scholarly journals MUTATIONS IN THE PHO80 GENE CONFER PERMEABILITY TO 5'-MONONUCLEOTIDES IN SACCHAROMYCES CEREVISIAE

Genetics ◽  
1982 ◽  
Vol 102 (3) ◽  
pp. 341-359
Author(s):  
Linda F Bisson ◽  
Jeremy Thorner
Keyword(s):  
Inorganic Phosphate ◽  
Phosphate Transport ◽  
Culture Conditions ◽  
Yeast Cells ◽  
Wild Type ◽  
Coordinate Control ◽  
Complementation Groups ◽  
The Right ◽  
Yeast Mutants ◽  
Type Strains

ABSTRACT Yeast mutants permeable to dTMP (tup) were selected and two new complementation groups (tup5 and tup7) were identified. Assay of the levels of both acid and alkaline phosphatase in cells grown under either repressing (5 mm PO4  -3) or derepressing (0.03 mm PO4  -3) conditions indicated that, in general, tup mutations cause cells to be defective in their regulation of phosphatase synthesis. In addition, three of the tup mutations (tup1, tup4 and tup7) displayed markedly elevated rates of inorganic phosphate transport. The tup7 locus was found to be tightly centromere-linked on the right arm of chromosome XV, and was shown to be allelic with the pho80 regulatory locus on the basis of both genetic and biochemical criteria. Analysis of other mutations known to affect phosphatase levels (pho) indicated that some also conferred permeability to dTMP. Possible allelic relationships between tup genes and certain of these pho mutations are discussed. Regardless of the culture conditions, wild-type strains were not permeable to dTMP; in contrast, it was found in the course of this work that normal yeast cells were permeable to dUMP and that dUMP permeability was regulated by the concentration of inorganic phosphate present in the medium used to grow the cells. Thus, permeability to 5′-mononucleotides appears to be under coordinate control with phosphatase synthesis.

scholarly journals Phosphatases ofCoprinus lagopus: the conditions for their production and the genetics of the alkaline phosphatase

1971 ◽  
Vol 18 (2) ◽  
pp. 153-166 ◽  
Author(s):  
Jane North ◽  
D. Lewis
Keyword(s):  
Alkaline Phosphatase ◽  
Acid Phosphatase ◽  
Inorganic Phosphate ◽  
Aerial Mycelium ◽  
Wild Type ◽  
Complementation Groups ◽  
Phosphate Source ◽  
Type Strains ◽  
Phosphate Medium ◽  
High Phosphate

SUMMARY1.Coprinus lagopusproduces two non-specific phosphatases: a constitutive acid phosphatase, and an alkaline phosphatase which is repressed during growth on media with a high inorganic phosphate concentration.2. The alkaline phosphatase is also repressed whenCoprinusis grown on an organic phosphate source; but if the acid phosphatase is selectively inhibited by fluoride the alkaline phosphatase is de-repressed and growth is comparable to that observed on an inorganic phosphate source.3. Alkaline phosphatase is not repressed in aerial mycelium or sporophores even when grown on high phosphate medium.4. Mutants altered in their capacity to synthesize alkaline phosphatase were selected from two compatible wild-type strains, H2 and H5.5. Mutants producing a higher level of alkaline phosphatase than wild-type (‘regulator’ mutants) fall into four (or possibly five) complementation groups. Assuming five separate genes, two pairs are linked; the remaining one is independent and on another chromosome.6. Mutants deficient in alkaline phosphatase synthesis fall into at least three groups. They were tested for linkage to ‘regulator’ loci but so far there is no evidence of this.

scholarly journals Peroxisome Maintenance Depends on De Novo Peroxisome Formation in Yeast Mutants Defective in Peroxisome Fission and Inheritance

2019 ◽  
Vol 20 (16) ◽  
pp. 4023 ◽  
Author(s):  
Justyna P. Wróblewska ◽  
Ida J. van der Klei
Keyword(s):  
De Novo ◽  
Hansenula Polymorpha ◽  
Yeast Cells ◽  
Wild Type ◽  
Double Deletion ◽  
Mother Cells ◽  
Yeast Mutants ◽  
Rescue Mechanism ◽  
Wild Type Yeast ◽  
In Cells

