Showing papers on "Gene interaction published in 1983"

Cellular Oncogenes and Multistep Carcinogenesis

Abstract: Two dozen cellular proto-oncogenes have been discovered to date through the study of retroviruses and the use of gene transfer. They form a structurally and functionally heterogeneous group. At least five distinct mechanisms are responsible for their conversion to active oncogenes. Recent work provides experimental strategies by which many of these oncogenes, as well as oncogenes of DNA tumor viruses, may be placed into functional categories. These procedures may lead to definition of a small number of common pathways through which the various oncogenes act to transform cells.

Differential expression of bithorax complex genes in the absence of the extra sex combs and trithorax genes.

Abstract: Each body segment of Drosophila follows a unique developmental pathway, controlled by the selective expression of homoeotic genes such as Sex combs reduced (Scr)and the bithorax complex (BX-C). Little is known about the regulation of these genes, though several potential activators or repressers have been described. For instance, absence of the extra sex combs (esc) gene product apparently causes adventitious expression of all the BX-C genes in most or all larval body segments. Absence of the trithorax (trx) gene appears to prevent Scr and BX-C expression but only in adult cells; differentiation of the larval segments is only slightly affected. I show here that the correct segmental differentiation of the larva does not require maternally deposited trx+ product, but that the esc mutant phenotype is suppressed by the removal of the trx gene, which implies that the BX-C can be differentially expressed in the absence of both the trx gene and the esc gene product.

X chromosome dosage and gene expression in Caenorhabditis elegans: Two unusual dumpy genes

Abstract: The phenotypes caused by mutations in two autosomal genes of the nematode Caenorhabditis elegans, dpy-21 V and dpy-26 IV, are markedly affected by X chromosome dosage, independent of sexual phenotype. At high X chromosome to autosome ratio, in 2A; 3X animals, these dumpy mutations are lethal; at intermediate ratio, in 2A; 2X animals, they cause dumpiness or lethality; at low ratio, in 2A; 1X animals they cause neither dumpiness nor lethality. One gene, dpy-26, exhibits a strong maternal effect. Interaction between these genes and two major sex-determining genes her-1 V and tra-1 III have been examined. The dumpy mutations partly suppress the masculinization of tra-1 2A;2X animals and also increase the fertility of most her-1 2A;1X hermaphrodites. It is suggested that these dumpy genes are involved in X chromosome dosage compensation, and in some aspects of sexual differentiation. The dpy-26 gene is compared with a similar Drosophila gene, daughterless.

A new H-2-linked class I gene whose expression depends on a maternally inherited factor.

Abstract: The maternally transmitted antigen (Mta) is expressed on the cells of most strains of mice1,2. It is a medial histocompatibility antigen3, that is, it is recognized by unrestricted cytotoxic T lymphocytes as are major H antigens, but unlike these it is a weak transplantation antigen and does not itself restrict the T-cell recognition of minor H antigens. All other medial H antigens are encoded by genes closely linked to the major histocompatibility complex3, H–2 in the mouse. By contrast, Mta appeared to follow extrachromosomal, maternal inheritance. Several substrains of NZB, NZO and non-inbred European NMRI mice are Mta-negative. Females of these strains bear only Mta− offspring, while females of the inbred Mta+ strains bear only Mta+ offspring. Repeated backcrossing from Mta+ females to NZB or NMRI males has shown that, given the right cytoplasmic genes, the chromosomal genes of these Mta− strains permit expression of Mta2. As the Mta type of a mouse cannot be influenced by embryo transfer or foster nursing2,4, we concluded that it was determined by a cytoplasmic factor (Mtf), transmitted through the egg. We now show that a gene, Hmt, closely linked to the H–2 complex, is also required for expression of Mta.

Epistatic Grouping of Repair-Deficient Mutants in Neurospora: Comparative Analysis of Two uvs-3 Alleles, uvs-6 and Their mus Double Mutant Strains.

Abstract: The nuclease halo mutant, nuh-4, of Neurospora crassa was identified conclusively as an allele of uvs-3, a gene involved in error-prone DNA repair. Like uvs-3, nuh-4 showed spontaneous mutator effects, and any previous contradictory findings were found to be due to newly arisen mutants. In normal strains the two alleles are noncomplementing and indistinguishable for sensitivity to UV and methyl methanesulfonate (MMS). Like uvs-3, nuh-4 lacked secretion of the extracellular enzyme, DNase A, a Ca++-dependent strand-nonspecific endonuclease which was found to be phosphate repressible. However, nuh-4 differed from uvs-3 in showing much higher conidial viability and lower sensitivity to ionizing radiation and mitomycin C.——Epistatic relationships of the two uvs-3 alleles with seven other MMS-sensitive mutants were determined and compared with those of the highly X-ray-sensitive mutant, uvs-6. Three epistatic groups were found, based on survival of double mutant strains relative to that of their component single mutant strains after treatment with MMS. Both, uvs-3 and nuh-4, were epistatic to mus-9 which also is a mutator. None of the three produced viable double mutants in crosses to uvs-6. On the other hand, uvs-6, but not the uvs-3 alleles, was found to be epistatic to mus-7 and mus-10. The excision-defective uvs-2 and mus-8 both showed synergism with the uvs-3 alleles and with uvs-6, forming a third, separate epistatic group.

