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Results for “Genetic Complementation Test”

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At least 109 records · Page 6Linked to original sources
PubMed1977

Specific neuroanatomical changes in chemosensory mutants of the nematode Caenorhabditis elegans.

Eight of nineteen chemotactic mutants of the nematode Caenorhabditis elegans have morphological defects in the sensory endings of neurons at the tip of the head. The mutants were obtained as worms swimming away from attractant or found amongst male potency mutants or mutants exhibiting erratic behavior. The nineteen mutants fall into at least twelve complementation groups. Mutants E1034 and E1035, alleles of che-1, show morphological alterations in the sensory endings of amphidial neurons and inner labial type 2 neurons, both prospective chemosensory neurons. Both mutants contain non-complementing ts sterile mutations linked to the chemosensory mutation. E1066 shows abnormalities in all the sheath cells associated with the sensory neurons and in the bundling pattern of the amphidial neurons. E1126 is structurally abnormal only in the sensory endings of inner labial type 2 neurons, supporting a chemosensory role for these neurons. E1033 (che-2) and E1124 (che-3) cause defects in the ciliary structure of all but one type of ciliated sensory neuron in the head. E1062 is grossly defective in head structure and the structure of the male copulatory organ, suggesting these opposite ends of the nematode rich in sensory structures share gene functions in embryogenesis. Our study illustrates the possibilities for genetic dissection of the development of a small set of nerves in a simple organism.

Animals↗
PubMed1976

Genetic control of the immune response to the radom linear terpolymer of L-glutamic acid, L-lysine and L-leucine (GLleu) by complementing Ir genes.

Three levels of humoral responsiveness (none, high or marginal) were noted following secondary immunization with random linear terpolymer of L-glutamic acid, L-lysine and L-leucine (GLleu). These immune responses were under dual H-2-linked Ir gene control. Gene complementation was observed in appropriate F1 offspring between two nonresponder strains and in selected intra-I region recombinants derived from crossing over between nonresponder parental haplotypes. One of the Ir-GLleu genes, beta, was localized within the I-A or I-B subregions. The other Ir-GLleu locus, termed alpha, was mapped in the I-C or S subregions. Differences in the strain distribution of immune responsiveness to GLleu and related terpolymer GLphe (which is also under complementing Ir gene control) are primarily attributable to differences among the Ir-GLleu and Ir-GLphe beta alleles. A correlation exists between the presence of the Ir-GLleu alpha(¿allele and the gene coding for specificity Ia.7.

Alleles↗
PubMed1992

Characterization of a complex chromosomal rearrangement maps the locus for in vitro complementation of xeroderma pigmentosum group D to human chromosome band 19q13.

Microcell-mediated chromosome transfer (MMCT) is a powerful genetic technique that permits the transfer of a single chromosome from one mammalian cell to another. The utility of MMCT for gene mapping strategies is critically dependent on the careful characterization of the chromosomes being transferred. We have recently reported the identification of a single rearranged human chromosome, designated Tneo, which corrects the UV sensitivity and excision repair defect of cells of xeroderma pigmentosum genetic complementation group D (XP-D) in culture (Flejter WL et al., Proc Natl Acad Sci USA 89:261-265, 1992). Additionally, those studies demonstrated a role for the excision repair cross-complementing 2 (ERCC2) gene in the observed phenotypic correction. We now report the results of detailed conventional and molecular cytogenetic characterization of the complementing Tneo chromosome. This analysis revealed a complex rearrangement involving material from human chromosomes 16, 17, and 19. Characterization of deletions of Tneo which retained or lost XP-D complementing ability mapped the gene responsible for phenotypic correction to a small region of the terminal q-arm of this chromosome. This region includes the previously described human DNA repair gene cluster located in the region 19q13.2-q13.3, a result consistent with the notion that the in vitro correction of XP-D cells by the Tneo chromosome is rendered by the ERCC2 locus. The data illustrate the potential value of detailed cytogenetic characterization of a human chromosome present in a somatic cell hybrid, even when that material involves complex rearrangements.

Cell Line↗
PubMed1992

Human RAG2, like RAG1, is on chromosome 11 band p13 and therefore not linked to ataxia telangiectasia complementation groups.

