scholarly journals INDUCTION OF MITOTIC CROSSING OVER IN SACCHAROMYCES CEREVISIAE BY BREAKDOWN PRODUCTS OF DIMETHYLNITROSAMINE, DIETHYLNITROSAMINE, 1-NAPHTHYLAMINE AND 2-NAPHTHYLAMINE FORMED BY AN IN VITRO HYDROXYLATION SYSTEM

Genetics ◽  
1973 ◽  
Vol 74 (3) ◽  
pp. 433-442
Author(s):  
V W Mayer
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitotic Recombination ◽  
Crossing Over ◽  
Genetic Damage ◽  
Nitroso Group ◽  
Damage Potential ◽  
Test Conditions

ABSTRACT Dimethylnitrosamine and diethylnitrosamine, two potent carcinogens, are nonmutagenic when tested directly in microorganisms. Likewise 1-naphthylamine and 2-naphthylamine are also nonmutagenic but the N-hydroxy derivatives are mutagenic in microorganisms. Apparently these compounds require metabolism to breakdown products which are then the proximately active agents, and microorganisms lack the enzymes necessary to effect this conversion. These compounds are mutagenic in Saccharomyces after conversion to breakdown products in an in vitro hydroxylation medium. The induction of mitotic crossing over in Saccharomyces cerevisiae by breakdown products of dimethylnitrosamine, diethylnitrosamine, 1-naphthylamine and 2-naphthylamine formed in the Udenfriend hydroxylation medium is reported in this communication. Mitotic crossing over was detected as red sectored colonies resulting from induced homozygosity of the ade2 marker. Dimethylamine and diethylamine, which lack the nitroso group of the nitrosamines, did not induce mitotic crossing over under any of the test conditions. To further confirm that the induced sectored colonies were the result of mitotic crossing over they were tested for the presence of reciprocal products. The expected reciprocal products were found in over 67% of the isolates tested. The significance and practicality of using mitotic recombination as an indicator of genetic damage potential of chemicals is discussed.

scholarly journals Spontaneous mitotic recombination in yeast: the hyper-recombinational rem1 mutations are alleles of the RAD3 gene.

Genetics ◽  
1988 ◽  
Vol 119 (2) ◽  
pp. 289-301
Author(s):  
B A Montelone ◽  
M F Hoekstra ◽  
R E Malone
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Gene Conversion ◽  
Excision Repair ◽  
Mitotic Recombination ◽  
Crossing Over ◽  
Wild Type ◽  
Recombination Repair ◽  
Mitotic Gene Conversion ◽  
Type Gene ◽  
Repair Genes

Abstract The RAD3 gene of Saccharomyces cerevisiae is required for UV excision-repair and is essential for cell viability. We have identified the rem1 mutations (enhanced spontaneous mitotic recombination and mutation) of Saccharomyces cerevisiae as alleles of RAD3 by genetic mapping, complementation with the cloned wild-type gene, and DNA hybridization. The high levels of spontaneous mitotic gene conversion, crossing over, and mutation conferred upon cells by the rem1 mutations are distinct from the effects of all other alleles of RAD3. We present preliminary data on the localization of the rem1 mutations within the RAD3 gene. The interaction of the rem1 mutant alleles with a number of radiation-sensitive mutations is also different than the interactions reported for previously described (UV-sensitive) alleles of RAD3. Double mutants of rem1 and a defect in the recombination-repair pathway are inviable, while double mutants containing UV-sensitive alleles of RAD3 are viable. The data presented here demonstrate that: (1) rem1 strains containing additional mutations in other excision-repair genes do not exhibit elevated gene conversion; (2) triple mutants containing rem1 and mutations in both excision-repair and recombination-repair are viable; (3) such triple mutants containing rad52 have reduced levels of gene conversion but wild-type frequencies of crossing over. We have interpreted these observations in a model to explain the effects of rem1. Consistent with the predictions of the model, we find that the size of DNA from rem1 strains, as measured by neutral sucrose gradients, is smaller than wild type.

Ca-, Mg- és K-sók hatása egyes nehézfémek Saccharomyces cerevisiae törzsekre gyakorolt toxicitására

2008 ◽  
Vol 57 (1) ◽  
pp. 161-175
Author(s):  
Nikoletta Tóth ◽  
Hamuda Hosam E. A. F. Bayoumi ◽  
Attila Palágyi ◽  
Mihály Kecskés
Keyword(s):  
Saccharomyces Cerevisiae