Transfer inhibition of RP4 by F factor

Abstract: When RP4 and F factors were brought together into one E. coli cell, the F factor reduced 500–1000-fold the frequency of transfer of RP4. However, F had almost no effect on the surface exclusion and pilus formation by RP4. In contrast, RP4 did not affect the transfer of F. Using in vitro recombinant DNA techniques, a gene of F responsible for the above-mentioned transfer inhibition of RP4 was located within the BamHI fragment (40.4–42.8 kb) of the mini-F sequence on F. From the result of product analysis using minicells, the responsible gene in the BamHI fragment was inferred to encode the 33 K protein.

Competition between ABO and Le gene specified enzymes. II. Quantitative analysis of A and B antigens in saliva of ABH nonsecretors.

Abstract: One B- and two A-specific radioimmunoassays detected A and B antigenic determinants in saliva of ABH nonsecretors. The A or B antigens found in saliva of nonsecretors had lower efficiency and higher heterogeneity, in the inhibition of the A or B assays, as compared to A or B antigens in saliva of ABH secretors. In the 3 assays, samples of nonsecretor Lewis positive donors (Lea) had less A or B antigens than samples of nonsecretor Lewis negative donors (Lec), suggesting that there is a competition between A or B and Le gene-specified products.

Regulatory interactions among the cya, crp and pts gene products in Salmonella typhimurium

Abstract: A well-characterized set of pts deletion mutants of Salmonella typhimurium were used to re-evaluate the purported role of the PTS in the inducer exclusion process and in regulation cAMP synthesis. During the course of these studies a class of secondary mutations was isolated which suppress the inhibition of cAMP synthesis caused by pts mutations. These suppressor mutations were traced to the crp locus and tentatively designated as acr (adenylate cyclase regulation) mutations. A new model is proposed in which CRP rather than adenylate cyclase is believed to be the central regulatory element in the catabolite repression phenomenon.

Topological and Quantitative Relationships in Evolving Genomes

Abstract: The network properties of the circuitry (topology) of gene interactions are to be distinguished from the quantitative aspects of these interactions. The difference between homologous and analogous morphological structures is best founded on this distinction. It is proposed that gene interaction topologies change very slowly during evolution, while quantitative aspects of gene action and interaction change faster. “Islands” of extremely old sectors of gene interaction topology may have been preserved. Cases of apparent convergent evolution of morphological features thus may contain a component of parallel evolution, which renders the independent appearance of such similar structures more plausible. Two types of gene interaction topology, a trans-spatiotemporal interaction topology and a stage-and-tissue-specific interaction topology need to be distinguished. Pathways for changes in gene interaction topology include gene duplication, heterochrony (the switch of the activity of a gene from one developmental time to another) and hetero histosis (the switch of the activity of a gene from one tissue to another). It is surmised that even higher organisms are built on the basis of a surprisingly small number of genes controlling polypeptides with significantly different functions, though in the same context the importance of the presence of a multiplicity of only slightly diverged gene duplicates is recognized. Even quantitative aspects of gene action and interaction are often conserved over rather long evolutionary periods. When quantitative relationships between gene activities change during evolution, they mostly are expected not to affect the network properties of the gene interaction system.

Interactions Between the MAT locus and the rad52-1 mutation in yeast.

Abstract: The directed and controlled switching of mating type which occurs in homothallic forms of the yeast Saccharomyces cerevisiaee is dependent upon the presence of the wild type RAD52 gene. The RAD52 gene is also required for spontaneous mitotic and meiotic recombination. It has been observed that the two haploid mating types of yeast respond differently to the presence of the rad52-1 mutation and the gene conferring the ability to switch mating type (the HO allele). Cells of genotype MATa rad52-1 HO remain as stable haploids instead of switching; cells with genotype MATα rad52-1 HO are inviable. However, some laboratory strains of yeast harbor a MATa allele which, like MATα, is inviable. Both allelic forms of a switch normally in wild type (RAD52) strains. This suggests that the difference between the two MATa alleles may help define the interaction which occurs between the mating type locus and the RAD52 gene product. The difference between the two MATa alleles is not due to major sequence rearrangements, but probably reflects a change of relatively few base pairs. Normally wild type haploid cells which contain the HO gene switch mating type, and then opposite mating types fuse to form MATa/MATα diploids. In such diploids the HO gene is not expressed, and switching does not occur. Strains which have only a (or only α) information of both MAT and the silent copies switch repeatedly. Digestion of DNA from such strains with appropriate restriction enzymes generates two fragments of DNA resulting from a spontaneous double stranded break in the MAT locus (Strathern et al. 1982). Viable MATa HO rad52-1 strains do not have these fragments.