There is an ongoing debate on how peroxisomes form: by growth and fission of pre-existing peroxisomes or de novo from another membrane. It has been proposed that, in wild type yeast cells, peroxisome fission and careful segregation of the organelles over mother cells and buds is essential for organelle maintenance. Using live cell imaging we observed that cells of the yeast Hansenula polymorpha, lacking the peroxisome fission protein Pex11, still show peroxisome fission and inheritance. Also, in cells of mutants without the peroxisome inheritance protein Inp2 peroxisome segregation can still occur. In contrast, peroxisome fission and inheritance were not observed in cells of a pex11 inp2 double deletion strain. In buds of cells of this double mutant, new organelles likely appear de novo. Growth of pex11 inp2 cells on methanol, a growth substrate that requires functional peroxisomes, is retarded relative to the wild type control. Based on these observations we conclude that in H. polymorpha de novo peroxisome formation is a rescue mechanism, which is less efficient than organelle fission and inheritance to maintain functional peroxisomes.

scholarly journals Recombination Can either Help Maintain Very Short Telomeres or Generate Longer Telomeres in Yeast Cells with Weak Telomerase Activity

2011 ◽  
Vol 10 (8) ◽  
pp. 1131-1142 ◽  
Author(s):  
Evelina Basenko ◽  
Zeki Topcu ◽  
Michael J. McEachern
Keyword(s):  
Homologous Recombination ◽  
Telomere Length ◽  
Telomerase Activity ◽  
Telomere Maintenance ◽  
Yeast Cells ◽  
Colony Morphology ◽  
Wild Type ◽  
Telomeric Repeats ◽  
Yeast Mutants ◽  
Derivatives Of

ABSTRACT Yeast mutants lacking telomerase are able to elongate their telomeres through processes involving homologous recombination. In this study, we investigated telomeric recombination in several mutants that normally maintain very short telomeres due to the presence of a partially functional telomerase. The abnormal colony morphology present in some mutants was correlated with especially short average telomere length and with a requirement for RAD52 for indefinite growth. Better-growing derivatives of some of the mutants were occasionally observed and were found to have substantially elongated telomeres. These telomeres were composed of alternating patterns of mutationally tagged telomeric repeats and wild-type repeats, an outcome consistent with amplification occurring via recombination rather than telomerase. Our results suggest that recombination at telomeres can produce two distinct outcomes in the mutants we studied. In occasional cells, recombination generates substantially longer telomeres, apparently through the roll-and-spread mechanism. However, in most cells, recombination appears limited to helping to maintain very short telomeres. The latter outcome likely represents a simplified form of recombinational telomere maintenance that is independent of the generation and copying of telomeric circles.

scholarly journals Yeast mutants sensitive to antimicrotubule drugs define three genes that affect microtubule function.

Genetics ◽  
1990 ◽  
Vol 124 (2) ◽  
pp. 251-262 ◽  
Author(s):  
T Stearns ◽  
M A Hoyt ◽  
D Botstein
Keyword(s):  
Chromosome Loss ◽  
Gene Products ◽  
Wild Type ◽  
Tubulin Genes ◽  
New Genes ◽  
Complementation Groups ◽  
Yeast Mutants ◽  
Antimicrotubule Drugs ◽  
Tubulin Mutations ◽  
Microtubule Function

Abstract Three new genes affecting microtubule function in Saccharomyces cerevisiae were isolated by screening for mutants displaying supersensitivity to the antimicrotubule drug benomyl. Such mutants fall into six complementation groups: TUB1, TUB2 and TUB3, the three tubulin genes of yeast, and three new genes, which we have named CIN1, CIN2 and CIN4. Mutations in each of the CIN genes were also independently isolated by screening for mutants with increased rates of chromosome loss. Strains bearing mutations in the CIN genes are approximately tenfold more sensitive than wild type to both benomyl and to the related antimicrotubule drug, nocodazole. This phenotype is recessive for all alleles isolated. The CIN1, CIN2 and CIN4 genes were cloned by complementation of the benomyl-supersensitive phenotype. Null mutants of each of the genes are viable, and have phenotypes similar to those of the point mutants. Genetic evidence for the involvement of the CIN gene products in microtubule function comes from the observation that some tubulin mutations are suppressed by cin mutations, while other tubulin mutations are lethal in combination with cin mutations. Additional genetic experiments with cin mutants suggest that the three genes act together in the same pathway or structure to affect microtubule function.

