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At least 973 records · Page 54Linked to original sources
PubMed1985

A study of the host range and distribution of antibody to Akabane virus (genus bunyavirus, family Bunyaviridae) in Kenya.

Serum neutralizing antibody to Akabane virus (genus bunyavirus, family Bunyaviridae) was found in a high proportion (50-95%) of cattle sampled in Kenya, while sheep and goats had fewer positive (13-33%). Camel and horse sera also contained antibody to the virus (70% and 50% respectively). The antibody was found in animals from the high altitude temperature type of grasslands, drier bushed and wooded grasslands and the semi-desert. No arthrogryposis nor hydranencephaly has been encountered in Kenya which might be related to this widespread virus infection. A wide range of Kenyan wild ruminants had antibody to Akabane virus in their sera, as also did zebra.

Altitude↗
PubMed1992

Expansion of insecticidal host range of Bacillus thuringiensis by in vivo genetic recombination.

We describe a novel approach for the insertion of an insecticidal toxin gene into a resident plasmid in Bacillus thuringiensis (Bt). A gene encoding a coleopteran-specific toxin was cloned within a fragment of IS232 and inserted into a plasmid thermosensitive for replication in Bt. The plasmid was used to transform a Bt strain toxic to lepidoptera, and the transformants were then selected at non-permissive temperature for clones in which the vector had integrated into a copy of IS232 present on a resident plasmid. A second recombination event was selected such that the vector was eliminated and the newly introduced toxin gene was conserved. The resulting strain contained only DNA of Bt origin, and displayed insecticidal activity against both lepidoptera and coleoptera.

Bacillus thuringiensis↗
PubMed2000

Mobility assays confirm the broad host-range activity of the Minos transposable element and validate new transformation tools.

Fast and reliable methods for assessing the mobility of the transposable element Minos have been developed. These methods are based on the detection of excision and insertion of Minos transposons from and into plasmids which are co-introduced into cells. Excision is detected by polymerase chain reaction (PCR) with appropriate primers. Transposition is assayed by marker rescue in Escherichia coli, using a transposon plasmid that carries a tetracycline resistance gene and a target plasmid carrying a gene that can be selected against in E. coli. Using both assays, Minos was shown to transpose in Drosophila melanogaster cells and embryos, and in cultured cells of a mosquito, Aedes aegypti, and a lepidopteran, Spodoptera frugiperda. In all cases, mobility was dependent on the presence of exogenously supplied transposase, and both excision and transposition were precise. The results indicate that Minos can transpose in heterologous insect species with comparable efficiencies and therefore has the potential to be used as a transgenesis vector for diverse species.

Aedes↗
PubMed1975

Mapping of biological functions on RNA of avian tumor viruses: location of regions required for transformation and determination of host range.

A map of the large T1 oligonucleotides of the RNA of Prague Rous sarcoma virus, strain B (Pr RSVb) has recently been established (Coffin and Billeter, submitted for publication). Since the RNA of Rous associated virus, type 1 (RAV-1) lacks many of the large 1 oligonucleotides of Pr RSV-B and contains others not present in the latter, the RNA of recombinants between RAV-1 and Pr RSV-B could be analyzed with regard to the origin of its sequences. Recombinants were selected for transforming capacity (characteristic for Pr RSV-B) and ability to grow on C/B chicken fibroblasts (characteristic for RAV-1). Four out of five recombinants examined had undergone at least two crossovers. The set of Pr RSV-B-specific oligonucleotides present in all recombinants defined an RNA region near the poly(A) segment; this must contain genetic information required for transformation required for transformation (the onc function). All recombinants lost a set of contiguous Pr RSV-B-specific oligonucleotides and concomitantly acquired a set of RAV-1-specific oligonucleotides. These define a region in the middle section of the oligonucleotide map, all or some of which must be required for determining growth capacity on C/B cells (the env function).

