PubMed Health⌕ Search

Biomedical subjects

F K Zimmermann

Publications and source records attributed to F K Zimmermann.

At least 91 records · Page 5Linked to original sources
PubMed1977

Mutants of Saccharomyces cerevisiae resistant to carbon catabolite repression.

Mutants with defective carbon catabolite repression have been isolated in the yeast Saccharomyces cerevisiae using a selective procedure. This was based on the fact that invertase is a glucose repressible cell wall enzyme which slowly hydrolyses raffinose to yield fructose and that the inhibitory effects of 2-deoxyglucose can be counteracted by fructose. Repressed cells were plated on a raffinose--2-doexyglucose medium and the resistant cells growing up into colonies were tested for glucose non-repressible invertase and maltase. The yield of regulatory mutants was very high. All were equally derepressed for invertase and maltase, no mutants were obtained with only non-repressible invertase synthesis which was the selected function. A total of 61 mutants isolated in different strains were allele tested and could be attributed to three genes. They were all recessive. Mutants in one gene had reduced hexokinase activities, the other class, located in a centromere linked gene, had elevated hexokinase levels and was inhibited by maltose. Mutants in a third gene were isolated on a 2-deoxyglucose galactose medium and had normal hexokinase levels. A partial derepression was observed for malate dehydrogenase in all mutants. Isocitrate lyase, however, was still fully repressible.

Carbon↗
PubMed1977

Genetics of carbon catabolite repression in Saccharomycess cerevisiae: genes involved in the derepression process.

A recessive mutant cat1-1, wild type CAT1, was isolated in Saccharomyces cerevisiae. It did not grow on glycerol nor ferment maltose even with fully constitutive, glucose resistant maltase synthesis. It prevented derepression of isocitrate lyase, fructose-1,6-diphosphatase and maltase in a constitutive but glucose sensitive maltase mutant. Derepression of malate dehydrogenase was retarded and slowed down. Sucrose fermentation and invertase synthesis was not affected. Respiration was normal. From this mutant, two reverse mutants were isolated. One was recessive, acted as a suppressor of cat1-1 and was called cat2-1, wild type CAT2; the other was dominant and allelic to CAT1 and designated CAT1-2d and cat2-1 caused an earlier derepression of enzymes studied but did not affect the repressed nor the fully derepressed enzyme levels. CAT1-2d and cat2-1 did not show any additive effects. It is proposed that carbon catabolite repression acts in two ways. The direct way represses synthesis of sensitive enzymes, during growth on repressing carbon sources whereas the other way regulates the derepression process. After alleviation of carbon catabolite repression, gene CAT1 becomes active and prevents the activity of CAT2 which functions as a repressor of sensitive enzyme synthesis. The CAT2 gene product has to be eliminated before derepression can actually occur. The time required for this causes a delay in derepression after the depletion of a repressible carbon source. cat1-1 cannot block CAT2 activity and therefore, derepression is blocked. cat2-1 is inactive and derepression can start after carbon catabolite repression has ceased. CAT1-2d permanently active as a repressor of CAT2 and eliminates the delay in derepression.

Carbon↗
PubMed1977

Study on cytological effects of carofur -- a new mutagen.

Chinese hamster cells (line V-79) and human leukocytes in vitro and mice of the CBA strain were treated with carofur (also called nifurprazinum), an antibacterial agent of pharmaceutical importance. At concentrations as low as 20 ppm, the in vitro treatments of cells of Chinese hamster and human lymphocytes expressed chromosome aberrations, almost exclusively of deletion type. This effect resembles that of fluorodeoxyuridine but may not necessarily reflect the same basic mechanism involved. When Chinese hamster cells were treated with 5 ppm or more of carofur for 24 hr, a 3-fold increase in the frequency of somatic sister chromatid exchanges was observed. An interesting phenomenon of "centromeric association" was observed in the bone marrow cells of mice treated with carofur, where the centromeres of the acrocentric chromosomes were oriented towards each other in groups of 2's or more.

Animals↗
PubMed1976

Thermal inactivation of maltase and its application to temperature-sensitive mutants of yeast.

Three maltases have been detected in each of a variety of strains of Saccharomyces. These are present in constant relative amounts in a particular strain and are characterized by reproducible first order thermal decay constants. Four of six mutants, temperature-sensitive for maltose fermentation, lack the maltase of intermediate stability. This deficiency appears to be the basis of the temperature sensitivity, and it is concluded that these strains carry a mutation in the structural gene for that maltase.

Genes↗
PubMed1976

The role of mitochondria in carbon catabolite repression in yeast.

