Showing papers on "Chromosomal region published in 1975"

HL-A system and diabetes mellitus.

Abstract: HL-A antigens were determined in 100 patients with diabetes mellitus. When the data are combined with that from other studies, there is a definite positive association of acute-onset juvenile diabetes mellitus with HL-A8 and W15. Four families are described in which two or more members with this type of diabetes are present, and in each family, affected individuals share a haplotype including HL-A8 or W15. These findings are consistent with the possible role of immune response genes in the HL-A chromosomal region which might control the immune response to virus infections capable of producing islet cell damage.

Genetic control of glutamine synthetase in Klebiella aerogenes.

Abstract: Mutations at two sites, glnA and glnB, of the Klebsiella aerogenes chromosome result in the loss of glutamine synthetase. The locations of these sites on the chromosome were established by complementation by episomes of Escherichia coli and by determination of their linkage to other genetic sites by transduction with phage P1. The glnB gene is located at a position corresponding to 48 min on the Taylor map of the E. coli chromosome; it is linked to tryA, nadB, and GUA. The glnA gene is at a position corresponding to 77 min on the Taylor map and is linked to rha and metB; it is also closely linked to rbs, located in E. coli at 74 min, indicating a difference in this chromosomal region between E. coli and K. aerogenes. Mutations in the glnA site can also lead to nonrepressible synthesis of active glutamine synthetase. The examination of the fine genetic structure of glnA revealed that one such mutation is located between two mutations leading to the loss of enzymatic activity. This result, together with evidence that the structural gene for glutamine synthetase is at glnA, suggests that glutamine synthetase controls expression of its own structural gene by repression.

Genetic and Physiological Studies on the Site of Action of Distamycin A

Abstract: Two new genetic loci of Bacillus subtilis are identified by mutations that confer resistance to distamycin A and to other antibacterial agents. The chromosomal region where they map probably contains a cluster of genes whose products are related to membrane structure and function. Some of the biological effects of distamycin A are still in evidence in the resistant mutants indicating that the drug possibly acts at multiple sites. Most biological effects of the drug (including the phenotypic correction of a morphopoietic mutation) are likely to be due to the interaction of distamycin A with membrane (or surface) structures. Images

Cellular Distribution of Rabbit IgA Allotypes

Abstract: Intestinal tissue from rabbits heterozygous at one or both of the α-chain subclass loci, i.e., f or g , was examined with mixtures of rhodamine-labeled and fluorescein-labeled antibodies each directed against one of the allelic products of the f or g locus. Individual plasma cells were stained by only one fluorescent reagent and thus exhibited both allelic exclusion and subclass exclusion. In contrast, the epithelial cells of the Lieberkuhn9s glands did not exhibit allelic exclusion. Studies with rabbits heterozygous at the f and g loci revealed that the ratio of the number of cells expressing maternal-type f cells to paternal-type f is equal to the ratio of the number of maternal-type g cells to paternal-type g cells. These data are used to suggest that the expression of each of the genes in the heavy chain chromosomal region of a particular allogroup is under the same control.

Genetic and Biochemical Characterization of a Ribosomal Mutant of Bacillus subtilis Resistant to Sporangiomycin

Abstract: The antibiotic sporangiomycin affects the growth of Bacillus subtilis by inhibiting protein synthesis. Mutants of B. subtilis resistant to sporangiomycin have been isolated. One of these, PB 1690, has been further studied. The analysis of subcellular fractions from the mutant has shown that the biochemical effect of the mutation is an alteration of a site on the 50S ribosomal subunit responsible for the binding of the antibiotic: the mutant ribosomes do not bind sporangiomycin and are capable of carrying out phenylalanine polymerization in the presence of sporangiomycin. The resistance mutation maps on the chromosomal region where the ribosomal markers map. The mutant strain is also resistant to the action of the chemically related antibiotic thiostrepton. Treatment of B. subtilis ribosomes with LiCl results in the detachment of a group of proteins including the one responsible for sporangiomycin resistance. Active ribosomes can be reconstructed by mixing “split proteins” and “core particles” of either parental or mutant origin. The fate of the mutant protein can now be followed by assaying reconstructed ribosomes for capacity to bind sporangiomycin and for resistance to the action of the antibiotic in the reactions for phenylalanine polymerization.

Dependence of heterochromatin differential staining on the time of its reduplication and the degree of condensation

Abstract: A comparison of the chromosomes banding pattern after G-and C-staining with the time of DNA reduplication and the degree of chromosome condensation, was carried out using Chinese hamster metaphase chromosomes. Chromosome condensation was studied under 5-bromodeoxyuridine and 5-bromodeoxycytidine treatment. All the chromosomal segments stained with C-technique are also stainable with G-technique, while only some G-positive segments are capable to be C-bands. C-bands are heterochromatic segments characterized by extremely late replication and great delay in condensation under the analog action, while G-bands are segments with earlier labelling and irregular decondensation. The data obtained suggest a close correlation between the capability of chromosomal region of G- and C- staining and the degree of its heterochromatinization.