cytokinesis. Well-characterised sporulation genes of different functions were expressed in vegetative cells and ectopic expression of these genes was found not to be lethal. It was ascertained through strain competition studies that ectopic expression of the genes IME1, SMK1, SPR3 and DIT1 during mitotic growth did not affect cellular fitness. The expression of NDT80 in vegetative cells, however, caused a marked reduction in fitness and cells were also further compromised in the absence of the Sum1p repressor that regulates NDT80 transcription. The role of NDT80 as a transcriptional activator of middle sporulation genes, rather than the over-expression of NDT80 as a protein, caused the reduction of cell viability. Transcriptional regulation of the middle sporulation-specific gene SPR3 by the meiosis-specific Set3p repressor complex was investigated using synchronous sporulation cultures of the W303a/?? strain commonly used for sporulation studies. In a mutant W303a/?? ??set3/??set3 strain, lacking a key component of the Set3p repression complex, the transcription of SPR3 was uncharacteristically expressed at higher levels and derepressed during late sporulation. This SPR3 expression was consistent for both SPR3 transcript and SPR3::lacZ reporter protein studies. This preliminary work will enable future studies, using SPR3 promoter deletions fused to a lacZ reporter, aimed at determining the region of the SPR3 promoter that the Set3p complex may interact with to transcriptionally repress the gene during sporulation.
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Becker, John van Wyk. "Plant defence genes expressed in tobacco and yeast." Thesis, Stellenbosch : University of Stellenbosch, 2002. http://hdl.handle.net/10019/2924.

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Kaeberlein, Matt (Matt Robert) 1971. "Genetic analysis of longevity in Saccharomyces cerevisiae." Thesis, Massachusetts Institute of Technology, 2002. http://hdl.handle.net/1721.1/8318.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2002.
Includes bibliographical references.
Aging is a universal process that affects organisms from yeast to humans. Replicative life span in the budding yeast, Saccharomyces cerevisiae is defined as the number of daughter cells produced by a mother cell prior to senescence. The isolation and characterization of genes and interventions that extend mother cell life span can provide insight into the mechanisms of aging. One cause of aging in yeast is the accumulation of extrachromosomal ribosomal DNA circles (ERCs) in the mother cell nucleus. ERCs are formed by homologous recombination within the ribosomal DNA (rDNA) caused by the presence of a stalled replication fork. Mutation of the replication fork block protein Foblp dramatically reduces ERCs and extends life span. A central regulator of longevity in yeast is the silencing protein Sir2p. Deletion of SIR2 shortens life span and overexpression of SIR2 extends life span. Sir2p promotes silenced chromatin at the rDNA by catalyzing a novel NAD-dependent histone deacetylation reaction. This rDNA silencing function is likely to promote long life span by inhibiting rDNA recombination and, hence, the formation of ERCs. Sir2p is required for life span extension by caloric restriction (CR), demonstrating the important role that this protein plays in the aging process. CR is thought to activate Sir2p by increasing the amount of NAD that is available as a substrate for Sir2p. The finding that osmotic stress extends life span by a mechanism that genetically mimics CR supports this. High osmolarity causes a metabolic shift from fermentation to an NAD-generating glycerol biosynthesis pathway.
(cont.) Life span extension by high osmolarity requires both Sir2p and glycerol biosynthesis. SSD1-V defines the only known Sir2p independent pathway that promotes long life span. SSD1-V functions in many different cellular processes and the mechanism(s) by which it extends life span is not known. SSDI-V functions in a pathway parallel to the longevity promoting protein Mpt5p for cell integrity and interacts genetically with the aging gene UTH1 in several, apparently unrelated, cellular processes. Further defining the molecular nature of this Sir2p-independent longevity pathway will provide insight into the aging process in yeast and, perhaps, higher organisms as well.
by Matt Kaeberlein.
Ph.D.
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Traini, Mathew Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Modelling aspects of neurodegeneration in Saccharomyces cerevisiae." Publisher:University of New South Wales. Biotechnology & Biomolecular Sciences, 2009. http://handle.unsw.edu.au/1959.4/43383.