Ataxia telangiectasia (A-T) is an inherited, recessive, cancer-prone disease with associated immunodeficiency and chromosome abnormalities involving TCR loci. The latter phenomena implicate errors of the enzyme(s) responsible for assembly of antigen receptor genes (recombinase) in disease pathogenesis. Here we report the location of a human recombination activating gene (RAG2), in addition to RAG1, on chromosome 11, band p13, thereby formally demonstrating linkage of these genes in humans and showing that they are not linked to the known locus responsible for the A-T syndrome.

Ataxia Telangiectasia↗
PubMed1990

Transactivation of anthocyanin biosynthetic genes following transfer of B regulatory genes into maize tissues.

The C1, B and R genes regulating the maize anthocyanin biosynthetic pathway encode tissue-specific regulatory proteins with similarities to transcriptional activators. The C1 and R regulatory genes are usually responsible for pigmentation of seed tissues, and the B-Peru allele of B, but not the B-I allele, can substitute for R function in the seed. In this study, members of the B family of regulatory genes were delivered to intact maize tissues by high velocity microprojectiles. In colorless r aleurones or embryos, the introduction of the B-Peru genomic clone or the expressed cDNAs of B-Peru or B-I resulted in anthocyanin-producing cells. Luciferase produced from the Bronze1 anthocyanin structural gene promoter was induced 100-fold when co-introduced with the expressed B-Peru or B-I cDNAs. This quantitative transactivation assay demonstrates that the proteins encoded by these two B alleles are equally able to transactivate the Bronze1 promoter. Analogous results were obtained using embryogenic callus cells. These observations suggest that one major contribution towards tissue-specific anthocyanin synthesis controlled by the various alleles of the B and R genes is the differential expression of functionally similar proteins.

Alleles↗
PubMed1991

Transient replication of BPV-1 requires two viral polypeptides encoded by the E1 and E2 open reading frames.

Bovine papillomavirus (BPV) DNA is maintained as an episome with a constant copy number in transformed cells and is stably inherited. To study BPV replication we have developed a transient replication assay based on a highly efficient electroporation procedure. Using this assay we have determined that in the context of the viral genome two of the viral open reading frames, E1 and E2, are required for replication. Furthermore we show that when produced from expression vectors in the absence of other viral gene products, the full length E2 transactivator polypeptide and a 72 kd polypeptide encoded by the E1 open reading frame in its entirety, are both necessary and sufficient for replication BPV in C127 cells.

Animals↗
PubMed1986

Highly adherent mutants of SV40-transformed mouse fibroblasts: genetic and biochemical characterization.

Mutants of SV40-transformed mouse fibroblasts have been isolated that have greatly increased cell-substratum adherence. The adherent phenotype (COL-) is recessive, and all mutants analyzed belong to one complementation group. No consistent qualitative differences between wild-type and mutant cells were found with respect to the protein content of the substrate-attached material (SAM), a cell surface fraction left after removal of cells from the substrate with a gentle Ca2+-chelating agent. However, the mutants yielded 2.5-10-fold more SAM than the parental cell line, and the SAM deposited by mutants was able to mediate attachment of transformed cells to a much greater degree than was the SAM from the parental cell line. The mutation, which appears to control the generation of footpads, was shown to cosegregate with resistance to the drug 6-thioguanine, which suggests X-linkage.

Animals↗
PubMed1975

Assembly of the tail of bacteriophage T4.

The protein products of at least 21 phage genes are needed for the formation of the tail of bacteriophage T4. Cells infected with amber mutants defective in these genes are blocked in the assembly process. By characterizing the intermediate structures and unassembled proteins accumulating in mutant-infected cells, we have been able to delineate most of the gene-controlled steps in tail assembly. Both the organized structures and unassembled proteins serve as precursors for in vitro tail assembly. We review here studies on the initiation, polymerization, and termination of the tail tube and contractile sheath and the genetic control of these processes. These studies make clear the importance of the baseplate; if baseplate formation is blocked (by mutation) the tube and sheath subunits remain essentially unaggregated, in the form of soluble subunits. Seventeen of the 21 tail genes specify proteins involved in baseplate assembly. The genes map contiguously in two separate clusters, one of nine genes and the other of eight genes. Recent studies show that the hexagonal baseplate is the end-product of two independent subassembly pathways. The proteins of the first gene cluster interact to form a structure which probably represents one-sixth of the outer radius. The products of the other gene cluster interact to form the central part of the baseplate. Most of the phage tail precursor proteins appear to be synthesized in a nonaggregating form; they are converted to a reactive form upon incorporation into preformed substrate complexes, without proteolytic cleavage. Thus reactive sited are limited to growing structures.

