Journal articles: 'Saccharomyces cerevisiae – Genetics'

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Belda, Ignacio, Javier Ruiz, Antonio Santos, Nïel Van Wyk, and Isak S. Pretorius. "Saccharomyces cerevisiae." Trends in Genetics 35, no. 12 (December 2019): 956–57. http://dx.doi.org/10.1016/j.tig.2019.08.009.

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Elias-Arnanz, Montserrat, Antoine A. Firmenich, and P. Berg. "Saccharomyces cerevisiae." MGG Molecular & General Genetics 252, no. 5 (1996): 530. http://dx.doi.org/10.1007/s004380050260.

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McCusker, J. H., K. V. Clemons, D. A. Stevens, and R. W. Davis. "Genetic characterization of pathogenic Saccharomyces cerevisiae isolates." Genetics 136, no. 4 (April 1, 1994): 1261–69. http://dx.doi.org/10.1093/genetics/136.4.1261.

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Abstract Saccharomyces cerevisiae isolates from human patients have been genetically analyzed. Some of the characteristics of these isolates are very different from laboratory and industrial strains of S. cerevisiae and, for this reason, stringent genetic tests have been used to confirm their identity as S. cerevisiae. Most of these clinical isolates are able to grow at 42 degrees, a temperature that completely inhibits the growth of most other S. cerevisiae strains. This property can be considered a virulence trait and may help explain the presence of these isolates in human hosts. The ability to grow at 42 degrees is shown to be polygenic with primarily additive effects between loci. S. cerevisiae will be a useful model for the evolution and genetic analysis of fungal virulence and the study of polygenic traits.

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Joseph, Sarah B., and David W. Hall. "Spontaneous Mutations in Diploid Saccharomyces cerevisiae." Genetics 168, no. 4 (December 2004): 1817–25. http://dx.doi.org/10.1534/genetics.104.033761.

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Lebrun, Éléonore, Emmanuelle Revardel, Cécile Boscheron, Rong Li, Eric Gilson, and Geneviève Fourel. "Protosilencers in Saccharomyces cerevisiae Subtelomeric Regions." Genetics 158, no. 1 (May 1, 2001): 167–76. http://dx.doi.org/10.1093/genetics/158.1.167.

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Abstract Saccharomyces cerevisiae subtelomeric repeats contain silencing elements such as the core X sequence, which is present at all chromosome ends. When transplaced at HML, core X can enhance the action of a distant silencer without acting as a silencer on its own, thus fulfilling the functional definition of a protosilencer. Here we show that an ACS motif and an Abf1p-binding site participate in the silencing capacity of core X and that their effects are additive. In addition, in a variety of settings, core X was found to bring about substantial gene repression only when a low level of silencing was already detectable in its absence. Adjoining an X-STAR sequence, which naturally abuts core X in subtelomeric regions, did not improve the silencing capacity of core X. We propose that protosilencers play a major role in a variety of silencing phenomena, as is the case for core X, which acts as a silencing relay, prolonging silencing propagation away from telomeres.

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Papacs, Laurie Ann, Yu Sun, Erica L. Anderson, Jianjun Sun, and Scott G. Holmes. "REP3-Mediated Silencing in Saccharomyces cerevisiae." Genetics 166, no. 1 (January 2004): 79–87. http://dx.doi.org/10.1534/genetics.166.1.79.

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Naumov, G. I., E. S. Naumova, and C. A. Michels. "Genetic variation of the repeated MAL loci in natural populations of Saccharomyces cerevisiae and Saccharomyces paradoxus." Genetics 136, no. 3 (March 1, 1994): 803–12. http://dx.doi.org/10.1093/genetics/136.3.803.

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Abstract In Saccharomyces cerevisiae, the gene functions required to ferment the disaccharide maltose are encoded by the MAL loci. Any one of five highly sequence homologous MAL loci identified in various S. cerevisiae strains (called MAL1, 2, 3, 4 and 6) is sufficient to ferment maltose. Each is a complex of three genes encoding maltose permease, maltase and a transcription activator. This family of loci maps to telomere-linked positions on different chromosomes and most natural strains contain more than one MAL locus. A number of naturally occurring, mutant alleles of MAL1 and MAL3 have been characterized which lack one or more of the gene functions encoded by the fully functional MAL loci. Loss of these gene functions appears to have resulted from mutation and/or rearrangement within the locus. Studies to date concentrated on the standard maltose fermenting strains of S. cerevisiae available from the Berkeley Yeast Stock Center collection. In this report we extend our genetic analysis of the MAL loci to a number of maltose fermenting and nonfermenting natural strains of S. cerevisiae and Saccharomyces paradoxus. No new MAL loci were discovered but several new mutant alleles of MAL1 were identified. The evolution of this gene family is discussed.

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Musiyaka, V. K., A. A. Gladun, V. V. Sarnackaya, and R. I. Gvozdyak. "Antimutagenic activity of Saccharomyces cerevisiae strains." Biopolymers and Cell 16, no. 4 (July 20, 2000): 284–88. http://dx.doi.org/10.7124/bc.000573.

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Natsoulis, G., W. Thomas, M. C. Roghmann, F. Winston, and J. D. Boeke. "Ty1 transposition in Saccharomyces cerevisiae is nonrandom." Genetics 123, no. 2 (October 1, 1989): 269–79. http://dx.doi.org/10.1093/genetics/123.2.269.