scholarly journals TWO CHROMOSOMAL GENES REQUIRED FOR KILLING EXPRESSION IN KILLER STRAINS OF SACCHAROMYCES CEREVISIAE

Genetics ◽  
1976 ◽  
Vol 82 (3) ◽  
pp. 429-442
Author(s):  
Reed B Wickner ◽  
Michael J Leibowitz
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Molecular Weight ◽  
Mutant Phenotype ◽  
Wild Type ◽  
Double Stranded Rna ◽  
Killer Strain ◽  
Chromosomal Genes ◽  
Complementation Groups ◽  
Killer Plasmid ◽  
Type Strains

ABSTRACT The killer character of yeast is determined by a 1.4 × 106 molecular weight double-stranded RNA plasmid and at least 12 chromosomal genes. Wild-type strains of yeast that carry this plasmid (killers) secrete a toxin which is lethal only to strains not carrying this plasmid (sensitives). —— We have isolated 28 independent recessive chromosomal mutants of a killer strain that have lost the ability to secrete an active toxin but remain resistant to the effects of the toxin and continue to carry the complete cytoplasmic killer genome. These mutants define two complementation groups, kex1 and kex2. Kex1 is located on chromosome VII between ade5 and lys5. Kex2 is located on chromosome XIV, but it does not show meiotic linkage to any gene previously located on this chromosome. —— When the killer plasmid of kex1 or kex2 strains is eliminated by curing with heat or cycloheximide, the strains become sensitive to killing. The mutant phenotype reappears among the meiotic segregants in a cross with a normal killer. Thus, the kex phenotype does not require an alteration of the killer plasmid. —— Kex1 and kex2 strains each contain near-normal levels of the 1.4 × 106 molecular weight double-stranded RNA, whose presence is correlated with the presence of the killer genome.

Multistress resistance of Saccharomyces cerevisiae is generated by insertion of retrotransposon Ty into the 5' coding region of the adenylate cyclase gene

1988 ◽  
Vol 8 (12) ◽  
pp. 5555-5560
Author(s):  
H Iida
Keyword(s):  
Heat Treatment ◽  
Saccharomyces Cerevisiae ◽  
Heat Shock ◽  
Adenylate Cyclase ◽  
Uv Light ◽  
Yeast Cells ◽  
Wild Type ◽  
Coding Region ◽  
Resistant Mutants ◽  
Type Strains

Heat shock-resistant mutants, which were isolated by their ability to withstand lethal heat treatment, were characterized. Resistance was demonstrated to be a consequence of insertion of retrotransposon Ty into either the 5' coding or noncoding region, close to the putative initiation codon of the adenylate cyclase gene CYR1 (or CDC35). These heat shock-resistant mutants contained about threefold lower adenylate cyclase activity than wild-type strains. The mutants were also observed to be resistant to other stresses such as UV light and ethanol. These results demonstrate that multistress resistance, which may confer a survival advantage to yeast cells, can be generated by transposition of a Ty element into CYR1.

scholarly journals Deletion of Yeast p24 Genes Activates the Unfolded Protein Response

2001 ◽  
Vol 12 (4) ◽  
pp. 957-969 ◽  
Author(s):  
William J. Belden ◽  
Charles Barlowe
Keyword(s):  
Unfolded Protein Response ◽  
Yeast Cells ◽  
Secretory Proteins ◽  
Wild Type ◽  
Vitro Assay ◽  
Unfolded Protein ◽  
Extracellular Secretion ◽  
The Unfolded Protein Response ◽  
Protein Response ◽  
Type Strains

Yeast cells lacking a functional p24 complex accumulate a subset of secretory proteins in the endoplasmic reticulum (ER) and increase the extracellular secretion of HDEL-containing ER residents such as Kar2p/BiP. We report that a loss of p24 function causes activation of the unfolded protein response (UPR) and leads to increasedKAR2 expression. The HDEL receptor (Erd2p) is functional and traffics in p24 deletion strains as in wild-type strains, however the capacity of the retrieval pathway is exceeded. Other conditions that activate the UPR and elevate KAR2 expression also lead to extracellular secretion of Kar2p. Using an in vitro assay that reconstitutes budding from the ER, we detect elevated levels of Kar2p in ER-derived vesicles from p24 deletion strains and from wild-type strains with an activated UPR. Silencing the UPR byIRE1 deletion diminished Kar2p secretion under these conditions. We suggest that activation of the UPR plays a major role in extracellular secretion of Kar2p.

scholarly journals Multistress resistance of Saccharomyces cerevisiae is generated by insertion of retrotransposon Ty into the 5' coding region of the adenylate cyclase gene.

