Toxicité génétique du chlorure de méthylmercure (CH3HgCl) sur les mitochondries de Saccharomyces cerevisiae

1983 ◽  
Vol 29 (9) ◽  
pp. 1149-1153 ◽  
Author(s):  
J. Phipps ◽  
D. R. Miller
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dose Response ◽  
Resistant Mutant ◽  
Dna Lesions ◽  
Organic Form ◽  
Yeast Saccharomyces Cerevisiae ◽  
Mechanism Of Toxicity

Among the strains of the yeast Saccharomyces cerevisiae we investigated, the organic form of mercury:methylmercury (II) does not seem to induce any cytoplasmic mutant "petite colonie" rho−. However, it induces a significant number of the erythromycin-resistant mutant Eryr. A dose response is shown. These effects are discussed in the view of the part that discrete DNA lesions could take in the explanation of the mechanism of toxicity of the organomercurial.

8-Azaguanine Resistant Mutant of the Yeast,Saccharomyces cerevisiae

1986 ◽  
Vol 50 (5) ◽  
pp. 1339-1340
Author(s):  
Naoko Sato ◽  
Makoto Shimosaka ◽  
Yasuki Fukuda ◽  
Kousaku Murata ◽  
Akira Kimura
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Resistant Mutant ◽  
Yeast Saccharomyces Cerevisiae

scholarly journals A heat shock-resistant mutant of Saccharomyces cerevisiae shows constitutive synthesis of two heat shock proteins and altered growth.

1984 ◽  
Vol 99 (4) ◽  
pp. 1441-1450 ◽  
Author(s):  
H Iida ◽  
I Yahara
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Heat Shock ◽  
Type Strain ◽  
Wild Type Strain ◽  
Growth Control ◽  
Protein S ◽  
Resistant Mutant ◽  
Wild Type ◽  
Yeast Saccharomyces Cerevisiae ◽  
Sulfur Starvation

A heat shock-resistant mutant of the budding yeast Saccharomyces cerevisiae was isolated at the mutation frequency of 10(-7) from a culture treated with ethyl methane sulfonate. Cells of the mutant are approximately 1,000-fold more resistant to lethal heat shock than those of the parental strain. Tetrad analysis indicates that phenotypes revealed by this mutant segregated together in the ratio 2+:2- from heterozygotes constructed with the wild-type strain of the opposite mating type, and are, therefore, attributed to a single nuclear mutation. The mutated gene in the mutant was herein designated hsr1 (heat shock response). The hsr1 allele is recessive to the HSR1+ allele of the wild-type strain. Exponentially growing cells of hsr1 mutant were found to constitutively synthesize six proteins that are not synthesized or are synthesized at reduced rates in HSR1+ cells unless appropriately induced. These proteins include one hsp/G0-protein (hsp48A), one hsp (hsp48B), and two G0-proteins (p73, p56). Heterozygous diploid (hsr1/HSR1+) cells do not synthesize the proteins constitutively induced in hsr1 cells, which suggests that the product of the HSR1 gene might negatively regulate the synthesis of these proteins. The hsr1 mutation also led to altered growth of the mutant cells. The mutation elongated the duration of G1 period in the cell cycle and affected both growth arrest by sulfur starvation and growth recovery from it. We discuss the problem of which protein(s) among those constitutively expressed in growing cells of the hsr1 mutant is responsible for heat shock resistance and alterations in the growth control.

scholarly journals Effect of Yeast (Saccharomyces cerevisiae) Supported by Selenium and Zinc on Lipid Profile of Local Sheep Males

2019 ◽  
Vol 12 (1) ◽  
pp. 89-96
Author(s):  
Mohannad Aremmt ◽  
T Mohammed ◽  
saad Alrawi
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Synergistic Effect ◽  
Lipid Profile ◽  
Animal Health ◽  
The Other ◽  
Control Group ◽  
Organic Form ◽  
Yeast Saccharomyces Cerevisiae ◽  
The Third ◽  
Group 3