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Abstract A large collection of Ty1 insertions in the URA3 and LYS2 loci was generated using a GAL1-Ty1 fusion to augment the transposition frequency. The sites of insertion of most of these Ty elements were sequenced. There appears to be a gradient of frequency of insertion from the 5' end (highest frequency) to the 3' end (lowest frequency) of both loci. In addition we observed hotspots for transposition. Twelve of the 82 Ty1 insertions in the URA3 locus were inserted in exactly the same site. Hotspots were also observed in the LYS2 locus. All hotspots were in the transcribed part of the genes. Alignment of the sites of insertion and of the neighboring sequences only reveals very weak sequence similarities.

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Roman, H., and M. M. Ruzinski. "Mechanisms of gene conversion in Saccharomyces cerevisiae." Genetics 124, no. 1 (January 1, 1990): 7–25. http://dx.doi.org/10.1093/genetics/124.1.7.

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Abstract In red-white sectored colonies of Saccharomyces cerevisiae, derived from mitotic cells grown to stationary phase and irradiated with a light dose of x-rays, all of the segregational products of gene conversion and crossing over can be ascertained. Approximately 80% of convertants are induced in G1, the remaining 20% in G2. Crossing over, in the amount of 20%, is found among G1 convertants but most of the crossovers are delayed until G2. About 20% of all sectored colonies had more than one genotype in one or the other sector, thus confirming the hypothesis that conversion also occurs in G2. The principal primary event in G2 conversion is a single DNA heteroduplex. It is suggested that the close contact that this implies carries over to G2 when crossing over and a second round of conversion occurs.

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Zhang, Hengshan, Aditi Chatterjee, and Keshav K. Singh. "Saccharomyces cerevisiae Polymerase ζ Functions in Mitochondria." Genetics 172, no. 4 (February 1, 2006): 2683–88. http://dx.doi.org/10.1534/genetics.105.051029.

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Wykoff, Dennis D., and Erin K. O'Shea. "Phosphate Transport and Sensing in Saccharomyces cerevisiae." Genetics 159, no. 4 (December 1, 2001): 1491–99. http://dx.doi.org/10.1093/genetics/159.4.1491.

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Abstract Cellular metabolism depends on the appropriate concentration of intracellular inorganic phosphate; however, little is known about how phosphate concentrations are sensed. The similarity of Pho84p, a high-affinity phosphate transporter in Saccharomyces cerevisiae, to the glucose sensors Snf3p and Rgt2p has led to the hypothesis that Pho84p is an inorganic phosphate sensor. Furthermore, pho84Δ strains have defects in phosphate signaling; they constitutively express PHO5, a phosphate starvation-inducible gene. We began these studies to determine the role of phosphate transporters in signaling phosphate starvation. Previous experiments demonstrated a defect in phosphate uptake in phosphate-starved pho84Δ cells; however, the pho84Δ strain expresses PHO5 constitutively when grown in phosphate-replete media. We determined that pho84Δ cells have a significant defect in phosphate uptake even when grown in high phosphate media. Overexpression of unrelated phosphate transporters or a glycerophosphoinositol transporter in the pho84Δ strain suppresses the PHO5 constitutive phenotype. These data suggest that PHO84 is not required for sensing phosphate. We further characterized putative phosphate transporters, identifying two new phosphate transporters, PHO90 and PHO91. A synthetic lethal phenotype was observed when five phosphate transporters were inactivated, and the contribution of each transporter to uptake in high phosphate conditions was determined. Finally, a PHO84-dependent compensation response was identified; the abundance of Pho84p at the plasma membrane increases in cells that are defective in other phosphate transporters.

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Gradolatto, Angeline, Richard S. Rogers, Heather Lavender, Sean D. Taverna, C. David Allis, John D. Aitchison, and Alan J. Tackett. "Saccharomyces cerevisiae Yta7 Regulates Histone Gene Expression." Genetics 179, no. 1 (May 2008): 291–304. http://dx.doi.org/10.1534/genetics.107.086520.

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Jordan, I. King, and John F. McDonald. "Tempo and Mode of Ty Element Evolution in Saccharomyces cerevisiae." Genetics 151, no. 4 (April 1, 1999): 1341–51. http://dx.doi.org/10.1093/genetics/151.4.1341.

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Abstract The Saccharomyces cerevisiae genome contains five families of long terminal repeat (LTR) retrotransposons, Ty1–Ty5. The sequencing of the S. cerevisiae genome provides an unprecedented opportunity to examine the patterns of molecular variation existing among the entire genomic complement of Ty retrotransposons. We report the results of an analysis of the nucleotide and amino acid sequence variation within and between the five Ty element families of the S. cerevisiae genome. Our results indicate that individual Ty element families tend to be highly homogenous in both sequence and size variation. Comparisons of within-element 5′ and 3′ LTR sequences indicate that the vast majority of Ty elements have recently transposed. Furthermore, intrafamily Ty sequence comparisons reveal the action of negative selection on Ty element coding sequences. These results taken together suggest that there is a high level of genomic turnover of S. cerevisiae Ty elements, which is presumably in response to selective pressure to escape host-mediated repression and elimination mechanisms.

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Saito, T. L. "SCMD: Saccharomyces cerevisiae Morphological Database." Nucleic Acids Research 32, no. 90001 (January 1, 2004): 319D—322. http://dx.doi.org/10.1093/nar/gkh113.

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Guacci, V., and D. B. Kaback. "Distributive disjunction of authentic chromosomes in Saccharomyces cerevisiae." Genetics 127, no. 3 (March 1, 1991): 475–88. http://dx.doi.org/10.1093/genetics/127.3.475.

