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Author (up) Aertsen, A.; Michiels, C.W. file  url
openurl 
  Title SulA-dependent hypersensitivity to high pressure and hyperfilamentation after high-pressure treatment of Escherichia coli lon mutants Type Journal Article
  Year 2005 Publication Research in Microbiology Abbreviated Journal Res Microbiol  
  Volume 156 Issue 2 Pages 233-237  
  Keywords Colony Count, Microbial; Culture Media; Escherichia coli--genetics, growth & development; Escherichia coli Proteins--genetics, metabolism; Gene Expression Regulation, Bacterial; Hydrostatic Pressure; Mutation; Protease La--genetics; SOS Response (Genetics); Ultraviolet Rays  
  Abstract High-pressure treatment (>100 MPa) is known to induce several heat shock proteins as well as an SOS response in Escherichia coli. In the current work, we have investigated properties with respect to high-pressure treatment of mutants-deficient in Lon, a pressure-induced ATP-dependent protease that belongs to the heat shock regulon but that also has a link to the SOS regulon. We report that lon mutants show increased pressure sensitivity and exhibit hyperfilamentation during growth after high-pressure treatment. Both phenotypes could be entirely attributed to the action of the SOS protein SulA, a potent inhibitor of the cell division ring protein FtsZ and a specific target of the Lon protease, since they were suppressed by knock-out of SulA. Introduction of the lexA1 allele, which effectively blocks the entire SOS response, also suppressed the high pressure hypersensitivity of lon mutants, but not their UV hypersensitivity. These results indicate the existence of a SulA-dependent pathway of high-pressure-induced cell filamentation, and suggest involvement of the SOS response, and particularly of SulA, in high-pressure-mediated cell death in E. coli strains which are compromised in Lon function.  
  Call Number Serial 301  
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Author (up) Arimoto-Kobayashi, S.; Sakata, H.; Mitsu, K.; Tanoue, H. file  url
openurl 
  Title A possible photosensitizer: Tobacco-specific nitrosamine, 4-(N-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), induced mutations, DNA strand breaks and oxidative and methylative damage with UVA Type Journal Article
  Year 2007 Publication Mutation Research Abbreviated Journal Mutat Res  
  Volume 632 Issue 1-2 Pages 111-120  
  Keywords Base Sequence; DNA Breaks; DNA Methylation--drug effects, radiation effects; Dose-Response Relationship, Drug; Models, Biological; Molecular Sequence Data; Mutation; Nitrosamines--toxicity; Oxidative Stress--drug effects, radiation effects; Photosensitizing Agents--toxicity; Salmonella typhimurium; Tobacco--chemistry; Ultraviolet Rays--adverse effects  
  Abstract We discovered the directly acting mutagenicity of the tobacco-specific nitrosamine, 4-(N-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), with UVA light (320-400nm) in Ames bacteria and phage M13mp2 in the absence of metabolic activation. We have investigated the spectrum of mutations caused by UVA-activated NNK. The majority (57%) of induced sequence changes were comprised of GC to CG, GC to TA and GC to AT. This suggested that modification of guanine residues was responsible for these mutations. Hence, we explored the formation of 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxodG) and O(6)-methylguanine (O(6)meG) in the DNA. When calf thymus DNA was treated with NNK and UVA, the amount of 8-oxodG/dG and O(6)meG/G in the DNA increased up to 20-fold and 100-fold, respectively, compared with the untreated control. DNA strand breaks were observed following NNK and UVA treatment, and the strand breaks were suppressed in the presence of scavengers for oxygen and NO radical. The formation of NO was also observed in NNK solutions irradiated with UVA. We analyzed the photodynamic spectrum of mutation induction, 8-oxodG formation and NO formation using monochromatic radiation. The patterns of the action spectra were comparable to the absorption spectrum of NNK. We conclude that NNK may act as a photosensitizer in response to UVA to produce NO and other oxidative and alkylative intermediates following the formation of 8-oxodG and O(6)meG in DNA, which may lead to mutations and DNA strand breaks.  
