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J Soska

Publications and source records attributed to J Soska.

At least 37 records · Page 2Linked to original sources
PubMed1984

The immI region of Salmonella phage P22. 1. Characterisation of the mutants P22 cir4-1, P22 cir5-1 and P22 cir6-1.

Salmonella phage mutants P22 cir4-1, P22 cir5-1 and P22 cir6-1 at 37 degrees C form more or less clear plaques. The mutants complement each other and clear mutations of the immC region (Prell et al. 1983). The mutants exhibit a strongly reduced frequency of lysogenisation, but form stable prophages. The low frequency of lysogenisation of P22 cir5-1 and of P22 cir6-1 is suppressed by an additional ant- mutation. Similarly, about 50% of turbid plaque revertants of both mutants carry ant- suppressor mutations. This suggests interference by the cir5-1 and cir6-1 mutations with the expression of gene ant. In contrast, the cir4-1 mutation seems not to interfere with ant expression, the latent periods of P22 cir4-1 and P22 cir5-1 are reduced and extended, respectively. The geneticly related Salmonella phage L carries a gene able to complement P22 cir4-1.

Genes, Viral↗
PubMed1984

The immI region of Salmonella phage P22. 2. The influence of the cir mutations on the regulation of antirepressor synthesis.

The effects were studied of three clear plaque mutations of phage P22 (cir4-1, cir5-1 and cir6-1) on antirepressor synthesis. The mutant site cir4-1 has no influence on the expression of gene ant. The cir5-1 and cir6-1 mutations prevent the repression of early ant synthesis shortly after infection: P22 cir5-1 exhibits a strong ant-overproduction because it renders the cir5 repressor protein defective for turning off early ant expression (Harvey et al. 1981). P22 cir6-1 exhibits only a low level of constitutive ant synthesis insensitive to cir5-directed repression. Complementation experiments between P22 wild type or mutant in the cir5 or cir6 sites reveal the following phenotypes of the cir6-1 mutation: (1) The cir6-1 site behaves as a weak promotor site insensitive to cir5-directed repression of ant synthesis. (2) In the P22 cir5-1 cir6-1 double recombinant the cir6-1 site is cis dominant preventing ant overproduction as observed in simple P22 cir5-1 infections. (3) Some of the deficient phenotypes of P22 cir6-1 can be complemented by co-infecting P22 mutants carrying a cir6+ allele. These results are explained by the following model: The active cir5 repressor protein is a dimer (or oligomer) and the cir5-1 and cir6-1 mutations map in different domains influencing the repressing as well as the dimer forming activities of this protein. Which particular cir6-1 phenotype is observed depends on the experimental conditions employed, and on the promotor site (either pANT or cir6-1) from which ant expression procedes.(ABSTRACT TRUNCATED AT 250 WORDS)

Gene Expression Regulation↗
PubMed1984

[Personal experience with in vitro fertilization and embryo transfer].

The causes of sterility could be better characterized in 49 so called complex laparoscopies with estimation of sperm ascension and extraction of oocytes following hormonal stimulation. Oocytes could be obtained in sterility operations. They have been fertilized and transferred into the tubes, with the result of 2 pregnancies after 49 such procedures. Up to now there is no late pregnancy after 115 in vitro fertilizations and 53 embryo transfer into the uterus.

Embryo Transfer↗
PubMed1981

Repression of ant synthesis early in the lytic cycle of phage P22.

Using SDS-polyacrylamide gel electrophoresis to study the early expression of P22 genes we show that early expression of the ant-gene (imm I region) is turned off after 6-8 min, independent of the 'late' acting mnt-repressor. A semi-clear mutant called cir5 is defective for this early ant turn-off. The mutation cir5 maps in the imm I region of P22 between genes mnt and ant. P22 cir5 mutants are defective for a repressor which acts in trans to regulate early ant synthesis. There appears to be no absolute requirement of the cir5 allele for the establishment of lysogeny. The overproduction of ant in the P22 cir5 mutant leads to a marked increase in abortive infections, killing the infected cells. The cir5-phenotype can be suppressed by an ant- mutation.

Gene Expression Regulation↗
PubMed1981

Mutagenic activities of simple nitrofuran derivatives. I. Comparison of related compounds in the phage inductest, chloroplast-bleaching and bacterial-repair and mutagenicity tests.

Several simple furan and nitrofuran compounds were tested for mutagenicity and related biological activities, in the Ames test, the bacterial repair test, the prophage-induction test and the chloroplast-bleaching test. Only those compounds having the nitro-group were found to be active in the test. If the nitro-group was in the beta instead of the alpha position, the mutagenic activity was much reduced (0.3 revertants per nanomole, the other simple nitrofurans producing 5-15 reversions per nanomole, as did 5-nitrofuran and 5,2-dinitrofuran). The vinyl-group-containing compound, 5-nitro-2-furylacrylic acid, was by one decadic order more effective both in the Ames test and in the prophage-induction test. In the repair tests all nitrofurans displayed a much higher dependence on the recA-repair system than on the uvrA system. For 2 compounds, the dinitrofuran and, especially, the 5-nitrofuraldehyde, the urA cells were even less sensitive than the wild-type cells.

Animals↗
PubMed1980

[Laparoscopic aspiration of Graafian follicle--its action on ovocyte ultrastructure (author's transl)].

The ultrastructure of human ovocytes was studied, the latter having been obtained laparoscopically following induced ovulation, using clomiphene and HCG. Optimum vacuum size for aspiration was tested on embryonated rat ova. It was found to be between 10 kPa and 30 kPa, that is between 100 and 300 mm H2O. Ultrastructural alteration was recordable neither from human nor from rat ovocytes. No change in ultrastructure was obtained either from subsequent in vitro culturing, and some of the ovocytes were embryonated with good success.

Animals↗