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At least 1,585 records · Page 88Linked to original sources
PubMed1986

Genetic mapping of a major site of phosphorylation in adenovirus type 2 E1A proteins.

Adenovirus early region 1A (E1A) encodes two acidic phosphoproteins which are required for transactivation of viral transcription, efficient viral DNA replication in phase G0-arrested human cells, and oncogenic transformation of rodent cells. Biochemical analysis of in vivo 32P-labeled adenovirus type 2 E1A proteins purified with monoclonal antibodies demonstrated that these proteins were phosphorylated at multiple serine residues. Two-dimensional phosphotryptic peptide maps of wild-type and mutant E1A proteins were used to locate a major site of E1A protein phosphorylation at serine-219 of the large E1A protein. Although this serine fell within a consensus sequence for phosphorylation by the cyclic AMP-dependent protein kinases, experiments with mutant CHO cells defective in these enzymes indicated that it was not. Oligonucleotide-directed mutagenesis was used to substitute an alanine for serine-219. This mutation prevented phosphorylation at this site. Nonetheless, the mutant was indistinguishable from the wild type for early gene transactivation, replication on G0-arrested WI-38 cells, and transformation of cloned rat embryo fibroblast cells.

Adenovirus Early Proteins↗
PubMed1986

Human parainfluenza virus type 3: messenger RNAs, polypeptide coding assignments, intergenic sequences, and genetic map.

cDNA clones of mRNAs for the major nucleocapsid protein (NP), the nucleocapsid P protein plus the nonstructural C protein (P+C), and the matrix protein (M) of human parainfluenza virus type 3 (PF3) were identified by hybrid arrest and hybrid selection of in vitro translation. Previously, cDNA clones were identified and sequenced for the hemagglutinin-neuraminidase glycoprotein (HN) and the fusion glycoprotein (F) mRNAs (N. Elango, J. E. Coligan, R. C. Jambou, and S. Venkatesan, J. Virol. 57:481-489, 1986; M. K. Spriggs, R. A. Olmsted, S. Venkatesan, J. E. Coligan, and P. L. Collins, Virology 152:241-251, 1986). Synthetic oligonucleotides, designed from nucleotide sequences of the cDNAs, were used to direct dideoxynucleotide sequencing of gene junctions in PF3 genomic RNA (vRNA). From sequencing of vRNA, a sixth viral gene was detected and identified as the large nucleocapsid protein (L) gene by hybridization of a synthetic oligonucleotide to intracellular PF3 mRNAs separated by gel electrophoresis. The order of the six PF3 genes on vRNA was 3'-NP-P+C-M-F-HN-L-5'. The five intergenic regions consisted of the trinucleotide 3'-GAA. The PF3 genes initiated with semiconserved 10-nucleotide gene-start sequences and terminated with semiconserved 12-nucleotide gene-end sequences. The M gene terminated with an aberrant gene-end sequence; analysis of intracellular mRNA showed that this aberrant sequence correlated with a disproportionately high accumulation of readthrough mRNA. These studies showed that PF3 encodes six unique mRNAs (NP, P+C, M, F, HN, and L) that encode seven proteins (NP, P, C, M, F, HN, and L) and provided evidence of a close relationship between PF3 and Sendai (murine parainfluenza type 1) viruses.

Base Sequence↗
PubMed1984

Cloning and genetic mapping of SNF1, a gene required for expression of glucose-repressible genes in Saccharomyces cerevisiae.