Avian Sarcoma Viruses↗
PubMed1984

Structural genes of dinitrogenase and dinitrogenase reductase are transcribed from two separate promoters in the broad host range cowpea Rhizobium strain IRc78.

The nucleotide sequence of the structural gene (nifD) coding for the alpha-subunit of dinitrogenase along with its flanking sequences has been determined in cowpea Rhizobium IRc78. The coding sequence consists of 1500 nucleotides, which corresponds to a predicted amino acid sequence of 500 residues and a molecular weight of 56,025. Nucleotide homology to nifD from the blue-green alga, Anabaena, and Parasponia Rhizobium, are 63% and 90%, respectively. Cowpea Rhizobium IRc78 nifD and nifK (encodes the beta-subunit of dinitrogenase) genes are linked, separated by 69 nucleotides. In contrast to fast-growing rhizobia, the structural genes of dinitrogenase (nifDK) are transcribed from a different promoter than the structural gene of dinitrogenase reductase (nifH). Transcription of nifDK initiates 41 nucleotides upstream of the start codon for the nifDK operon. Two transcription initiation sites, localized at 152 and 114 nucleotides upstream of the start codon, were determined for the nifH operon. Two nucleotide sequences, a hexamer (G-G-T-T-G-C) and a pentamer (T-G-G-C-A), centered at approximately -15 and -25, respectively, are conserved in the nifD and nifH promoter regions and are not present in the 69-nucleotide nifDK junction. No sequence homology other than a possible ribosome binding site, T-T-G-A-[unk]-G-G-A, located 14 nucleotides upstream of the initiation codon was detected between the transcribed but untranslated leader regions of nifD and nifH.

Journal Article↗
PubMed1988

Avian reovirus mRNAs are nonfunctional in infected mouse cells: translational basis for virus host-range restriction.

Avian reovirus S1133 penetrates and uncoats in suspension cultures of mouse L cells. The multiple species of viral transcripts are produced in the cytoplasm of the infected cell, but they fail to associate with polysomes, consistent with the absence of viral protein synthesis. The selective block in avian virus mRNA translation is not overcome by coinfection with mammalian reovirus type 3, which replicates in mouse L cells, or by hypertonic shock or exposure to a low concentration of cycloheximide. Although the avian viral transcripts are inactive in vivo, RNA extracted from infected, nonpermissive L cells directs the synthesis of a normal spectrum of viral proteins in rabbit reticulocyte lysates. These results indicate that avian viral transcription is not restricted in mouse cells and that viral replication is prevented at the level of initiation of protein synthesis.

Animals↗
PubMed1998

Replication origin of the broad host range plasmid RK2. Positioning of various motifs is critical for initiation of replication.

The 393-base pair minimal origin, oriV, of plasmid RK2 contains three iterated motifs essential for initiation of replication: consensus sequences for binding the bacterial DnaA protein, DnaA boxes, which have recently been shown to bind the DnaA protein; 17-base pair direct repeats, iterons, which bind the plasmid encoded replication protein, TrfA; and A + T-rich repeated sequences, 13-mers, which serve as the initial site of helix destabilization. To investigate how the organization of the RK2 origin contributes to the mechanism of replication initiation, mutations were introduced into the minimal origin which altered the sequence and/or spacing of each particular region relative to the rest of the origin. These altered origins were analyzed for replication activity in vivo and in vitro, for localized strand opening and for DnaB helicase mediated unwinding. Mutations in the region between the iterons and the 13-mers which altered the helical phase or the intrinsic DNA curvature prevented strand opening of the origin and consequently abolished replication activity. Insertions of more or less than one helical turn between the DnaA boxes and the iterons also inactivated the replication origin. In these mutants, however, strand opening appeared normal but the levels of DnaB helicase activity were substantially reduced. These results demonstrate that correct helical phasing and intrinsic DNA curvature are critical for the formation of an open complex and that the DnaA boxes must be on the correct side of the helix to load DnaB helicase.

Bacterial Proteins↗