The role of mitochondria in carbon catabolite repression in Saccharomyces cerevisiae was investigated by comparing normal, respiratory competent (RHO) strains with their mitochondrially inherited, respiratory deficient mutant derivatives (rho). Formation of maltase and invertase was used as an indicator system for the effect of carbon catabolite repression on carbon catabolic reactions. Fermentation rates for glucose, maltose and sucrose were the same in RHO and rho strains. Specific activities of maltase and invertase were usually higher in the rho-mutants. A very pronounced difference in invertase levels was observed when cells were grown on maltose; rho-mutants had around 30 times more invertase than their RHO parent strains. The fact that rho-mutants were much less sensitive to carbon catabolite repression of invertase synthesis than their RHO parents was used to search for the mitochondrial factor(s) or function(s) involved in carbon catabolite repression. A possible metabolic influence of mitochondria on this system of regulation was tested after growth of RHO strains under anaerobic conditions (no respiration nor oxidative phosphorylation), in the presence of KCN (respiration inhibited), dinitrophenol (uncoupling of oxidative phosphorylation) and of both inhibitors anaerobic conditions and dinitrophenol had no effect on the extent of invertase repression. KCN reduced the degree of repression but not to the level found in rho-mutants. A combination of both inhibitors gave the same results as with KCN alone. Erythromycin and chloramphenicol were used as specific inhibitors of mitochondrial protein synthesis. Erythromycin prevented the formation of mitochondrial respiratory systems but did not induce rho-mutants under the conditions used. However, repression of invertase was as strong as in the absence of the inhibitor. Chloramphenicol led only to a slight reduction of the respiratory systems and did not affect invertase levels. A combination of both antibiotics had about the same effect as growth in the presence of KCN. The results showed that mitochondria are involved in carbon catabolite repression and they cause an increase in the degree of repression. These effects cannot be due to mere metabolic activities nor to factors made on the mitochondrial protein synthesizing machinery. This regulatory role of mitochondria is observed as long as an intact mitochondrial genome is maintained.

Carbon↗
PubMed1975

Mutagen specificity in the induction of mitotic crossing-over in Saccharomyces cerevisiae.

A diploid yeast strain, D81, was constructed heterozygous for seven recessive markers linked on the left arm of chromosome VII to study the localization of induced mitotic crossing over. The mutagens used were carofur also called nifurprazinum (1-(5-nitro-2-furyl)-2-(6-amino-3-pyridazyl)-ethylene hydrochloride), diepoxybutane, ethylmethanesulfonate, nitrous acid and 1-nitrosoimidazolidinone-2. All agents induced high frequencies of mitotic crossing over at doses exerting only a low degree of killing. The distribution of recombinational events was compared for five intervals. The distribution pattern of spontaneous mitotic crossing over was different from all the patterns obtained after mutagenic treatments. Nitrous acid and diepoxybutane induced the same pattern, which was different from the patterns induced by carofur, EMS and 1-nitrosoimidazolidinone-2. The patterns induced by the latter three mutagens were again different amongst each other. Repeat experiments showed that the patterns induced by a given mutagen were reproducible. Tetrad analysis with a representative sample of segregants induced by diepoxybutane and carofur showed that the treatments actually induced mitotic crossing-over. The pattern of meiotic recombinational events was different from those of spontaneous and mutagen induced mitotic recombination. Inducibility of mitotic crossing-over was low at the proximal and distal ends of the chromosome arm and highest in the middle. Each interval showed a different response to those mutagens that differed in their patterns of induced mitotic crossing over. The observed mutagen specific effects are considered as an indication of mutagen specificity. No plausible explanation for mutagen specificity could be given. However, the data presented reveal the same situation as found in induction of chromosome breaks, as reported by other authors. Apparently, mutagen specificity is quite a general phenomenon even for genetic effects in larger intervals of a chromosome.

Chromosome Mapping↗
PubMed1975

Procedures used in the induction of mitotic recombination and mutation in the yeast Saccharomyces cerevisiae.

Techniques are described for the use of various yeast strains to detect the induction of (1) mitotic crossing-over, (2) mitotic gene conversion, (3) forward mutation and (4) reverse mutation. The technique for the detection of mitotic crossing over is based on a diploid that carries two different alleles of the gene locus ade2. These alleles differ in their extent of colony pigmentation engendered on low-adenine media, and they complement each other to the effect that the diploid is white. Mitotic crossing over results in the formation of twin-sectored colonies with a red and a pink sector. The technique for the detection of mitotic gene conversion is based on the use of a heteroallelic diploid carrying two non-complementing alleles that cause a nutritional requirement. Mitotic gene conversion leads to the restoration of intact and dominant wild-type alleles that alleviate the nutritional requirement so that convertant cells can be selected on a minimal medium. The forward mutation technique is based on the use of a haploid strain with a defect in the ade2-gene locus which causes the formation of red colonies. Induction of forward mutation in a number of other loci prevents the accumulation of this red pigment so that induction of mutation can be detected by the formation of pink and white colonies. The reverse mutation technique is based on the restoration or compensation of a mutational defect causing a growth requirement. Mutants can be selected for on a minimal medium.

Adenine↗