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The neurodegenerative disorders Alzheimer??s Disease (AD) and Parkinson??s Disease (PD) are characterised by the accumulation of misfolded amyloid beta 1-42 peptide (Aβ1-42) or α-synuclein, respectively. In both cases, there is extensive evidence to support a central role for these aggregation-prone molecules in the progression of disease pathology. However, the precise mechanisms through which Aβ1-42 and α-synuclein contribute to neurodegeneration remain unclear. Organismal, cellular and in vitro models are under development to allow elucidation of these mechanisms. A cellular system for the study of intracellular Aβ1-42 misfolding and localisation was developed, based on expression of an Aβ1-42-GFP fusion protein in the model eukaryote Saccharomyces cerevisiae. This system relies on the known inverse relationship between GFP fluorescence, and the propensity to misfold of an N-terminal fusion domain. To discover cellular processes that may affect the misfolding and localisation of intracellular Aβ1-42, the Aβ1-42-GFP reporter was transformed into the S. cerevisiae genome deletion mutant collection and screened for fluorescence. 94 deletion mutants exhibited increased Aβ1-42-GFP fluorescence, indicative of altered Aβ1-42 misfolding. These mutants were involved in a number of cellular processes with suspected relationships to AD, including the tricarboxylic acid cycle, chromatin remodelling and phospholipid metabolism. Detailed examination of mutants involved in phosphatidylcholine synthesis revealed the potential for phospholipid composition to influence the intracellular aggregation and localisation of Aβ1-42. In addition, an existing S. cerevisiae model of α-synuclein pathobiology was extended to study the effects of compounds that have been hypothesized to be environmental risk factors leading to increased risk of developing PD. Exposure of cells to aluminium, dieldrin and compounds generating reactive oxygen species enhanced the toxicity of α- synuclein expression, supporting suggested roles for these agents in the onset and development of PD. Expression of α-synuclein-GFP in phosphatidylcholine synthesis mutants identified in the Aβ1-42-GFP fluorescence screen resulted in dramatic alteration of α-synuclein localisation, indicating a common involvement of phospholipid metabolism and composition in modulating the behaviours of these two aggregation-prone proteins.
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Owuama, C. I. "Genetic transformation of Saccharomyces cerevisiae with chimaeric plasmids." Thesis, University of Liverpool, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381362.

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Hill, James. "Genetic manipulation and biochemical studies of Saccharomyces cerevisiae." Thesis, University of Warwick, 1991. http://wrap.warwick.ac.uk/110498/.

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The brewing properties of an industrial strain of Saccharomyces cerevisiae were investigated by laboratory scale brewing trials in the presence or absence of an uncoupler of oxidative phosphorylation (SX-1). When SX-1 was added the change in specific gravity of brewing wort with respect to time was less, yeast produced less biomass and more ethanol per unit drop in specific gravity than the control. Similar fermentation properties were observed for C2, a haploid laboratory yeast strain with the ability to ferment maltose. Recombinant DNA technology was used to generate a C2 pet mutant, specifically in the ATP12 gene, which encodes a protein essential for mitochondrial ATP synthesis. In brewing trials a comparison of C2 and C2:AATP 12 shows similar results to C2 fermentations in the presence or absence of SX-1 although the effects of SX-1 are more dramatic than with C2:AA TP 12. Together, the results of chemical studies and gene disruption mutagenesis suggest that mitochondrial ATP synthesis affects nuclear functions, although the possibility that results obtained are a consequence of changes to the yeast mitochondrial DNA cannot be eliminated. Problems experienced with yeast DNA transformation protocols lead to the development of a new transformation method that is quicker and more efficient than the standard protocol. Initial studies revealed that DMSO could enhance yeast transformation efficiency, and that the optimal concentration of DMSO used is strain specific. The point at which DMSO was added was found to be important, with maximal transformation efficiency achieved when DMSO was added just before heat shocking. The optimised protocol for S. cerevisiae JRY188 routinely enhanced transformation IS- to 25-fold compared with a control transformation protocol. The osmotic condition was found to be important for DNA uptake as transformation was inhibited if yeast were washed in 1M sorbitol and selected on plates containing the same. Significantly, DMSO enhanced transformation even in the absence of captions, therefore this method may prove useful for yeasts which transform poorly by existing cationic-based yeast transformation methods.
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Byrne, Kerry. "Genetic analysis of thiamine metabolism in Saccharomyces cerevisiae." Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/30304.