Centrifugation, Density Gradient↗
PubMed1988

A nuclear gene required for the expression of the linear DNA-associated killer system in the yeast Kluyveromyces lactis.

The killer system of Kluyveromyces lactis is associated with two linear DNA plasmids, pGKL1 and pGKL2. The killer toxin and the immunity determinant are coded for by pGKL1. Mutations which block the expression of the killer character have been isolated. These mutations reside in a single chromosomal gene which we have named KEX1. The KEX1 gene of K. lactis has been cloned by complementation of kex1 mutations by using a recombinant plasmid pool containing the entire Kluyveromyces lactis genome, on a multicopy plasmid KEp6, which contains the Saccharomyces cerevisiae URA3 gene as a marker. Genetic analyses of strains carrying a disrupted kex1 allele demonstrated that the cloned DNA corresponded to the KEX1 gene. The cloned KEX1 gene of K. lactis has low but significant sequence homology with the KEX2 gene of Saccharomyces cerevisiae. In vivo complementation of the kex1 mutation of K. lactis by the KEX2 gene of S. cerevisiae, and complementation of the kex2 mutation of S. cerevisiae by the KEX1 gene of K. lactis, demonstrated that KEX1 of K. lactis is functionally related to the KEX2 gene of S. cerevisiae. K. lactis diploids homozygous for kex1 are deficient for sporulation.

Cloning, Molecular↗
PubMed1991

Genetic transformation of auxotrophic mutants of the filamentous yeast Trichosporon cutaneum using homologous and heterologous marker genes.

A transformation system for the filamentous yeast Trichosporon cutaneum based on auxotrophic markers is presented and techniques for the induction, isolation and characterization of mutants are described. A number of auxotrophic mutants were isolated and characterized by using biosynthetic precursors and/or inhibitors. A mutant unable to grow in the presence of ornithine could be complemented successfully by spheroplast transformation experiments using the cloned Aspergillus nidulans ornithine transcarbamoylase gene (argB gene) as selection marker with an efficiency of 5-100 transformants per microgram of DNA. In these transformants the heterologous argB gene was present in multiple tandem copies and the transforming DNA was found to remain stable after more than 50 generations in non-selective media. The same mutant could be complemented by a T. cutaneum cosmid gene library and a complementary cosmid was subsequently isolated from this library by a sib-selection strategy. This cosmid transformed T. cutaneum spheroblasts with an efficiency of 50-200 colonies per microgram of DNA. Southern blot analyses were consistent with the view that the transforming sequences became stably integrated into the host genome at the homologous site.

Arginine↗
PubMed1992

DNA transformations of Candida tropicalis with replicating and integrative vectors.

The alkane-assimilating yeast Candida tropicalis was used as a host for DNA transformations. A stable ade2 mutant (Ha900) obtained by UV-mutagenesis was used as a recipient for different vectors carrying selectable markers. A first vector, pMK16, that was developed for the transformation of C. albicans and carries an ADE2 gene marker and a Candida autonomously replicating sequence (CARS) element promoting autonomous replication, was compatible for transforming Ha900. Two transformant types were observed: (i) pink transformants which easily lose pMK16 under non-selective growth conditions; (ii) white transformants, in which the same plasmid exhibited a higher mitotic stability. In both cases pMK16 could be rescued from these cells in Escherichia coli. A second vector, pADE2, containing the isolated C. tropicalis ADE2, gene, was used to transform Ha900. This vector integrated in the yeast genome at homologous sites of the ade2 locus. Different integration types were observed at one or both ade2 alleles in single or in tandem repeats.

Alcohol Dehydrogenase↗