This study was conducted to investigate the effect of (Saccharomyces cerevisiae) supported with zinc and selenium on the lipid profile. of Twenty-one Iraqi males sheep were used aged (1-1.5) years and the weight mean approximately (38±4) kg. experiment animals used divided randomly into three treated groups each group have 7 males. All males were fed on the same ration. The first group was considered as a control group without treatment (T1), the second group (T2) were given yeast enriched with zinc (Saccharomyces cerevisiae -zinc) with dosage (0.2 g/kg/bw), the third group (3) was given yeast enriched with selenium (Saccharomyces cerevisiae-selenium) with dosage (0.03 g/kg/bw). The results showed significant (P≤0.05) differences control group compare with the other two-treated groups (T3 and T2) in triglyceride, LDL , VLDL and HDL . The results indicate to significant differences (P≤0.05) of (T2 and T3) compare with the control group by HDL . From the results concluded that there synergistic effect of Saccharomyces cerevisiae with zinc and selenium as organic form (Saccharomyces cerevisiae-zinc/selenium) could be attributed to improved animal health.

scholarly journals Detection of the DNA primary structure modifications induced by the base analog 6-n-hydroxylaminopurine in the alpha-test in yeast saccharomyces cerevisiae

2020 ◽  
Vol 18 (3) ◽  
pp. 357-366
Author(s):  
Anna S. Zhuk ◽  
Elena I. Stepchenkova ◽  
Sergey G. Inge-Vechtomov
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Dna Lesions ◽  
Genetic Toxicology ◽  
Yeast Saccharomyces Cerevisiae ◽  
Genetic Changes ◽  
Mating Type Switching ◽  
Base Modifications ◽  
Type Switch ◽  
Chromosome Iii

Background. The alpha-test allows to detect inherited genetic changes of different types, as well as phenotypic expression of primary DNA lesions before the lesions are fixed by repair. Here we investigate ability of the alpha-test to detect base modifications induced by 6-N-hydroxylaminopurine (HAP) and determine frequency of inherited and non-inherited genetic changes in yeast strains treated with HAP. Materials and methods. The alpha-test is based on mating type regulation and detects cell type switch from to a in heterothallic yeast Saccharomyces cerevisiae. The frequency of mating type switching reflects level of both spontaneous and induced by a mutagen DNA instability. The alpha-test may be performed in two variants: illegitimate hybridization and cytoduction. Conducting both complementary tests and analysis of phenotypes of the illegitimate hybrids and cytoductants allows to detect the full spectrum of genetic events that lead to mating type switching, such as chromosome III loss and chromosome III arm loss, mutations and temporary lesions, recombination and conversion. Results. HAP increases the frequency of illegitimate hybridization by 5-fold, and illegitimate cytoduction by 10-fold. A large proportion of the primary lesions induced by HAP causes temporary mating type switch and the remainder parts are converted into inherited point mutations. Conclusion. The alpha-test can detect HAP-induced base modifications and may be used to investigate the ratio between correct and error-prone processing of such primary DNA lesions. Like other genetic toxicology tests the alpha-test has limitations, which are discussed.

scholarly journals 8-Azaguanine resistant mutant of the yeast, Saccharomyces cerevisiae.

1986 ◽  
Vol 50 (5) ◽  
pp. 1339-1340 ◽  
Author(s):  
Naoko SATO ◽  
Makoto SHIMOSAKA ◽  
Yasuki FUKUDA ◽  
Kousaku MURATA ◽  
Akira KIMURA
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Resistant Mutant ◽  
Yeast Saccharomyces Cerevisiae

A Saccharomyces cerevisiae mutant defines a new locus essential for resistance to the antitumour drug bleomycin

1996 ◽  
Vol 42 (8) ◽  
pp. 835-843 ◽  
Author(s):  
Dindial Ramotar ◽  
Jean-Yves Masson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Hydrogen Peroxide ◽  
Dna Repair ◽  
Chromosomal Translocation ◽  
Normal Growth ◽  
Fold Increase ◽  
Growth Conditions ◽  
Dna Lesions ◽  
Methyl Methanesulfonate ◽  
Yeast Saccharomyces Cerevisiae

