[Gene RAD31 is identical to gene MEC1 of yeast Saccharomyces cerevisiae].

The earlier identified gene RAD31 was mapped on the right arm of chromosome II in the region of gene MEC1 localization. Epistatic analysis demonstrated that the rad31 mutation is an allele of the MEC1 gene, which allows further designation of the rad31 mutation as mec1-212. Mutation mec1-212, similar to deletion alleles of this gene, causes sensitivity to hydroxyurea, disturbs the check-point function, and suppresses UV-induced mutagenesis. However, this mutation significantly increases the frequency of spontaneous canavanine-resistance mutations induced by disturbances in correcting errors of DNA replication and repair, which distinguishes it from all identified alleles of gene MEC1.

[The Rdh54 protein role in regulation of DNA repair in yeast Saccharomyces cerevisiae].

In this work, we present the evidences of the involvement of Rdh54 in coordination of DNA repair by several pathways. Previously, we isolated rdh54-29 point mutation demonstrating unique properties different from the full deletion of RDH54 gene. Epistatic interaction between rdh54-29 and apn1delta mutations discloses the function of Rdh54p in the process of base excision repair. However, rdh54-29 mutant exhibits sensitivity to many DNA damaging agents including UV light, methylmethanesulphonate and nitrous acid. Such pleiotrophic effect of rdh54-29 mutation may indicate the role of Rdh54p in the regulation of different DNA repair systems. To check this hypothesis, we estimated the effect of rdh54-29 mutation on recombination and mutagenesis. The data confirm the involvement of Rdh54p in coordination of different DNA repair systems including mutagenic and recombinagenic pathways as well as nucleotide excision repair. Rdh54p presumably operates via chromatin remodulation at the site of damage rendering DNA accessible to the DNA repair enzymes.

[RAD29 and RAD31--new genes from Saccharomyces cerevisiae yeasts, participating in control of DNA repair. II. Clarification of possible functions of these genes]. / RAD29 i RAD31--novye geny drozhzhei Saccharomyces cerevisiae, uchastvuiushchie v kontrole reparatsii DNK. II. Vyiasnenie vozmozhnykh funktsii étikh genov.

Possible functions of previously described genes RAD29 and RAD31 involved in DNA repair were determined by analyzing the interaction between these genes and mutations in the genes of the three basic epistatic groups: RAD3 (nucleotide excision repair), RAD6 (error-prone mutagenic repair system), RAD52 (recombination repair pathway), and also the apn1 mutation that blocks the synthesis of major AP endonuclease (base excision repair). The results obtained in these studies and the estimation of the capability for excision repair of lesions induced by 8-metoxipsoralen and subsequent exposure to long-wavelength UV light in mutants for these genes led to the assumption that the RAD29 and RAD31 genes are involved in yeast DNA repair control.

[RAD29 and RAD31--new genes from Saccharomyces cerevisiae yeasts, participating in control of DNA repair. Isolation and genetic study of mutants]. / RAD29 i RAD31--novye geny drozhzhei Saccharomyces cerevisiae, uchastvuiushchie v kontrole reparatsii DNK. Izoliatsiia i geneticheskoe izuchenie mutantov.

Base excision repair (BER) and nucleotide excision repair (NER) are two main cellular responses to DNA damage induced by various physical and chemical factors. After exposure of the strain that carries the NER-blocking rad2 mutation to UV light, several mutants hypersensitive to the UV light lethal action and simultaneously sensitive to methylmethanesulphonate (MMS) were isolated. Two of these mutants (Uvs64 and Uvs212) were examined in detail. The mutants were found to carry recessive, monogenically inherited lesions that had pleiotropic, though different, phenotypes: both mutants were also sensitive to nitrous acid (HNO2), whereas Uvs212 was sensitive to hydrogen peroxide as well. Moreover, the homozygote for the uvs212 mutation, but not for uvs64, blocks the sporulation. Since the mutations examined were not allelic to any of the known rad mutations that cause MMS sensitivity or to each other, it is concluded that two new genes involved in the control of yeast DNA repair were detected. Furthermore, these genes were mapped to different regions of the right arm of chromosome 2 where repair genes were not found. Thus, two new genes, designated RAD29(UVS64) and RAD31(UVS212) and probably involved in base excision repair, were identified.

RAD58 (XRS4)--a new gene in the RAD52 epistasis group.

The RAD58 (XRS4) gene of Saccharomyces cerevisiae has been previously identified as a DNA repair gene. In this communication, we show that RAD58 also encodes an essential meiotic function. The spore inviability of rad58 strains is not rescued by a spo13 mutation. The rad50 mutation suppresses spore inviability of a spo13 rad58 strain suggesting that RAD58 acts after RAD50 in meiotic recombination. The rad58-4 mutation does not prevent mitotic recombination events. Haploid rad58 cells fail to carry out G2-repair of gamma-induced lesions, whereas rad58/rad58 diploids are able to perform some diploid-specific repair of these lesions.

[A system for analysis of yeast mutants deficient in the genetic recombination process]. / Sistema dlia analiza mutantov drozhzhei s narusheniiami protsessa geneticheskoi rekombinatsii.