  Call Number Serial 86  
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Author (up) Backberg, M.; Meister, B. file  url
openurl 
  Title Abnormal cholinergic and GABAergic vascular innervation in the hypothalamic arcuate nucleus of obese tub/tub mice Type Journal Article
  Year 2004 Publication Synapse (New York, N.Y.) Abbreviated Journal Synapse  
  Volume 52 Issue 4 Pages 245-257  
  Keywords Acetylcholine/*metabolism; Adaptor Proteins, Signal Transducing; Animals; Arcuate Nucleus of Hypothalamus/blood supply/*metabolism; Blood Vessels/innervation; Carrier Proteins/metabolism; Glutamate Decarboxylase/metabolism; Immunohistochemistry; *Membrane Transport Proteins; Mice; Mutation; Obesity/*physiopathology; Polymerase Chain Reaction; Presynaptic Terminals/metabolism; Proteins/*genetics; Synaptophysin/metabolism; Vesicular Acetylcholine Transport Proteins; *Vesicular Transport Proteins; gamma-Aminobutyric Acid/*metabolism  
  Abstract Tubby and tubby-like proteins (TULPs) are encoded by members of a small gene family. An autosomal recessive mutation in the mouse tub gene leads to blindness, deafness, and maturity-onset obesity. The mechanisms by which the mutation causes the obesity syndrome has not been established. We compared obese tub/tub mice and their lean littermates in order to find abnormalities within the mediobasal hypothalamus, a region intimately associated with the regulation of body weight. Using an antiserum to the vesicular acetylcholine transporter (VAChT), a marker for cholinergic neurons, many unusually large VAChT-immunoreactive (-ir) nerve terminals, identified by colocalization with the synaptic vesicle protein synaptophysin, were demonstrated in the hypothalamic arcuate nucleus of obese tub/tub mice. Double-labeling showed that VAChT-ir nerve endings also contained glutamic acid decarboxylase (GAD), a marker for gamma-aminobutyric acid (GABA) neurons. The VAChT- and GAD-ir nerve terminals were in close contact with blood vessels, identified with antisera to platelet endothelial cell adhesion molecule-1 (PECAM; also called CD31), laminin, smooth muscle actin (SMA), and glucose transporter-1 (GLUT1). Such large cholinergic and GABAergic nerve terminals surrounding blood vessels were not seen in the arcuate nucleus of lean tub/+ mice. The presence of abnormal cholinergic/GABAergic vascular innervation in the arcuate nucleus suggests that alterations in this region, which contains neurons that receive information from the periphery and which relays information about the energy status to other parts of the brain, may be central in the development of the obese phenotype in animals with an autosomal recessive mutation in the tub gene.  
  Call Number Serial 1460  
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Author (up) Baron, J.M.; Higgins, J.M.; Dzik, W.H. file  url
doi  openurl
  Title A revised timeline for the origin of Plasmodium falciparum as a human pathogen Type Journal Article
  Year 2011 Publication Journal of Molecular Evolution Abbreviated Journal J Mol Evol  
  Volume 73 Issue 5-6 Pages 297-304  
  Keywords Animals; Cytochromes b/*genetics; *Evolution, Molecular; Gorilla gorilla/parasitology; Host-Parasite Interactions/*genetics; Humans; Malaria/*genetics/parasitology; Mitochondrial Proteins/*genetics; Mutation Rate; Plasmodium falciparum/*genetics/pathogenicity  
  Abstract While Plasmodium falciparum is known to have had a strong effect on human evolution, the time period when P. falciparum first infected ancestors of modern humans has remained uncertain. Recent advances demonstrated that P. falciparum evolved from ancestors of gorilla parasites via host switching. Here, we estimate the range of dates during which this host switch may have occurred. DNA sequences of portions of the mitochondrial cytochrome b gene obtained from gorilla parasites closely related to human P. falciparum were aligned and compared against similar sequences from human P. falciparum. Time estimates were calculated by applying a previously established parasite cytochrome b gene mutation rate (0.012 mutations per site per million years) and by modeling uncertainty in a Monte-Carlo simulation. We estimate a 95% confidence interval for when P. falciparum first infected ancestors of modern humans to be 112,000 and 1,036,000 years ago (median estimate, 365,000 years ago). This confidence interval suggests that P. falciparum first infected human ancestors much more recently than the previous recognized estimate of 2.5 million years ago. The revised estimate may inform our understanding of certain aspects of human-malaria co-evolution. For example, this revised date suggests a closer relationship between the entry of P. falciparum in humans and the appearance of many red blood cell polymorphisms considered to be genetic adaptations to malaria. In addition, the confidence interval lies within the timeframe dating the dawn of Homo sapiens, suggesting that P. falciparum may have undergone host switching as a Plasmodia adaptation specific for our species.  