A functional SNF1 gene product is required to derepress expression of many glucose-repressible genes in Saccharomyces cerevisiae. Strains carrying a snf1 mutation are unable to grow on sucrose, galactose, maltose, melibiose, or nonfermentable carbon sources; utilization of these carbon sources is regulated by glucose repression. The inability of snf1 mutants to utilize sucrose results from failure to derepress expression of the structural gene for invertase at the RNA level. We isolated recombinant plasmids carrying the SNF1 gene by complementation of the snf1 defect in S. cerevisiae. A 3.5-kilobase region is common to the DNA segments cloned in five different plasmids. Transformation of S. cerevisiae with an integrating vector carrying a segment of the cloned DNA resulted in integration of the plasmid at the SNF1 locus. This result indicates that the cloned DNA is homologous to sequences at the SNF1 locus. By mapping a plasmid marker linked to SNF1 in this transformant, we showed that the SNF1 gene is located on chromosome IV. We then mapped snf1 to a position 5.6 centimorgans distal to rna3 on the right arm; snf1 is not extremely closely linked to any previously mapped mutation.

Chromosome Mapping↗
PubMed2003

Genetic mapping of a new Lafora progressive myoclonus epilepsy locus (EPM2B) on 6p22.

BACKGROUND: Lafora disease is a progressive myoclonus epilepsy with polyglucosan accumulations and a peculiar neurodegeneration with generalised organellar disintegration. It causes severe seizures, leading to dementia and eventually death in early adulthood. METHODS: One Lafora disease gene, EPM2A, has been identified on chromosome 6q24. Locus heterogeneity led us to search for a second gene using a genome wide linkage scan in French-Canadian families. RESULTS: We mapped a second Lafora disease locus, EPM2B, to a 2.2 Mb region at 6p22, a region known to code for several proteins, including kinesins. Kinesins are microtubule dependent motor proteins that are involved in transporting cellular components. In neurones, they play a major role in axonal and dendritic transport. CONCLUSION: Analysis of the present locus in other non-EPM2A families will reveal whether there is further locus heterogeneity. Identification of the disease gene will be of major importance towards our understanding of the pathogenesis of Lafora disease.

Chromosome Mapping↗
PubMed1984

Genetic mapping in the Mexican axolotl, Ambystoma mexicanum.

In the Mexican axolotl, Ambystoma mexicanum, gynogenetic diploids can be produced by suppressing the release of the second polar body in eggs activated with irradiated sperm. If the female is heterozygous for a particular mutation, some of the progeny will be homozygous for the mutation. The proportion depends on the distance from the centromere and can be used to determine the gene--centromere (or gene-kinetochore) distance. The mapping function is based on the Neurospora tetrad mapping function. Several variations on this function, based on considerations of how coincidence varies with map distance, are considered. Three genes have been mapped: c at 5.9, t at 24.3, and m at 59.1 map units from their respective centromeres. Four other genes (a, ax, p, and the sex locus) appear to be distant from their centromeres but precise map distances cannot be determined. Based on these data, the total length of the genome has been estimated as at least 2600 map units.

Ambystoma↗
PubMed1999

Chromosomal location and genetic mapping of the mismatch repair gene homologs MSH2, MSH3, and MSH6 in rye and wheat

The efficiency of homeologous recombination is influenced by mismatch repair genes in bacteria, yeast, and mammals. To elucidate a possible role of these genes in homeologous pairing and cross-compatibility in plants, gene probes of wheat (Triticum aestivum) specific for the mismatch repair gene homologues MSH2, MSH3, and MSH6 were used to map them to their genomic positions in rye (Secale cereale). Whereas MSH2 was mapped to the short arm of chromosome 1R, MSH3 was mapped to the long arm of chromosome 2R and MSH6 to the long arm of chromosome 5R. Southern blots with nullisomic-tetrasomic (NT) lines of wheat indicated the presence of the sequences on the respective homeologous group of wheat chromosomes. Additionally, an MSH6-specific homologue could also be detected on homoeologous group 3 of wheat. However, in the well-known, highly homoeologous pairing wheat mutant ph1b the MSH6-specific sequence is not within the deleted part of chromosome 5BL, indicating that the pairing phenotype is not due to a loss of one of the mismatch repair genes tested.

Journal Article↗
PubMed2001

Genetic mapping and functional studies of a natural inhibitor of the insulin receptor tyrosine kinase: the mouse ortholog of human alpha2-HS glycoprotein.

