A cDNA sequence encoding glutamine synthetase is preferentially expressed in nodules of Vigna aconitifolia.
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Three new full-length cDNAs coding for porcine somatotropin (PST) have been cloned. The sequence data indicate a high degree of polymorphism in the PST sequence. All six known PST sequences are different.
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Serological heterogeneity in HLA-B46 antigens has been described. Previous studies have identified B*4601 as the allele encoding the "strong" B46 antigen found in Chinese populations. Serological characterization of a Vietnamese family revealed a "weak" B46 antigen. Complementary DNA for the HLA-A, B and C alleles of three family members were cloned and the coding regions sequenced. The allele encoding the weak B46 antigen has the same coding sequence as B*4601, demonstrating that the antigenic differences are not due to polymorphism in the amino acid sequence of the HLA-B heavy chain. The recently described HLA-B*1525 and HLA-Cw*0403 alleles were also found to segregate in this Vietnamese family.
A number of human single gene disorders are now known to result from abnormal expansion of trinucleotide repeats. Spinal muscular bulbar atrophy, myotonic dystrophy, Huntington's Disease, spinocerebellar ataxia and dentatorubral-pallidoluysian atrophy are all caused by expansions of CAG repeats. Abnormal expansion of trinucleotide repeats has only so far been described in humans, and no mouse models exist for these diseases. In order to investigate trinucleotide repeat stability in mice, the Genbank and EMBL nucleotide databases were screened to find genes containing CAG repeats. Of the sequences selected, 32 were from mouse, and in 12 of these the repeat was in transcribed sequence and contained at least seven perfect repeats. These repeats were then analysed by PCR to evaluate the degree of variability of repeat length in the various genes. Two of the genes containing variable length CAG repeats, seven in absentia homologue 1b (Sinh1b), and choline acetyl transferase (Chat), which had not previously been mapped in the mouse genome, were mapped by linkage analysis in an interspecific backcross. Sinh1b maps very distally on the X chromosome, and Chat maps to chromosome 14.
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DNA sequences complementary to the double-stranded RNA coding for the neutralization antigen (glycoprotein VP7) of simian rotavirus SA11 have been cloned. The VP7 gene consists of 1,062 nucleotides, containing an uninterrupted coding sequence of 978 nucleotides which specifies a glycoprotein of 326 amino acids. The significance of a second possible initiation site 30 nucleotides downstream from the first is discussed. Partial amino acid sequence of this glycoprotein showed unequivocally that the cloned segment (segment 9) codes for glycoprotein VP7 of SA11. The resulting amino acid sequence contained only one carbohydrate acceptor site. Possible sites of membrane interaction and antigenic determinants are discussed based on the analysis of the hydrophobicity and hydrophilicity profiles of VP7.
Intracisternal A-particle retrotransposons (IAPs) are retroviruslike elements that are defective in envelope protein synthesis and exist without an extracellular stage. We have isolated a novel class of cDNAs that are related to known IAP elements in the nucleotide and deduced protein sequence of gag and pol genes but also contain a previously unidentified reading frame between the pol gene and putative U3 region. Analysis of the deduced protein sequence reveals features of the putative protein that are characteristic of retroviral envelope proteins. The isolated cDNAs represent transcripts of multiple retroid elements in the mouse genome that were termed IAPE (intracisternal A-particle-related elements coding for envelope). IAPE env genes exist in approximately 200 copies per haploid genome as integral parts of the majority of these retroid elements. Four major IAPE subgroups could be distinguished after EcoRI digestion of genomic DNA.
Mutations in ARHGEF6, encoding a guanine nucleotide exchange factor for Rho GTPases, have been shown to cause X-chromosomal non-specific mental retardation (MRX) in human. Here we report the identification and characterization of the orthologous mouse gene, Arhgef6. The gene transcript of approximately 4.4 kb is present in various mouse tissues indicating ubiquitous expression as found for human ARHGEF6. The open reading frame encodes a polypeptide of 771 amino acids with high homology to human ARHGEF6. The structural motifs of both proteins are conserved including an N-terminal CH domain, followed by an SH3 domain, and a tandem organization of the DH and PH domains. Analysis of the temporal expression pattern revealed that Arhgef6 is strongly expressed in the very early embryo and somewhat less in later stages. A genomic cosmid clone containing Arhgef6 exons 1 and 2 has been isolated and used for mapping the gene on the mouse X chromosome.
Members of the NFAT (nuclear factors of activated T cells) gene family have been investigated in numerous organisms, including man and mouse. All NFATs may be synthesized in several isoforms differing in amino or carboxy termini due to 5' and 3' alternative splicing of the corresponding mRNA. Recently, we mapped the murine Nfat5 gene to chromosome 8D. In the present paper we describe for the first time the complete sequence and primary structure of murine Nfat5, two new spliced isoforms, and the expression of murine Nfat5 in embryonic and adult mouse tissues.
Mutations in the gene encoding seipin cause Berardinelli-Seip congenital lipodystrophy 2, with symptoms including near-absence of adipose tissue and altered glucose tolerance. Radiation hybrid analysis localized the seipin gene (Bscl2) in rat to a major quantitative trait locus in rat chromosome 1 linked to glucose intolerance in the Goto-Kakizaki (GK) rat model of Type 2 diabetes. We determined the genomic organization of Bscl2 and screened coding exons and flanking intron sequences for mutations in GK, Wistar and Brown Norway rats, as well as in the Otsuka Long-Evans Tokushima Fatty (OLETF) diabetic rat. Two silent single nucleotide polymorphisms that were identified also were found in non-diabetic rat strains. We conclude that mutations in the gene for seipin are unlikely to contribute to diabetes in GK and OLETF rats.
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