PubMed · 9634840
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A P Blanchard, L Hood. 1996. Sequence to array: probing the genome's secrets.. https://doi.org/10.1038/nbt1296-1649
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Ehrlichia infections are more and more common in the USA and Europe. The genetics and genome organization of Ehrlichia are little studied due to great difficulties in cultivating these bacteria. Pulse gel electrophoresis was first used to determine the sizes of a genome of 3 representatives of the genus Ehrlichia. The sizes of a genome was established for E. sennetsu (881 kb), for E. risticii (867 kb), E. chaffeensis (1,236 kb).
Organophosphorus (OP) compounds inhibit mitochondrial enzymes, respiration, and ATP generation, in addition to inducing structural changes such as matrix swelling. This implicates mitochondria as primary subcellular targets for these compounds. In this study, the health and function of cellular mitochondria following OP compound exposure were assessed by evaluating the mitochondrial transmembrane potential (DeltaPsi(m)). This was done by measuring the changes in DeltaPsi(m) in SH-SY5Y human neuroblastoma cells incubated with the cationic fluorochrome, rhodamine 123 (5 microg/ml), and the OP compounds tri-ortho-tolyl phosphate (TOTP), triphenyl phosphite (TPPi), or parathion for 7.5 to 960 minutes. OP compounds (100 microM to 1 mM) induced significant concentration-dependent mitochondrial hyperpolarization with peak maxima occurring at 60 (TOTP, TPPi) or 120 (parathion) min. Following this, the mitochondrial membranes gradually depolarized. Pretreatment with cyclosporin A (500 nM, 30 h), a mitochondrial permeability transition pore (PTP) inhibitor, decreased the hyperpolarization. In contrast, 30-h pretreatment with the muscarinic receptor agonist carbachol (1 mM) significantly increased DeltaPsi(m) and delayed subsequent depolarization. Hyperpolarization and subsequent depolarization of mitochondrial membranes occurred 16 to 24 h prior to a loss of substrate adhesion or an increase in DNA fragmentation, indicating that mitochondria were a primary target in OP compound-initiated cytotoxicity.
We screened 93 lesion mimic mutants of rice for resistance to the blast fungus, Magnaporthe grisea, and found eight mutants that exhibited significant resistance to the fungus. We called these mutants cdr (cell death and resistance) and further analyzed three of them. Two mutations, cdr1 and cdr2, were recessive and one, Cdr3, was dominant. Many small brownish lesions developed over the entire leaf of the mutants 20-50 days after sowing. TUNEL staining revealed that DNA fragmentation occurred in leaf blade cells of the homozygous Cdr3 mutants. Autofluorescence and callose deposition were visible in leaf cells of these three mutants. Activation of two defense-related genes, PBZ1 and PR1, was observed in the leaves of the mutants; high expression of PBZ1 was correlated with the lesion formation in the three mutants, whereas PR1 was constitutively expressed in the cdr2 and Cdr3 mutants irrespective of the lesion formation. Levels of momilactone A, a major phytoalexin of rice, in these mutants were increased approximately 100-400-fold relative to the wild-type levels. Suspension-cultured cells of the cdr1 and cdr2 but not Cdr3 produced higher levels of H2O2 than the wild type when treated with calyculin A, an inhibitor of protein phosphatase 1. These results suggest that biochemical lesions of cdr1 and cdr2 lie in the early signaling steps leading to activation of the NADPH oxidase and that type-1 protein phosphatase is operative in protein dephosphorylation involved in NADPH oxidase activation.