Fetuin/alpha2-HS glycoprotein (alpha2-HSG) homologs have been identified in several species including rat, sheep, pig, rabbit, guinea pig, cattle, mouse and human. Multiple physiological roles for these homologs have been suggested, including ability to bind to hydroxyapatite crystals and to specifically inhibit the tyrosine kinase (TK) activity of the insulin receptor (IR). In this study we report the identification, cloning, and characterization of the mouse Ahsg gene and its function as an IR-TK inhibitor. Genomic clones derived from a mouse Svj 129 genomic library were sequenced in order to characterize the intron-exon organization of the mouse Ahsg gene, including an 875 bp subclone containing 154 bp upstream from the transcription start site, the first exon, and part of the first intron. A second genomic subclone harboring a 3.45 kb Bgl II fragment contained exons 2, 3 and 4 in addition to two adjacent elements within the first intron-a repetitive element of the B1 family (92 bp) and a 271 bp tract of (T,C)n*(A,G)n. We have mapped mouse Ahsg at 16 cM adjacent to the Diacylglycerol kinase 3 (Dagk3) gene on chromosome 16 by genotyping interspecific backcross panels between C57BL/6J and Mus spretus. The position is syntenic with human chromosome 3q27, where the human AHSG gene resides. Using recombinant mouse alpha2-HSG expressed from a recombinant baculovirus, we demonstrate that mouse alpha2-HSG inhibits insulin-stimulated IR autophosphorylation and IR-TKA in vitro. In addition, mouse alpha2-HSG (25 microg/ml) completely abolishes insulin-induced DNA synthesis in H-35 rat hepatoma cells. Based on the sequence data and functional analysis, we conclude that the mouse Ahsg gene is the true ortholog of the human AHSG gene.

Amino Acid Sequence↗
PubMed1998

Detailed genetic mapping around a putative prostate-specific membrane antigen locus on human chromosome 11p11.2.

Physical mapping of the human prostate-specific membrane antigen gene (FOLH) has not been straightforward. Previously, localisations of this gene to either 11p11.2 or 11q14 have been described. This raised the possibility of the presence of more than one related FOLH gene in man. We now present detailed characterisation of the region around a FOLH gene in a 500-kb non-chimaeric YAC clone, putatively assigned to 11p11.2. This clone contains two known microsatellites, D11S1326 and D11S1357 which have been previously mapped unequivocally to the 11p11.2 region at 62.5 cM. This data strongly supports the original 11p11.2 localisation of FOLH. The YAC clone also has a putative EST at each of its ends and these have thus been physically positioned on this chromosome. However, the two regions previously highlighted at 11p11.2 and 11q14 are apparently extensively duplicated, as evidenced by the appearance of dual FISH signals with a number of different genomic probes selected across this 500-kb 11p11.2 region.

Animals↗
PubMed1998

Genetic mapping of mouse centromere protein (Incenp and Cenpe) genes.

Inner centromere protein (INCENP) and centromere protein E (CENPE) are two functionally important proteins of the higher eukaryotic centromere. Using a mouse Incenp genomic DNA and a mouse Cenpe cDNA to analyze recombinant inbred mouse sets, as well as interspecific backcross panels, we have mapped these genes to the proximal regions of mouse Chromosomes 19 and 6, respectively. Comparison of Cenpe and human CENPE, which maps to chromosome region 4q24-->q25, has further identified a new region of homology between the two species.

Animals↗
PubMed1988

Genetic mapping of the human polymeric immunoglobulin receptor gene to chromosome region 1q31----q41.

Polymeric immunoglobulin receptor (PIGR) is a transmembrane glycoprotein which is expressed by epithelial cells and is involved in the transcellular transport of polymeric immunoglobulins into secretions. We cloned the human gene for PIGR and used the clone to obtain probes to determine the chromosomal localization of PIGR. Analysis of somatic cell hybrids and in situ chromosomal hybridization localized the human PIGR gene locus to 1q31----q41.

Blotting, Southern↗