1988 ◽  
Vol 8 (12) ◽  
pp. 5555-5560 ◽  
Author(s):  
H Iida
Keyword(s):  
Heat Treatment ◽  
Saccharomyces Cerevisiae ◽  
Heat Shock ◽  
Adenylate Cyclase ◽  
Uv Light ◽  
Yeast Cells ◽  
Wild Type ◽  
Coding Region ◽  
Resistant Mutants ◽  
Type Strains

Heat shock-resistant mutants, which were isolated by their ability to withstand lethal heat treatment, were characterized. Resistance was demonstrated to be a consequence of insertion of retrotransposon Ty into either the 5' coding or noncoding region, close to the putative initiation codon of the adenylate cyclase gene CYR1 (or CDC35). These heat shock-resistant mutants contained about threefold lower adenylate cyclase activity than wild-type strains. The mutants were also observed to be resistant to other stresses such as UV light and ethanol. These results demonstrate that multistress resistance, which may confer a survival advantage to yeast cells, can be generated by transposition of a Ty element into CYR1.

scholarly journals Doubling Ty1 element copy number in Saccharomyces cerevisiae: host genome stability and phenotypic effects.

Genetics ◽  
1991 ◽  
Vol 129 (4) ◽  
pp. 1043-1052
Author(s):  
J D Boeke ◽  
D J Eichinger ◽  
G Natsoulis
Keyword(s):  
Copy Number ◽  
Genome Stability ◽  
Genome Structure ◽  
Yeast Cells ◽  
Wild Type ◽  
Opposite Mating Type ◽  
Spore Viability ◽  
Normal Number ◽  
Yeast Strains ◽  
Type Strains

Abstract Haploid yeast strains bearing approximately double the normal number of Ty1 elements have been constructed using marked GAL/Ty1 fusion plasmids. The strains maintain their high transposon copy number and overall genome structure in the absence of selection. The strains bearing extra Ty1 copies are surprisingly similar phenotypically to the parental strain. The results suggest that the limit to transposon copy number, if any, has not been reached. When these strains are crossed by wild-type strains (i.e., bearing the normal complement of Ty1 elements) or by strains of opposite mating type also bearing excess Ty1 elements, normal to very slightly reduced spore viability is observed, indicating that increasing the extent of transposon homology scattered around the genome does not result in significant increases in frequency of ectopic reciprocal recombination. The results suggest that yeast cells have evolved mechanisms for coping with excess transposon copies in the genome.

scholarly journals Role of the PDR Gene Network in Yeast Susceptibility to the Antifungal Antibiotic Mucidin

2000 ◽  
Vol 44 (2) ◽  
pp. 418-420 ◽  
Author(s):  
Dana Michalkova-Papajova ◽  
Margita Obernauerova ◽  
Julius Subik
Keyword(s):  
Transcriptional Regulation ◽  
Gene Network ◽  
Wild Type ◽  
Gain Of Function ◽  
Antifungal Antibiotic ◽  
Yeast Strains ◽  
Yeast Mutants ◽  
Type Strains ◽  
Higher Sensitivity

ABSTRACT Yeast strains disrupted in the PDR1, PDR3, or PDR5 gene, but not in SNQ2, exhibited higher sensitivity to mucidin (strobilurin A) than did the isogenic wild-type strains. Different gain-of-function mutations in the PDR1and PDR3 genes rendered yeast mutants resistant to this antibiotic. Mucidin induced PDR5 expression, but the changes in the expression of SNQ2 were only barely detectable. The results indicate that PDR5 provides the link between transcriptional regulation by PDR1 andPDR3 and mucidin resistance of yeast.

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