  Call Number Serial 1123  
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Author (up) Berenstein, D. file  url
openurl 
  Title UV-inducible DNA repair in Acinetobacter calcoaceticus Type Journal Article
  Year 1987 Publication Mutation Research Abbreviated Journal Mutat Res  
  Volume 183 Issue 3 Pages 219-224  
  Keywords Acinetobacter/genetics/*radiation effects; Bacteriophages/genetics; Cell Division/radiation effects; DNA Repair/*radiation effects; Lysogeny/radiation effects; Mutation/radiation effects; Ultraviolet Rays  
  Abstract Bacterial mutation frequency after UV irradiation and phage mutation frequency under conditions of W-reactivation were determined in A. calcoaceticus. With the exception of streptomycin resistance, there was no increase in the frequency of the assayed markers above the background level. The increased survival of phage during W-reactivation was not followed by an increase in the frequency of mutation from turbid to clear plaque formers among phage survivors. The findings suggested that the UV-inducible repair pathway in A. calcoaceticus was error free. Post-irradiation incubation of UV-treated culture before phage infection resulted in a further increase of W-reactivation. As chloramphenicol inhibited this response, it was concluded that de novo protein synthesis was involved in the UV-inducible repair pathway in A. calcoaceticus.  
  Call Number Serial 409  
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Author (up) Biron, D.; Shibuya, M.; Gabel, C.; Wasserman, S.M.; Clark, D.A.; Brown, A.; Sengupta, P.; Samuel, A.D.T. file  url
openurl 
  Title A diacylglycerol kinase modulates long-term thermotactic behavioral plasticity in C. elegans Type Journal Article
  Year 2006 Publication Nature Neuroscience Abbreviated Journal Nat Neurosci  
  Volume 9 Issue 12 Pages 1499-1505  
  Keywords Animals; Association Learning/physiology; Behavior, Animal/*physiology; Body Temperature Regulation/physiology; Caenorhabditis elegans/*enzymology/genetics; Caenorhabditis elegans Proteins/genetics/*metabolism; Diacylglycerol Kinase/genetics/*metabolism; Gene Expression Profiling; Mutation; Neurons/enzymology; Thermosensing/*physiology  
  Abstract A memory of prior thermal experience governs Caenorhabditis elegans thermotactic behavior. On a spatial thermal gradient, C. elegans tracks isotherms near a remembered temperature we call the thermotactic set-point (T(S)). The T(S) corresponds to the previous cultivation temperature and can be reset by sustained exposure to a new temperature. The mechanisms underlying this behavioral plasticity are unknown, partly because sensory and experience-dependent components of thermotactic behavior have been difficult to separate. Using newly developed quantitative behavioral analyses, we demonstrate that the T(S) represents a weighted average of a worm's temperature history. We identify the DGK-3 diacylglycerol kinase as a thermal memory molecule that regulates the rate of T(S) resetting by modulating the temperature range of synaptic output, but not temperature sensitivity, of the AFD thermosensory neurons. These results provide the first mechanistic insight into the basis of experience-dependent plasticity in this complex behavior.  
  Call Number Serial 1679  
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Author (up) Brenner, S. file  url
openurl 
  Title The genetics of behaviour Type Journal Article
  Year 1973 Publication British Medical Bulletin Abbreviated Journal Br Med Bull  
  Volume 29 Issue 3 Pages 269-271  
  Keywords Animals; *Genetics, Behavioral; Mutation; Neurons/ultrastructure  
  Abstract Genes are understandably crucial to physiology, morphology and biochemistry, but the idea of genes contributing to individual differences in behaviour once seemed outrageous. Nevertheless, some scientists have aspired to understand the relationship between genes and behaviour, and their research has become increasingly informative and productive over the past several decades. At the forefront of behavioural genetics research is the fruitfly Drosophila melanogaster, which has provided us with important insights into the molecular, cellular and evolutionary bases of behaviour.  
  Call Number Serial 1603  
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Author (up) De, S. file  url
openurl 
  Title Somatic mosaicism in healthy human tissues Type Journal Article
  Year 2011 Publication Trends in Genetics : TIG Abbreviated Journal Trends Genet  
  Volume 27 Issue 6 Pages 217-223  
  Keywords Aging; Animals; DNA, Mitochondrial/genetics; Humans; *Mosaicism; Mutation  
  Abstract From the fertilization of an egg until the death of an individual, somatic cells can accumulate genetic changes, such that cells from different tissues or even within the same tissue differ genetically. The presence of multiple cell clones with distinct genotypes in the same individual is referred to as 'somatic mosaicism'. Many endogenous factors such as mobile elements, DNA polymerase slippage, DNA double-strand break, inefficient DNA repair, unbalanced chromosomal segregation and some exogenous factors such as nicotine and UV exposure can contribute to the generation of somatic mutations, thereby leading to somatic mosaicism. Such changes can potentially affect the epigenetic patterns and levels of gene expression, and ultimately the phenotypes of cells. Although recent studies suggest that somatic mosaicism is widespread during normal development and aging, its implications for heightened disease risks are incompletely understood. Here, I discuss the origins, prevalence and implications of somatic mosaicism in healthy human tissues.  