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Abstract Distributive disjunction is defined as the first division meiotic segregation of either nonhomologous chromosomes that lack homologs or homologous chromosomes that have not recombined. To determine if chromosomes from the yeast Saccharomyces cerevisiae were capable of distributive disjunction, we constructed a strain that was monosomic for both chromosome I and chromosome III and analyzed the meiotic segregation of the two monosomic chromosomes. In addition, we bisected chromosome I into two functional chromosome fragments, constructed strains that were monosomic for both chromosome fragments and examined meiotic segregation of the chromosome fragments in the monosomic strains. The two nonhomologous chromosomes or chromosome fragments appeared to segregate from each other in approximately 90% of the asci analyzed, indicating that yeast chromosomes were capable of distributive disjunction. We also examined the ability of a small nonhomologous centromere containing plasmid to participate in distributive disjunction with the two nonhomologous monosomic chromosomes. The plasmid appeared to efficiently participate with the two full length chromosomes suggesting that distributive disjunction in yeast is not dependent on chromosome size. Thus, distributive disjunction in S. cerevisiae appears to be different from Drosophila melanogaster where a different sized chromosome is excluded from distributive disjunction when two similar size nonhomologous chromosomes are present.

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Steele, D. F., and S. Jinks-Robertson. "An examination of adaptive reversion in Saccharomyces cerevisiae." Genetics 132, no. 1 (September 1, 1992): 9–21. http://dx.doi.org/10.1093/genetics/132.1.9.

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Abstract Reversion to Lys+ prototrophy in a haploid yeast strain containing a defined lys2 frameshift mutation has been examined. When cells were plated on synthetic complete medium lacking only lysine, the numbers of Lys+ revertant colonies accumulated in a time-dependent manner in the absence of any detectable increase in cell number. An examination of the distribution of the numbers of early appearing Lys+ colonies from independent cultures suggests that the mutations to prototrophy occurred randomly during nonselective growth. In contrast, an examination of the distribution of late appearing Lys+ colonies indicates that the underlying reversion events occurred after selective plating. No accumulation of Lys+ revertants occurred when cells were starved for tryptophan, leucine or both lysine and tryptophan prior to plating selectively for Lys+ revertants. These results indicate that mutations accumulate more frequently when they confer a selective advantage, and are thus consistent with the occurrence of adaptive mutations in yeast.

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18

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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Rattray, A. J., and L. S. Symington. "Multiple pathways for homologous recombination in Saccharomyces cerevisiae." Genetics 139, no. 1 (January 1, 1995): 45–56. http://dx.doi.org/10.1093/genetics/139.1.45.

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Abstract The genes in the RAD52 epistasis group of Saccharomyces cerevisiae are necessary for most mitotic and meiotic recombination events. Using an intrachromosomal inverted-repeat assay, we previously demonstrated that mitotic recombination of this substrate is dependent upon the RAD52 gene. In the present study the requirement for other genes in this epistasis group for recombination of inverted repeats has been analyzed, and double and triple mutant strains were examined for their epistatic relationships. The majority of recombination events are mediated by a RAD51-dependent pathway, where the RAD54, RAD55 and RAD57 genes function downstream of RAD51. Cells mutated in RAD55 or RAD57 as well as double mutants are cold-sensitive for inverted-repeat recombination, whereas a rad51 rad55 rad57 triple mutant is not. The RAD1 gene is not required for inverted-repeat recombination but is able to process spontaneous DNA lesions to produce recombinant products in the absence of RAD51. Furthermore, there is still considerably more recombination in rad1 rad51 mutants than in rad52 mutants, indicating the presence of another, as yet unidentified, recombination pathway.

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Preston, R. A., P. S. Reinagel, and E. W. Jones. "Genes required for vacuolar acidity in Saccharomyces cerevisiae." Genetics 131, no. 3 (July 1, 1992): 551–58. http://dx.doi.org/10.1093/genetics/131.3.551.

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Abstract Mutations that cause loss of acidity in the vacuole (lysosome) of Saccharomyces cerevisiae were identified by screening colonies labeled with the fluorescent, pH-sensitive, vacuolar labeling agent, 6-carboxyfluorescein. Thirty nine vacuolar pH (Vph-) mutants were identified. Four of these contained mutant alleles of the previously described PEP3, PEP5, PEP6 and PEP7 genes. The remaining mutants defined eight complementation groups of vph mutations. No alleles of the VAT2 or TFP1 genes (known to encode subunits of the vacuolar H(+)-ATPase) were identified in the Vph- screen. Strains bearing mutations in any of six of the VPH genes failed to grow on medium buffered at neutral pH; otherwise, none of the vph mutations caused notable growth inhibition on standard yeast media. Expression of the vacuolar protease, carboxypeptidase Y, was defective in strains bearing vph4 mutations but was apparently normal in strains bearing any of the other vph mutations. Defects in vacuolar morphology at the light microscope level were evident in all Vph- mutants. Strains that contained representative mutant alleles of the 17 previously described PEP genes were assayed for vacuolar pH; mutations in seven of the PEP genes (including PEP3, PEP5, PEP6 and PEP7) caused loss of vacuolar acidity.

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Kim, J., P. O. Ljungdahl, and G. R. Fink. "kem mutations affect nuclear fusion in Saccharomyces cerevisiae." Genetics 126, no. 4 (December 1, 1990): 799–812. http://dx.doi.org/10.1093/genetics/126.4.799.