Az utóbbi években egyre több tanulmány született a mikroorganizmusok nehézfém akkumulációjáról. A mikroszervezetek nehézfémekkel szembeni tűrőképességére és nehézfém felvételére a bioremediációs hasznosíthatóságuk miatt egyre nagyobb figyelmet fordítanak. A mikroorganizmusok tulajdonságai nagyon jól hasznosíthatóak a talajszennyezés monitorozásánál. A toxikus nehézfémek komoly ökológiai problémát jelentenek környezetünkben, ezért kiemelkedő fontosságú a nehézfémekkel szennyezett talajok tisztítása. In vitro , két S. cerevisiae törzs (NSS5099 és NSS7002) nehézfémekkel szembeni toleranciáját vizsgáltuk. A két törzs szaporodási kinetikáját olyan táptalajon tanulmányoztuk, amelyhez 50 µM koncentrációban adtunk Cu 2+ -, Pb 2+ -, Cd 2+ - vagy Ni 2+ -ionokat. A vizsgált nehézfémek élesztőtörzsekre gyakorolt toxicitása csökkenő sorrendben: Cu 2+ > Pb 2+ > Cd 2+ > Ni 2+ . A 350 µM koncentrációjú Cu 2+ , Pb 2+ vagy Cd 2+ és 450 µM koncentrációjú Ni 2+ 48 órás inkubációt követően 50%-kal csökkentette az élősejtek számát. Amikor a nehézfémek táptalajba történő adagolása előtt 50 mM Ca(HCO 3 ) 2 , 75 mM MgSO 4 , vagy 150 mM K 2 SO 4 -ot adtunk a közeghez csökkent a nehézfémek sejtekre gyakorolt toxicitása, és több sejt maradt életben. A 350 és 450 µM koncentrációban lévő nehézfémek toxicitását a fémsók 40%-kal csökkentették. A kapott eredmények alapján az NSS7002 törzs sokkal alkalmasabbnak bizonyult a nehézfémekkel szennyezett talajok tisztítására, mint az NSS5099._

scholarly journals The Conversion Gradient at HIS4 of Saccharomyces cerevisiae. II. A Role for Mismatch Repair Directed by Biased Resolution of the Recombinational Intermediate

Genetics ◽  
1999 ◽  
Vol 153 (2) ◽  
pp. 573-583 ◽  
Author(s):  
Henriette M Foss ◽  
Kenneth J Hillers ◽  
Franklin W Stahl
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Synthesis ◽  
Mismatch Repair ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Holliday Junction ◽  
Crossing Over ◽  
Gradient Type ◽  
Salient Features

AbstractSalient features of recombination at ARG4 of Saccharomyces provoke a variation of the double-strand-break repair (DSBR) model that has the following features: (1) Holliday junction cutting is biased in favor of strands upon which DNA synthesis occurred during formation of the joint molecule (this bias ensures that cutting both junctions of the joint-molecule intermediate arising during DSBR usually leads to crossing over); (2) cutting only one junction gives noncrossovers; and (3) repair of mismatches that are semirefractory to mismatch repair and/or far from the DSB site is directed primarily by junction resolution. The bias in junction resolution favors restoration of 4:4 segregation when such mismatches and the directing junction are on the same side of the DSB site. Studies at HIS4 confirmed the predicted influence of the bias in junction resolution on the conversion gradient, type of mismatch repair, and frequency of aberrant 5:3 segregation, as well as the predicted relationship between mismatch repair and crossing over.

scholarly journals Suppressor Analysis of the Saccharomyces cerevisiae Gene REC104 Reveals a Genetic Interaction With REC102

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1261-1272 ◽  
Author(s):  
Laura Salem ◽  
Natalie Walter ◽  
Robert Malone
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Null Allele ◽  
Genetic Interaction ◽  
In Vitro Mutagenesis ◽  
Conditional Mutations ◽  
Suppressor Analysis

Abstract REC104 is a gene required for the initiation of meiotic recombination in Saccharomyces cerevisiae. To better understand the role of REC104 in meiosis, we used an in vitro mutagenesis technique to create a set of temperature-conditional mutations in REC104 and used one ts allele (rec104-8) in a screen for highcopy suppressors. An increased dosage of the early exchange gene REC102 was found to suppress the conditional recombinational reduction in rec104-8 as well as in several other conditional rec104 alleles. However, no suppression was observed for a null allele of REC104, indicating that the suppression by REC102 is not “bypass” suppression. Overexpression of the early meiotic genes REC114, RAD50, HOP1, and RED1 fails to suppress any of the rec104 conditional alleles, indicating that the suppression might be specific to REC102.

scholarly journals Regulation of Mitotic Homeologous Recombination in Yeast: Functions of Mismatch Repair and Nucleotide Excision Repair Genes

Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 133-146 ◽  
Author(s):  
Ainsley Nicholson ◽  
Miyono Hendrix ◽  
Sue Jinks-Robertson ◽  
Gray F Crouse
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mismatch Repair ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Mitotic Recombination ◽  
Inverted Repeats ◽  
Replication Errors ◽  
Nucleotide Excision ◽  
Homeologous Recombination ◽  
Repair Genes

Abstract The Saccharomyces cerevisiae homologs of the bacterial mismatch repair proteins MutS and MutL correct replication errors and prevent recombination between homeologous (nonidentical) sequences. Previously, we demonstrated that Msh2p, Msh3p, and Pms1p regulate recombination between 91% identical inverted repeats, and here use the same substrates to show that Mlh1p and Msh6p have important antirecombination roles. In addition, substrates containing defined types of mismatches (base-base mismatches; 1-, 4-, or 12-nt insertion/deletion loops; or 18-nt palindromes) were used to examine recognition of these mismatches in mitotic recombination intermediates. Msh2p was required for recognition of all types of mismatches, whereas Msh6p recognized only base-base mismatches and 1-nt insertion/deletion loops. Msh3p was involved in recognition of the palindrome and all loops, but also had an unexpected antirecombination role when the potential heteroduplex contained only base-base mismatches. In contrast to their similar antimutator roles, Pms1p consistently inhibited recombination to a lesser degree than did Msh2p. In addition to the yeast MutS and MutL homologs, the exonuclease Exo1p and the nucleotide excision repair proteins Rad1p and Rad10p were found to have roles in inhibiting recombination between mismatched substrates.

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