  Call Number Serial 1775  
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Author (up) Diaz-Acosta, A.; Sandoval, M.L.; Delgado-Olivares, L.; Membrillo-Hernandez, J. file  url
doi  openurl
  Title Effect of anaerobic and stationary phase growth conditions on the heat shock and oxidative stress responses in Escherichia coli K-12 Type Journal Article
  Year 2006 Publication Archives of Microbiology Abbreviated Journal Arch Microbiol  
  Volume 185 Issue 6 Pages 429-438  
  Keywords Aerobiosis/physiology; Anaerobiosis/physiology; Bacterial Proteins/genetics; Electrophoresis, Polyacrylamide Gel; Escherichia coli K12/genetics/*growth & development/metabolism; Escherichia coli Proteins/genetics/*metabolism; Heat-Shock Proteins/genetics/metabolism; *Hot Temperature; Hydrogen Peroxide/pharmacology; Kinetics; Microbial Viability/drug effects; Mutation/genetics; Oxidation-Reduction; Oxidative Stress/*physiology; Oxygen/pharmacology; Protein Biosynthesis/drug effects; Sigma Factor/genetics  
  Abstract The natural living style of Escherichia coli occurs in the gastrointestinal tract, where most of its existence is spent under anaerobic conditions and in stationary phase of growth. Here we report on the heat shock response of E. coli K-12 cells growing in the presence or absence of oxygen. An rpoH mutant (impaired in the synthesis of the sigma(32) transcriptional factor) exhibited an increased sensitivity to heat shock but only in the exponential phase of aerobic growth, suggesting that in anaerobic growth conditions, and in aerobic stationary phase, sigma(32)-independent mechanisms are playing a prime role in protecting cells from heat stress. Our results demonstrated that sigma(S) is not involved in this protection system. Studies on the kinetics of synthesis of Heat shock proteins (Hsp) after an abrupt rise in temperature demonstrated that in the absence of oxygen, the synthesis of Hsp is triggered faster and is sustained for a longer period of time compared to aerobic growth conditions. Finally, the heated cells in the exponential phase of aerobic growth displayed a high concentration of oxidatively damaged proteins in the presence of 4 mM H(2)O(2), in sharp contrast to cultures of stationary phase or anaerobic growth.  
  Call Number Serial 298  
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Author (up) Driscoll, M.; Gerstbrein, B. file  url
openurl 
  Title Dying for a cause: invertebrate genetics takes on human neurodegeneration Type Journal Article
  Year 2003 Publication Nature Reviews. Genetics Abbreviated Journal Nat Rev Genet  
  Volume 4 Issue 3 Pages 181-194  
  Keywords Alzheimer Disease/genetics/pathology; Animals; Animals, Genetically Modified; Caenorhabditis elegans/cytology/genetics; Cell Death; Drosophila melanogaster/cytology/genetics; Humans; Hypoxia/genetics/pathology; Invertebrates/cytology/*genetics; Ion Channels/metabolism; Models, Neurological; Mutation; Nerve Degeneration/*genetics/*pathology; Neurons/drug effects/pathology; Parkinson Disease/genetics/pathology; Peptides/genetics  
  Abstract If invertebrate neurons are injured by hostile environments or aberrant proteins they die much like human neurons, indicating that the powerful advantages of invertebrate molecular genetics might be successfully used for testing specific hypotheses about human neurological diseases, for drug discovery and for non-biased screens for suppressors and enhancers of neurodegeneration. Recent molecular dissection of the genetic requirements for hypoxia, excitotoxicity and death in models of Alzheimer disease, polyglutamine-expansion disorders, Parkinson disease and more, is providing mechanistic insights into neurotoxicity and suggesting new therapeutic interventions. An emerging theme is that neuronal crises of distinct origins might converge to disrupt common cellular functions, such as protein folding and turnover.  
  Call Number Serial 1706  
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