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Abstract We have identified mutations in three genes of Saccharomyces cerevisiae, KEM1, KEM2 and KEM3, that enhance the nuclear fusion defect of kar1-1 yeast during conjugation. The KEM1 and KEM3 genes are located on the left arm of chromosome VII. Kem mutations reduce nuclear fusion whether the kem and the kar1-1 mutations are in the same or in different parents (i.e., in both kem kar1-1 X wild-type and kem X kar 1-1 crosses). kem 1 X kem 1 crosses show a defect in nuclear fusion, but kem 1 X wild-type crosses do not. Mutant kem 1 strains are hypersensitive to benomyl, lose chromosomes at a rate 10-20-fold higher than KEM+ strains, and lose viability upon nitrogen starvation. In addition, kem 1/kem 1 diploids are unable to sporulate. Cells containing a kem 1 null allele grow very poorly, have an elongated rod-shape and are defective in spindle pole body duplication and/or separation. The KEM 1 gene, which is expressed as a 5.5-kb mRNA transcript, contains a 4.6-kb open reading frame encoding a 175-kD protein.

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Wilke, C. M., and J. Adams. "Fitness effects of Ty transposition in Saccharomyces cerevisiae." Genetics 131, no. 1 (May 1, 1992): 31–42. http://dx.doi.org/10.1093/genetics/131.1.31.

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Abstract It has been suggested that the primary evolutionary role of transposable elements is negative and parasitic. Alternatively, the target specificity and gene regulatory capabilities of many transposable elements raise the possibility that transposable element-induced mutations are more likely to be adaptively favorable than other types of mutations. Populations of Saccharomyces cerevisiae containing large amounts of variation for Ty1 genomic insertions were constructed, and the effects of Ty1 copy number on two components of fitness, yield and growth rate were determined. Although mean stationary phase density decreased with increased Ty1 copy number, the variance and range increased. The distributions of stationary phase densities indicate that many Ty1 insertions have negative effects on fitness, but also that some may have positive effects. To test directly for adaptively favorable Ty1 insertions, populations containing large amounts of variability for Ty1 copy number were grown in continuous culture. After 98-112 generations the frequency of clones containing zero Ty1 elements had decreased to approximately 0.0, and specific Ty1-containing clone families had predominated. Considering that most of the genetic variation in the populations was due to Ty1 transposition, and that Ty1 insertions had, on average, a negative effect on fitness, we conclude that Ty1 transposition events were directly responsible for the production of adaptive mutations in the clones that predominated in the populations.

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Harvey, Anne C., Stephen P. Jackson, and Jessica A. Downs. "Saccharomyces cerevisiae Histone H2A Ser122 Facilitates DNA Repair." Genetics 170, no. 2 (March 21, 2005): 543–53. http://dx.doi.org/10.1534/genetics.104.038570.

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Veron, Marie, Yanfei Zou, Qun Yu, Xin Bi, Abdelkader Selmi, Eric Gilson, and Pierre-Antoine Defossez. "Histone H1 of Saccharomyces cerevisiae Inhibits Transcriptional Silencing." Genetics 173, no. 2 (April 2, 2006): 579–87. http://dx.doi.org/10.1534/genetics.105.050195.

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Barton, Arnold B., Yuping Su, Jacque Lamb, Dianna Barber, and David B. Kaback. "A Function for Subtelomeric DNA in Saccharomyces cerevisiae." Genetics 165, no. 2 (October 1, 2003): 929–34. http://dx.doi.org/10.1093/genetics/165.2.929.

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Abstract The subtelomeric DNA sequences from chromosome I of Saccharomyces cerevisiae are shown to be inherently poor substrates for meiotic recombination. On the basis of these results and prior observations that crossovers near telomeres do not promote efficient meiosis I segregation, we suggest that subtelomeric sequences evolved to prevent recombination from occurring where it cannot promote efficient segregation.

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Natsoulis, G., F. Winston, and J. D. Boeke. "The SPT10 and SPT21 genes of Saccharomyces cerevisiae." Genetics 136, no. 1 (January 1, 1994): 93–105. http://dx.doi.org/10.1093/genetics/136.1.93.

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Abstract Mutations in the SPT10 and SPT21 genes were originally isolated as suppressors of Ty and LTR (delta) insertion mutations in Saccharomyces cerevisiae, and the genes were shown to be required for normal transcription at a number of loci in yeast. Now we have cloned, sequenced, mapped and mutagenized SPT10 and SPT21. Since the spt10 mutation used to clone SPT10 resulted in very poor transformation efficiency, a novel method making use of the kar1-1 mutation was used. Neither SPT gene is essential for growth, and constructed null alleles cause phenotypes similar to those caused by spontaneous mutations in the genes. spt10 null alleles are strong suppressor mutations and cause extremely slow growth. Certain spt10 spontaneous alleles are good suppressors but have a normal growth rate, suggesting that the SPT10 protein may have two distinct functions. An amino acid sequence motif that is similar to the Zn-finger motif was found in SPT10. Mutation of the second Cys residue in this motif resulted in loss of complementation of the suppression phenotype but a normal growth rate. Thus, this motif may reside in a part of the SPT10 protein that is important for transcriptional regulation but not for normal growth. Both the SPT10 and SPT21 proteins are relatively tolerant of large deletions; in both cases deletions of the C-terminus resulted in at least partially functional proteins; also, a large internal deletion in SPT21 was phenotypically wild type.

