The REC41 gene of Saccharomyces cerevisiae: isolation and genetic analysis.

Recombination-deficient strains have been proven useful for the understanding of the genetic control of homologous recombination. As the genetic screens used to isolate recombination-deficient (rec(-)) yeast mutants have not been saturated, we sought to develop a simple colony color assay to identify mutants with low or elevated rates of recombination. Using this system we isolated a collection of rec(-) mutants.

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.

[Analysis of maintenance of redundant genetic structures in the yeast Saccharomyces cerevisiae: effect of mutations cdc28-srm and srm1].

The effects of nuclear gene mutations cdc28-srm and srm1 on the maintenance of various recombinant facultative genetic structures (FGSs) in Saccharomyces cerevisiae were studied. These structures are ARS1 TRP1 mini-coils, noncentromeric circular plasmids containing various ARS elements, and extended linear yeast artificial chromosomes (YAC). These mutations led to an increase in the mitotic stability of some of the FGS tested and the disturbed maintenance of the others.

[The xrs2 gene controls recombination repair in yeast].

The XRS2 mutants of Saccharomyces cerevisiae are sensitive to ionizing and UV irradiation, have altered rates of spontaneous and induced mitotic recombination and are defective in meiosis. Haploid xrs2 cells bearing a mutation in RAD51 or RAD52 genes are more sensitive to gamma-rays than respective single mutants. On the other hand, double mutants xrs2-6 and rad50-1 (cdc40-1, radH) have the same radiosensitivity as the single mutants.

[Rec41--a new gene, participating in the control of recombination in Saccharomyces cerevisiae yeast].

We isolated a collection of rec- mutants. The mutant rec41 from this collection was studied in detail. The mutant demonstrated a reduced level of interplasmid recombination, did not grow at the elevated temperature (36 degrees C) and was sensitive to gamma-rays but not to ultraviolet irradiation.

[A system for analysis of yeast mutants deficient in the genetic recombination process].

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.

[A new system of selecting yeast mutants with disrupted genetic recombination processes].

A new convenient system for isolation of the yeast mutants deficient in the genetical recombination is proposed. The chimeric plasmids constructed to carry the noncomplimenting mutant copy of the yeast ADE2 gene and different selectable yeast markers (LEU2 or TRP1 genes) are the basis for the system. Interplasmid intragenic recombination of ADE2 gene alleles in yeast cells transformed by two chimeric plasmids results in appearance of the secondary white prototrophic clones covering the primary red colony.

The start gene CDC28 and the genetic stability of yeast.

The cdc28-srm mutation in Saccharomyces cerevisiae decreases spontaneous and induced mitochondrial rho- mutability and the mitotic stability of native chromosomes and recombinant circular minichromosomes. The effects of cdc28-srm on the genetic stability of cells support the hypothesis that links cell cycle regulation in yeast to changes in chromatin organization dependent on the start gene CDC28 (Hayles and Nurse, 1986).

[Genetic analysis of mitochondrial rho-mutability in Saccharomyces yeasts. VI. Quantitative characteristics of the effect of mutation srm5 on the mitochondrial stability of natural and recombinant genetic structures].

The srm5 mutation diminishes the spontaneous rho- mutation rate by an order of magnitude. Frequency of rho- mutations is 500 times lower in homozygous cultures, as compared with those of normal SRM+/SRM+ diploids. The rate of spontaneous loss of extra chromosome IV is about 25 times higher in srm5 disomes, as compared with SRM+ ones.

[Genetic control of plasmid recombination in the cotransformation of Saccharomyces cerevisiae: the role of RAD52 and FLP genes].

In our earlier works we observed high frequency of recombination between two chimeric plasmids of different types, when they were introduced into yeast cells via cotransformation. Incapability of one of these plasmids to replicate autonomously in yeast cell is the necessary condition for such recombination. The high efficiency of this process point to the differences between interplasmid recombination and other types of yeast recombination.

[Insertion of transposon Tn9 into the spinal (Escherichia coli-Saccharomyces cerevisiae) plasmids and the expression of the prokaryotic gene of chloramphenicol resistance in yeast cells].

Transposon Tn9 carrying camr gene which controls resistance to chloramphenicol has been introduced in vivo (in cells of Escherichia coli) into two chimeric shuttle plasmids pYF91 and YEp13. These plasmids consist of the different parts of the E. coli plasmid pBR322, the yeast 2mkm DNA plasmid and the yeast LEU2 structural gene.

[Repair and mutagenesis in Escherichia coli cells on induction in the DNA of monoadducts and cross-links by light-activated 8-methoxypsoralen. Dependence on the uvrA and polA genes].

Relative efficiency of (psoralen + near UV)-induced monoadducts and inter-strand cross-links of Escherichia coli cells has been studied, as well as the role of uvrA and polA genes in these processes. Inter-strand cross-links have been shown to be more effective, as compared with monoadducts both in cell inactivation and in mutagenesis. At least 3 ways for repair of DNA carrying monoadducts have been found, and only 2 for DNA carrying inter-strand cross-links, each of these being controlled by genes uvrA and polA in different modes.