A system of molecular-genetic methods intended for analysis of yeast Rec-mutants was developed. A number of plasmids containing noncomplementing mutations in the ADE2 gene and different selective markers were constructed. The system was based upon the phenomenon of interplasmid intragenic recombination during transformation and mitotic division. Transformation of yeast cells with the plasmid containing two long right repeats allowed to estimate the efficiency of intraplasmid crossing-over. The system also allows to study plasmid-chromosomal interaction. To check up the system proposed, a well known rad50 and rad52 mutants were used. The rad52-1 mutation was found sharply decreased the levels both intra- and interplasmid recombination events. On the other hand, rad50-1 mutation has not influences or stimulates the processes. Thus, the system proposed efficiently distinguishes the mutants deficient in different stages of recombinational process.

[Genetic and biochemical study of yeast acid phosphatases. XI. Gene ACP80 controls inorganic phosphate transport]. / Genetiko-biokhimicheskoe izuchenie kislykh fosfataz drozhzhei. Soobshchenie XI. Gen ACP80 kontroliruet transport neorganicheskogo fosfata.

Mutations in the gene ACP80 which simultaneously lead to constitutive synthesis of repressible acid phosphatases, resistance to 1 X 10(-3) M sodium arsenate and to the disturbance of phosphate uptake in the cell were obtained. Mutations suppressible by ochre suppressors in this gene were identified. The conclusion that the gene ACP80 encodes a protein which participates in the phosphate transport into the cell, was drawn. A selective method for isolation of mutations in this gene is proposed.

[Genetico-biochemical study of the acid phosphatases of Saccharomyces cerevisiae yeasts. X. Analysis of mutations arising in gene acp3]. / Genetiko-biokhimicheskoe izuchenie kislykh fosfataz drozhzhei Saccharomyces cerevisiae. Soobshchenie X. Analiz mutatsii, voznikaiushchikh v gene acp3.

Mutations leading to decrease or absence of orthophosphate-repressible acid phosphatase activity have been studied. It is shown that these mutations can arise in three genes: acp1, acp2 and acp3, which are not linked. Genes acp1 and acp2 have been studied previously; the existence of the gene acp3 is demonstrated in this paper. It is established that all mutations in the acp3 gene are recessive, are leaky and epistatic to the constitutive mutations in all known regulatory genes for acid phosphatase II synthesis - acp4, acp80, acp81, acp82, acp83, and acp84. The gene acp3 is not linked with these regulatory genes, but it is closely linked with the structural gene for constitutive acid phosphatase - pho1 (D=0.33+/-0.20 cM). The pho1 gene has been recently located on the right arm of chromosome II on the left of the gene lys2. Mutations lacking activity of constitutive and repressible acid phosphatases simultaneously have been found. It is shown that these mutations are allelic to mutations in the gene acp3 and pho1 simultaneously. Two hypotheses are proposed about the role of the gene acp3: the gene controls the positive factor for the repressible acid phosphatase synthesis or the structure of the enzyme.

[Genetico-biochemical study of acid phosphatases in Saccharomyces cerevisiae yeast. V. Genetic control of regulation of acid phosphatase II synthesis]. / Genetiko-biokhimicheskoe izuchenie kislykh fosfataz drozhzhei Saccharomyces cerevisiae. Soobshchenie V. Geneticheskii kontrol' reguliatsii sinteza kisloi fosfatazy II

Regulation of exocellular enzyme acid phosphatase 2 synthesis is studied. 21 mutants with consitutive synthesis of this enzyme are obtained by UV-irradiation. All mutants were recessive and were distributed among 3 complementation groups ACP80, ACP81, ACP82. Two groups, ACP80 and ACP81 corresponded to two different genes, which showed no linkage with ACP1, ACP2 and PHO1 genes. The type of synthesis of acid phosphatase 2 in strains acp1 acp80, acp1 acp81, acp2 acp80, acp2 acp81 is determined, and a conclusion is made about the participation of ACP2 gene in the regulation of acid phosphatase 2 synthesis. It is shown that some mutations in PHO1 gene, which block the activity of acid phosphatase 1, influence the activity and regulation of acid phosphatase 2.

[Genetic-biochemical study of acid phosphatases from Saccharomyces cerevisiae yeasts. IV. Genetic control of acid phosphatase II activity]. / Genetiko-biokhimicheskoe izuchenie kislykh fosfataz drozhzhei Saccharomyces cerevisiae. Soobshchenie IV. Geneticheskii kontrol' aktivnosti kisloi fosfatazy II

Genetic control of exocellular acid phosphatase of yeast Saccharomyces cerevisiae (acph 2) is studied. 64 mutants with the impaired activity of acid phosphatase have been obtained by UV-irradiation. All the mutations have been distributed among 4 genes: ACP1, ACP2, ACP3, ACP4 using functional and recombinational tests for allelism. It is shown that mutations in genes ACP1--ACP3 are recessive, but in the gene ACP4--dominant. The gene ACP4 is found to be located 0.41+/-0.064 in strains from centromere and to have no linkage with ACP1. Possible functions of genes studied are under discussion.