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Berg, Matthew D., Yanrui Zhu, Julie Genereaux, Bianca Y. Ruiz, Ricard A. Rodriguez-Mias, Tyler Allan, Alexander Bahcheli, Judit Villén, and Christopher J. Brandl. "Modulating Mistranslation Potential of tRNASer in Saccharomyces cerevisiae." Genetics 213, no. 3 (September 4, 2019): 849–63. http://dx.doi.org/10.1534/genetics.119.302525.

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Blacketer, M. J., P. Madaule, and A. M. Myers. "Mutational analysis of morphologic differentiation in Saccharomyces cerevisiae." Genetics 140, no. 4 (August 1, 1995): 1259–75. http://dx.doi.org/10.1093/genetics/140.4.1259.

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Abstract A genetic analysis was undertaken to investigate the mechanisms controlling cellular morphogenesis in Saccharomyces cerevisiae. Sixty mutant strains exhibiting abnormally elongated cell morphology were isolated. The cell elongation phenotype in at least 26 of the strains resulted from a single recessive mutation. These mutations, designated generically elm (elongated morphology), defined 14 genes; two of these corresponded to the previously described genes GRR1 and CDC12. Genetic interactions between mutant alleles suggest that several ELM genes play roles in the same physiological process. The cell and colony morphology and growth properties of many elm mutant strains are similar to those of wild-type yeast strains after differentiation in response to nitrogen limitation into the pseudohyphal form. Each elm mutation resulted in multiple characteristics of pseudohyphal cells, including elongated cell shape, delay in cell separation, simultaneous budding of mother and daughter cells, a unipolar budding pattern, and/or the ability to grow invasively beneath the agar surface. Mutations in 11 of the 14 ELM gene loci potentiated pseudohyphal differentiation in nitrogen-limited medium. Thus, a subset of the ELM genes are likely to affect control or execution of a defined morphologic differentiation pathway in S. cerevisiae.

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Pisat, Nilambari P., Abhinav Pandey, and Colin W. MacDiarmid. "MNR2 Regulates Intracellular Magnesium Storage in Saccharomyces cerevisiae." Genetics 183, no. 3 (August 31, 2009): 873–84. http://dx.doi.org/10.1534/genetics.109.106419.

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Magnesium (Mg) is an essential enzyme cofactor and a key structural component of biological molecules, but relatively little is known about the molecular components required for Mg homeostasis in eukaryotic cells. The yeast genome encodes four characterized members of the CorA Mg transporter superfamily located in the plasma membrane (Alr1 and Alr2) or the mitochondrial inner membrane (Mrs2 and Lpe10). We describe a fifth yeast CorA homolog (Mnr2) required for Mg homeostasis. MNR2 gene inactivation was associated with an increase in both the Mg requirement and the Mg content of yeast cells. In Mg-replete conditions, wild-type cells accumulated an intracellular store of Mg that supported growth under deficient conditions. An mnr2 mutant was unable to access this store, suggesting that Mg was trapped in an intracellular compartment. Mnr2 was localized to the vacuole membrane, implicating this organelle in Mg storage. The mnr2 mutant growth and Mg-content phenotypes were dependent on vacuolar proton-ATPase activity, but were unaffected by the loss of mitochondrial Mg uptake, indicating a specific dependence on vacuole function. Overexpression of Mnr2 suppressed the growth defect of an alr1 alr2 mutant, indicating that Mnr2 could function independently of the ALR genes. Together, our results implicate a novel eukaryotic CorA homolog in the regulation of intracellular Mg storage.

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Cannon, John F., Jackson B. Gibbs, and Kelly Tatchell. "SUPPRESSORS OF THE ras2 MUTATION OF SACCHAROMYCES CEREVISIAE." Genetics 113, no. 2 (June 1, 1986): 247–64. http://dx.doi.org/10.1093/genetics/113.2.247.

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ABSTRACT Saccharomyces cerevisiae contains two members of the ras gene family. Strains with disruptions of the RAS2 gene fail to grow efficiently on nonfermentable carbon sources. This growth defect can be suppressed by extragenic mutations called sra. We have isolated 79 independent suppressor mutations, 68 of which have been assigned to one of five loci. Eleven additional dominant mutations have not been assigned to a specific locus. Some sra1 and SRA4 and all SRA3 mutations were RAS independent, allowing growth of yeast cells that lack a functional RAS gene. Mutations in sra1, SRA3, SRA4 and sra6 are linked to his6, ino1, met3 and ade6, respectively. Some sra mutants have pleitropic phenotypes that affect glycogen accumulation, sporulation, viability, respiratory capacity and suppression of two cell-division-cycle mutations, cdc25 and cdc35. The proposed functions of many of the suppressor genes are consistent with the model in which RAS activates adenylate cyclase.

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Riles, L., and M. V. Olson. "Nonsense mutations in essential genes of Saccharomyces cerevisiae." Genetics 118, no. 4 (April 1, 1988): 601–7. http://dx.doi.org/10.1093/genetics/118.4.601.

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Abstract A new method for isolating nonsense mutations in essential yeast genes has been used to develop a collection of 115 ochre mutations that define 94 complementation groups. The mutants are isolated in a genetic background that includes an ochre suppressor on a metastable plasmid and a suppressible colony-color marker on a chromosome. When the parental strain is plated on a rich medium, the colonies display a pattern of red, plasmid-free sectors on a white background. Mutants containing an ochre mutation in any essential yeast gene give rise to nonsectoring, white colonies, since cell growth is dependent on the presence of the plasmid-borne suppressor. Analysis of the data suggests that mutations are being recovered from a pool of approximately 250 genes.