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A genetic analysis of thiamine metabolism has been carried out in the budding yeast, Saccharomyces cerevisiae. A collection of thiamine auxotrophic mutants were isolated following UV and Ty insertion mutagenesis. The mutations responsible for the auxotrophic phenotypes were characterised to different extents through complementation analysis, molecular cloning and enzyme assays. In total 171 mutants were analysed and all of these have been assigned to complementation groups, genes and/or functions. Some newly isolated mutations were found to be allelic with the known biosynthetic genes, THI4 and THI6 others were in the regulatory genes, THI2 and THI3 two more defined a new function for the transcription factor, Pdc2p, namely thiamine gene activation. In addition the previously known mutations, thil, thi2, and thi3, were complemented and the sequences of the wild-type THI1, THI2 and THI3 genes were found. From the deduced amino acid sequences roles for the gene products were hypothesised. The Thi2p was found to be homologous with the Gal4p transcription factor due to the presence of a Zn-finger motif therefore a DNA-binding transcription factor role was proposed for this protein. The Thi3p was found to be homologous to the structural proteins for the enzyme pyruvate decarboxylase. It contains a conserved sequence for TPP binding, the consensus motif having been found in all TPP-dependent enzymes. Therefore it is hypothesised here that Thi3p acts as a "TPP sensor" within the cell, such that deactivation of thiamine-regulated genes is exerted when TPP is bound to Thi3p. In the case of THI1, the complementing ORF was found to be a previously characterised gene, ILV2, which encodes the aceto-hydroxy acid synthase (AHAS) enzyme. AHAS catalyses the first step in the parallel biosyntheses of the branched-chain amino acids, isoleucine and valine, using TPP as a cofactor. It was hypothesised that thil encodes a functional AHAS which has a reduced affinity for TPP resulting in a thiamine auxotrophic phenotype. The thil allele was cloned and enzyme assays were carried out which supported this hypothesis. Sequencing analysis and site-directed mutagenesis revealed that the thil phenotype was produced as a result of a single point mutation which caused the conserved amino acid substitution D176E. Hence in this study an amino acid residue potentially important in the binding of TPP to the AHAS enzyme is identified.
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Pratt, Elizabeth Stratton. "Genetic and biochemical studies of Adr6, a component of the SWI/SNF chromatin remodeling complex /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/10288.

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James, Allan. "A genetic analysis of sulfate transporters in Saccharomyces cerevisiae and Saccharomyces pastorianus." Thesis, Heriot-Watt University, 2000. http://hdl.handle.net/10399/1525.

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Gundllapalli, Sarath B. "Genetic engineering of Saccharomyces cerevisiae for efficient polysaccharide utilisation /." Link to online version, 2005. http://hdl.handle.net/10019.1/1479.

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Books on the topic "Saccharomyces cerevisiae – Genetic aspects"

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R, Fink Gerald, ed. Guide to yeast genetics and molecular and cell biology. San Diego, Calif: Academic Press, 2002.

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R, Fink Gerald, ed. Guide to yeast genetics and molecular and cell biology. San Diego, Calif: Academic Press, 2002.

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Hill, James. Genetic manipulation and biochemical studies of Saccharomyces Cerevisiae. [s.l.]: typescript, 1991.

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Mortimer, Robert K. Genetic map of Saccharomyces cerevisiae: (as of November 1984). [Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory], 1985.