The antitumor drug bleomycin can produce a variety of lesions in the cellular DNA by a free radical dependent mechanism. To understand how these DNA lesions are repaired, bleomycin-hypersensitive mutants were isolated from the yeast Saccharomyces cerevisiae. We report here the analysis of one mutant, DRY25, that showed extreme sensitivity to bleomycin. This mutant also exhibited hypersensitivity to hydrogen peroxide and t-butyl hydroperoxide, but showed no sensitivity to other DNA-damaging agents, including γ-rays, ultraviolet light, and methyl methanesulfonate. Subsequent analysis revealed that strain DRY25 was severely deficient in the repair of bleomycin-induced DNA lesions. Under normal growth conditions, DRY25 displayed a 3-fold increase in the frequency of chromosomal translocation that was further stimulated by 5- to 15-fold when the cells were treated with either bleomycin or hydrogen peroxide, but not by methyl methanesulfonate, as compared with the wild type. Genetic analysis indicated that the mutant defect was independent of the nucleotide excision, postreplication, or recombinational DNA-repair pathways. These data suggest that one conceivable defect of DRY25 is that it lacks a protein that protects the cell against oxidative damage to DNA. A clone that fully complemented DRY25 defect was isolated and the possible roles of the complementing gene are discussed.Key words: yeast, bleomycin, DNA repair, mutations.

A Saccharomyces cerevisiae phleomycin-sensitive mutant, phl40, is defective in the RAD6 DNA repair gene

1996 ◽  
Vol 42 (12) ◽  
pp. 1263-1266 ◽  
Author(s):  
Chuan Hua He ◽  
Jean-Yves Masson ◽  
Dindial Ramotar
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Anticancer Agent ◽  
Radiation Treatment ◽  
Dna Lesions ◽  
Exact Nature ◽  
Repair Gene ◽  
Yeast Saccharomyces Cerevisiae ◽  
Dna Repair Gene ◽  
Cellular Dna

The antibiotic bleomycin is used as an anticancer agent for treating a variety of tumours. The antitumour effect of bleomycin is related to its ability to produce lesions such as apurinic/apyrimidinic sites and single- and double-strand breaks in the cellular DNA. Phleomycin is a structurally related form of bleomycin, but it is not used as an anticancer agent. While phleomycin can also damage DNA, neither the exact nature of these DNA lesions nor the cellular process that repairs phleomycin-induced DNA lesions is known. As a first step to understand how eukaryotic cells provide resistance to phleomycin, we used the yeast Saccharomyces cerevisiae as a model system. Several phleomycin-sensitive mutants were generated following γ-radiation treatment and among these mutants, phl40 was found to be the most sensitive to phleomycin. Molecular analysis revealed that the mutant phl40 harbored a mutation in the DNA repair gene RAD6. Moreover, a functional copy of the RAD6 gene restored full phleomycin resistance to strain phl40. Our findings indicate that the RAD6 protein is essential for yeast cellular resistance to phleomycin.Key words: yeast, phleomycin, DNA repair, RAD6.

scholarly journals The RAD7, RAD16, and RAD23 genes of Saccharomyces cerevisiae: requirement for transcription-independent nucleotide excision repair in vitro and interactions between the gene products.

1997 ◽  
Vol 17 (2) ◽  
pp. 635-643 ◽  
Author(s):  
Z Wang ◽  
S Wei ◽  
S H Reed ◽  
X Wu ◽  
J Q Svejstrup ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Nucleotide Excision Repair ◽  
Protein Complex ◽  
Excision Repair ◽  
Dna Lesions ◽  
Yeast Saccharomyces Cerevisiae ◽  
Free System ◽  
Nucleotide Excision ◽  
A Cell

Nucleotide excision repair (NER) is a biochemical process required for the repair of many different types of DNA lesions. In the yeast Saccharomyces cerevisiae, the RAD7, RAD16, and RAD23 genes have been specifically implicated in NER of certain transcriptionally repressed loci and in the nontranscribed strand of transcriptionally active genes. We have used a cell-free system to study the roles of the Rad7, Rad16, and Rad23 proteins in NER. Transcription-independent NER of a plasmid substrate was defective in rad7, rad16, and rad23 mutant extracts. Complementation studies with a previously purified NER protein complex (nucleotide excision repairosome) indicate that Rad23 is a component of the repairosome, whereas Rad7 and Rad16 proteins were not found in this complex. Complementation studies with rad4, rad7, rad16, and rad23 mutant extracts suggest physical interactions among these proteins. This conclusion was confirmed by experiments using the yeast two-hybrid assay, which demonstrated the following pairwise interactions: Rad4 with Rad23, Rad4 with Rad7, and Rad7 with Rad16. Additionally, interaction between the Rad7 and Rad16 proteins was demonstrated in vitro. Our results show that Rad7, Rad16, and Rad23 are required for transcription-independent NER in vitro. This process may involve a unique protein complex which is distinct from the repairosome and which contains at least the Rad4, Rad7, and Rad16 proteins.

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