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Naumov, Gennadi I., Elena S. Naumova, and Enrique D. Sancho. "Genetic reidentification of Saccharomyces strains associated with black knot disease of trees in Ontario and Drosophila species in California." Canadian Journal of Microbiology 42, no. 4 (April 1, 1996): 335–39. http://dx.doi.org/10.1139/m96-049.

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Using genetic hybridization analysis, electrophoretic karyotyping, and Southern hybridization with the ADC1 promoter probe, three biological sibling species, Saccharomyces cerevisiae, Saccharomyces paradoxus, and Saccharomyces bayanus, have been identified in Ontario and California. Saccharomyces kluyveri strains were revealed by karyotyping.Key words: genetical taxonomy, sibling species, Saccharomyces complex, electrophoretic karyotyping.

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Grunstein, M., and S. M. Gasser. "Epigenetics in Saccharomyces cerevisiae." Cold Spring Harbor Perspectives in Biology 5, no. 7 (July 1, 2013): a017491. http://dx.doi.org/10.1101/cshperspect.a017491.

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Lee, Won-Chul, Minho Lee, Jin Woo Jung, Kwang Pyo Kim, and Dongsup Kim. "SCUD: Saccharomyces Cerevisiae Ubiquitination Database." BMC Genomics 9, no. 1 (2008): 440. http://dx.doi.org/10.1186/1471-2164-9-440.

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Adt, Isabelle, Achim Kohler, Sabine Gognies, Julien Budin, Christophe Sandt, Abdelkader Belarbi, Michel Manfait, and Ganesh D. Sockalingum. "FTIR spectroscopic discrimination of Saccharomyces cerevisiae and Saccharomyces bayanus strains." Canadian Journal of Microbiology 56, no. 9 (September 2010): 793–801. http://dx.doi.org/10.1139/w10-062.

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In this study, we tested the potential of Fourier-transform infrared absorption spectroscopy to screen, on the one hand, Saccharomyces cerevisiae and non-S. cerevisiae strains and, on the other hand, to discriminate between S. cerevisiae and Saccharomyces bayanus strains. Principal components analysis (PCA), used to compare 20 S. cerevisiae and 21 non-Saccharomyces strains, showed only 2 misclassifications. The PCA model was then used to classify spectra from 14 Samos strains. All 14 Samos strains clustered together with the S. cerevisiae group. This result was confirmed by a routinely used electrophoretic pattern obtained by pulsed-field gel electrophoresis. The method was then tested to compare S. cerevisiae and S. bayanus strains. Our results indicate that identification at the strain level is possible. This first result shows that yeast classification and S. bayanus identification can be feasible in a single measurement.

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Huberman, Joel A., R. David Pridmore, Daniel J�ger, Ben Zonneveld, and Peter Philippsen. "Centromeric DNA from Saccharomyces uvarum is functional in Saccharomyces cerevisiae." Chromosoma 94, no. 3 (September 1986): 162–68. http://dx.doi.org/10.1007/bf00288490.

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Magasanik, Boris, and Chris A. Kaiser. "Nitrogen regulation in Saccharomyces cerevisiae." Gene 290, no. 1-2 (May 2002): 1–18. http://dx.doi.org/10.1016/s0378-1119(02)00558-9.

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Prado, Félix, Felipe Cortés-Ledesma, Pablo Huertas, and Andrés Aguilera. "Mitotic recombination in Saccharomyces cerevisiae." Current Genetics 42, no. 4 (January 2003): 185–98. http://dx.doi.org/10.1007/s00294-002-0346-3.

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Offley, Sarah R., and Martin C. Schmidt. "Protein phosphatases of Saccharomyces cerevisiae." Current Genetics 65, no. 1 (September 17, 2018): 41–55. http://dx.doi.org/10.1007/s00294-018-0884-y.

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Li, Q. R., A. R. Carvunis, H. Yu, J. D. J. Han, Q. Zhong, N. Simonis, S. Tam, et al. "Revisiting the Saccharomyces cerevisiae predicted ORFeome." Genome Research 18, no. 8 (August 1, 2008): 1294–303. http://dx.doi.org/10.1101/gr.076661.108.

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Dorsey, M., C. Peterson, K. Bray, and C. E. Paquin. "Spontaneous amplification of the ADH4 gene in Saccharomyces cerevisiae." Genetics 132, no. 4 (December 1, 1992): 943–50. http://dx.doi.org/10.1093/genetics/132.4.943.

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Abstract Five spontaneous amplifications of the ADH4 gene were identified among 1,894 antimycin A-resistant mutants isolated from a diploid strain after growth at 15 degrees. Four of these amplifications are approximately 40-kb linear extrachromosomal palindromes carrying telomere homologous sequences at each end similar to a previously isolated amplification. ADH4 is located at the extreme left end of chromosome VII, and the extrachromosomal fragments appear to be the fusion of two copies of the end of this chromosome. The fifth amplification is a chromosomal amplification carrying an extra copy of ADH4 on both homologs of chromosome VII. These results suggest that the ADH system can be used to study amplification in Saccharomyces cerevisiae.

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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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Galbraith, Anne M., Steven A. Bullard, Kai Jiao, Johnathan J. Nau, and Robert E. Malone. "Recombination and the Progression of Meiosis in Saccharomyces cerevisiae." Genetics 146, no. 2 (June 1, 1997): 481–89. http://dx.doi.org/10.1093/genetics/146.2.481.