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Craven, Rachel Anne. A genetic analysis of protein translocation in Saccharomyces cerevisiae. Manchester: University of Manchester, 1996.

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Donald, K. Allen G. Genetic and biochemical studies of mitochondria in the yeast saccharomyces cerevisiae. [s.l.]: typescript, 1991.

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Moraes, L. M. P. Genetic improvement of the yeast saccharomyces cerevisiae for alcoholic fermentation of starch. Manchester: UMIST, 1993.

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Prion diseases of mammals and yeast: Molecular mechanisms and genetic features. New York: Springer, 1997.

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Toivari, Mervi. Engineering the pentose phosphate pathway of Saccharomyces cerevisiae for production of ethanol and xylitol. [Espoo, Finland]: VTT Technical Research Centre of Finland, 2007.

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Saloheimo, Anu. Yeast Saccharomyces cerevisiae as a tool in cloning and analysis of fungal genes: Applications for biomass hydrolysis and utilisation. Espoo [Finland]: VTT Technical Research Centre of Finland, 2004.

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Book chapters on the topic "Saccharomyces cerevisiae – Genetic aspects"

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Siewers, Verena, Uffe H. Mortensen, and Jens Nielsen. "Genetic Engineering Tools for Saccharomyces cerevisiae." In Manual of Industrial Microbiology and Biotechnology, 287–301. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816827.ch20.

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Brendel, Martin. "Mutation Induction by Excess Deoxyribonucleotides in Saccharomyces Cerevisiae." In Genetic Consequences of Nucleotide Pool Imbalance, 425–34. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2449-2_26.

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Le Borgne, Sylvie. "Genetic Engineering of Industrial Strains of Saccharomyces cerevisiae." In Recombinant Gene Expression, 451–65. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-433-9_24.

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Goldman, Gustavo H. "Genetic Improvement of Xylose Utilization by Saccharomyces cerevisiae." In Routes to Cellulosic Ethanol, 153–63. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-92740-4_10.

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Weining, Song, and Dongyou Liu. "Genetic Manipulation and Genome Editing of Saccharomyces cerevisiae." In Molecular Food Microbiology, 329–36. 3rd ed. First edition. | Boca Raton : Taylor & Francis, 2021. |: CRC Press, 2021. http://dx.doi.org/10.1201/9781351120388-25.

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Ferguson, Lynnette R. "‘Petite’ Mutagenesis by Benzidine, DAT, DAB and CDA in Saccharomyces cerevisiae." In Comparative Genetic Toxicology, 195–203. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07901-8_24.

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Futcher, Bruce. "The Copy Number Control System of the 2μm Circle Plasmid of Saccharomyces Cerevisiae." In Genetic Engineering, 33–48. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-7084-4_3.

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Polleys, Erica J., and Catherine H. Freudenreich. "Genetic Assays to Study Repeat Fragility in Saccharomyces cerevisiae." In Methods in Molecular Biology, 83–101. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9784-8_5.

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Tuite, M. F., F. Izgu, C. M. Grant, and M. Crouzet. "Genetic Control of tRNA Suppression in Saccharomyces Cerevisiae: Allosuppressors." In Genetics of Translation, 393–402. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73139-6_32.

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Doheny, Kimberly Floy, John Puziss, Forrest Spencer, and Phil Hieter. "Genetic Approaches for Identifying Kinetochore Components in Saccharomyces Cerevisiae." In Chromosome Segregation and Aneuploidy, 93–110. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84938-1_8.

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Reports on the topic "Saccharomyces cerevisiae – Genetic aspects"

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Luther, Jamie, Holly Goodson, and Clint Arnett. Development of a genetic memory platform for detection of metals in water : use of mRNA and protein destabilization elements as a means to control autoinduction from the CUP1 promoter of Saccharomyces cerevisiae. Construction Engineering Research Laboratory (U.S.), June 2018. http://dx.doi.org/10.21079/11681/27275.

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