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Recombination is an essential part of meiosis; in almost all organisms, including Saccharomyces cerevisiae, proper chromosome segregation and the viability of meiotic products is dependent upon normal levels of recombination. In this article we examine the kinetics of the meiotic divisions in four mutants defective in the initiation of recombination. We find that mutations in any of three Early Exchange genes (REC104, REC114 or REC102) confer a phenotype in which the reductional division occurs earlier than in an isogenic wild-type diploid. We also present data confirming previous reports that strains with a mutation in the Early Exchange gene MEI4 undergo the first division at about the same time as wild-type cells. The rec104 mutation is epistatic to the mei4 mutation for the timing of the first division. These observations suggest a possible relationship between the initiation of recombination and the timing of the reductional division. These data also allow these four Early Exchange genes examined to be distinguished in terms of their role in coordinating recombination with the reductional division.

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Neff, M. W., and D. J. Burke. "Random segregation of chromatids at mitosis in Saccharomyces cerevisiae." Genetics 127, no. 3 (March 1, 1991): 463–73. http://dx.doi.org/10.1093/genetics/127.3.463.

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Abstract Previous experiments suggest that mitotic chromosome segregation in some fungi is a nonrandom process in which chromatids of the same replicative age are destined for cosegregation. We have investigated the pattern of chromatid segregation in Saccharomyces cerevisiae by labeling the DNA of a strain auxotrophic for thymidine with 5-bromodeoxyuridine. The fate of DNA strands was followed qualitatively by immunofluorescence microscopy and quantitatively by microphotometry using an anti-5-bromodeoxyuridine monoclonal antibody. Chromatids of the same replicative age were distributed randomly to daughter cells at mitosis. Quantitative measurements showed that the amount of fluorescence in the daughter nuclei derived from parents with hemilabeled chromosomes diminished in intensity by one half. The concentration of 5-bromodeoxyuridine used in the experiments had little effect on the frequency of either homologous or sister chromatid exchanges. We infer that the 5-bromodeoxyuridine was distributed randomly due to mitotic segregation of chromatids and not via sister chromatid exchanges.

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Yuan, L. W., and R. L. Keil. "Distance-independence of mitotic intrachromosomal recombination in Saccharomyces cerevisiae." Genetics 124, no. 2 (February 1, 1990): 263–73. http://dx.doi.org/10.1093/genetics/124.2.263.

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Abstract Many genetic studies have shown that the frequency of homologous recombination depends largely on the distance in which recombination can occur. We have studied the effect of varying the length of duplicated sequences on the frequency of mitotic intrachromosomal recombination in Saccharomyces cerevisiae. We find that the frequency of recombination resulting in the loss of one of the repeats and the intervening sequences reaches a plateau when the repeats are short. In addition, the frequency of recombination to correct a point mutation contained in one of these repeats is not proportional to the size of the duplication but rather depends dramatically on the location of the mutation within the repeated sequences. However, the frequency of mitotic interchromosomal reciprocal recombination is dependent on the distance separating the markers. The difference in the response of intrachromosomal and interchromosomal mitotic recombination to increasing lengths of homology may indicate there are different rate-limiting steps for recombination in these two cases. These findings have important implications for the maintenance and evolution of duplicated sequences.

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Kawakami, K., B. K. Shafer, D. J. Garfinkel, J. N. Strathern, and Y. Nakamura. "Ty element-induced temperature-sensitive mutations of Saccharomyces cerevisiae." Genetics 131, no. 4 (August 1, 1992): 821–32. http://dx.doi.org/10.1093/genetics/131.4.821.

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Abstract Temperature-sensitive mutants of Saccharomyces cerevisiae were isolated by insertional mutagenesis using the HIS3 marked retrotransposon TyH3HIS3. In such mutants, the TyHIS3 insertions are expected to identify loci which encode genes essential for cell growth at high temperatures but dispensable at low temperatures. Five mutations were isolated and named hit for high temperature growth. The hit1-1 mutation was located on chromosome X and conferred the pet phenotype. Two hit2 mutations, hit2-1 and hit2-2, were located on chromosome III and caused the deletion of the PET18 locus which has been shown to encode a gene required for growth at high temperatures. The hit3-1 mutation was located on chromosome VI and affected the CDC26 gene. The hit4-1 mutation was located on chromosome XIII. These hit mutations were analyzed in an attempt to identify novel genes involved in the heat shock response. The hit1-1 mutation caused a defect in synthesis of a 74-kD heat shock protein. Western blot analysis revealed that the heat shock protein corresponded to the SSC1 protein, a member of the yeast hsp70 family. In the hit1-1 mutant, the TyHIS3 insertion caused a deletion of a 3-kb DNA segment between the delta 1 and delta 4 sequences near the SUP4 locus. The 1031-bp wild-type HIT1 DNA which contained an open reading frame encoding a protein of 164 amino acids and the AGG arginine tRNA gene complemented all hit1-1 mutant phenotypes, indicating that the mutant phenotypes were caused by the deletion of these genes. The pleiotropy of the HIT1 locus was analyzed by constructing a disruption mutation of each gene in vitro and transplacing it to the chromosome. This analysis revealed that the HIT1 gene essential for growth at high temperatures encodes the 164-amino acid protein. The arginine tRNA gene, named HSX1, is essential for growth on a nonfermentable carbon source at high temperatures and for synthesis of the SSC1 heat shock protein.

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Lemmon, S. K., C. Freund, K. Conley, and E. W. Jones. "Genetic instability of clathrin-deficient strains of Saccharomyces cerevisiae." Genetics 124, no. 1 (January 1, 1990): 27–38. http://dx.doi.org/10.1093/genetics/124.1.27.

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Abstract Saccharomyces cerevisiae strains carrying a mutation in the clathrin heavy chain gene (CHC1) are genetically unstable and give rise to heterogeneous populations of cells. Manifestations of the instability include increases in genome copy number as well as compensatory genetic changes that allow better growing clathrin-deficient cells to take over the population. Increases in genome copy number appear to result from changes in ploidy as well as alterations in normal nuclear number. Genetic background influences the frequency at which cells with increased genome content are observed in different Chc- strains. We cannot distinguish whether genetic background affects the rate at which aberrant nuclear division events occur or a growth advantage of cells with increased nuclear and/or genome content. However, survival of chc1-delta cells does not require an increase in genome copy number. The clathrin heavy chain gene was mapped 1-2 cM distal to KEX1 on the left arm of chromosome VII by making use of integrated 2 mu plasmid sequences to destabilize distal chromosome segments and allow ordering of the genes.

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Cannon, J. F., J. R. Pringle, A. Fiechter, and M. Khalil. "Characterization of glycogen-deficient glc mutants of Saccharomyces cerevisiae." Genetics 136, no. 2 (February 1, 1994): 485–503. http://dx.doi.org/10.1093/genetics/136.2.485.

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Abstract Forty-eight mutants of Saccharomyces cerevisiae with defects in glycogen metabolism were isolated. The mutations defined eight GLC genes, the function of which were determined. Mutations in three of these genes activate the RAS/cAMP pathway either by impairment of a RAS GTPase-activating protein (GLC1/IRA1 and GLC4/IRA2) or by activating Ras2p (GLC5/RAS2). SNF1 protein kinase (GLC2) was found to be required for normal glycogen levels. Glycogen branching enzyme (GLC3) was found to be required for significant glycogen synthesis. GLC6 was shown to be allelic to CIF1 (and probably FDP1, BYP1 and GGS1), mutations in which were previously found to prevent growth on glucose; this gene is also the same as TPS1, which encodes a subunit of the trehalose-phosphate synthase. Mutations in GLC6 were capable of increasing or decreasing glycogen levels, at least in part via effects on the regulation of glycogen synthase. GLC7 encodes a type 1 protein phosphatase that contributes to the dephosphorylation (and hence activation) of glycogen synthase. GLC8 encodes a homologue of type 1 protein phosphatase inhibitor-2. The genetic map positions of GLC1/IRA1, GLC3, GLC4/IRA2, GLC6/CIF1/TPS1 (and the adjacent VAT2/VMA2), and GLC7 were clarified. From the data on GLC3, there may be a suppression of recombination near the chromosome V centromere, at least in some strains.

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Dornfeld, K. J., and D. M. Livingston. "Plasmid recombination in a rad52 mutant of Saccharomyces cerevisiae." Genetics 131, no. 2 (June 1, 1992): 261–76. http://dx.doi.org/10.1093/genetics/131.2.261.

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Abstract Using plasmids capable of undergoing intramolecular recombination, we have compared the rates and the molecular outcomes of recombination events in a wild-type and a rad52 strain of Saccharomyces cerevisiae. The plasmids contain his3 heteroalleles oriented in either an inverted or a direct repeat. Inverted repeat plasmids recombine approximately 20-fold less frequently in the mutant than in the wild-type strain. Most events from both cell types have continuous coconversion tracts extending along one of the homologous segments. Reciprocal exchange occurs in fewer than 30% of events. Direct repeat plasmids recombine at rates comparable to those of inverted repeat plasmids in wild-type cells. Direct repeat conversion tracts are similar to inverted repeat conversion tracts in their continuity and length. Inverted and direct repeat plasmid recombination differ in two respects. First, rad52 does not affect the rate of direct repeat recombination as drastically as the rate of inverted repeat recombination. Second, direct repeat plasmids undergo crossing over more frequently than inverted repeat plasmids. In addition, crossovers constitute a larger fraction of mutant than wild-type direct repeat events. Many crossover events from both cell types are unusual in that the crossover HIS3 allele is within a plasmid containing the parental his3 heteroalleles.

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Loidl, J. "Meiotic chromosome pairing in triploid and tetraploid Saccharomyces cerevisiae." Genetics 139, no. 4 (April 1, 1995): 1511–20. http://dx.doi.org/10.1093/genetics/139.4.1511.

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Abstract Meiotic chromosome pairing in isogenic triploid and tetraploid strains of yeast and the consequences of polyploidy on meiotic chromosome segregation are studied. Synaptonemal complex formation at pachytene was found to be different in the triploid and in the tetraploid. In the triploid, triple-synapsis, that is, the connection of three homologues at a given site, is common. It can even extend all the way along the chromosomes. In the tetraploid, homologous chromosomes mostly come in pairs of synapsed bivalents. Multiple synapsis, that is, synapsis of more than two homologues in one and the same region, was virtually absent in the tetraploid. About five quadrivalents per cell occurred due to the switching of pairing partners. From the frequency of pairing partner switches it can be deduced that in most chromosomes synapsis is initiated primarily at one end, occasionally at both ends and rarely at an additional intercalary position. In contrast to a considerably reduced spore viability (approximately 40%) in the triploid, spore viability is only mildly affected in the tetraploid. The good spore viability is presumably due to the low frequency of quadrivalents and to the highly regular 2:2 segregation of the few quadrivalents that do occur. Occasionally, however, quadrivalents appear to be subject to 3:1 nondisjunction that leads to spore death in the second generation.

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Journal articles on the topic 'Saccharomyces cerevisiae – Genetics'

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