bluuebunny/crossref_metadata_2025_split huggingface dataset:
Physiology and molecular aspects of Verticillium wilt diseases caused by V. dahliae and V. albo‐atrum
Authors: FRADIN EMILIE F. , THOMMA BART P. H. J. 
Published: January 2006

SUMMARYIntroduction:  Verticillium spp. are soil‐borne plant pathogens responsible for Verticillium wilt diseases in temperate and subtropical regions; collectively they affect over 200 hosts, including many economically important crops. There are currently no fungicides available to cure plants once they are infected.Taxonomy:  Kingdom: Fungi, phylum: Ascomycota, subphylum, Pezizomycotina, class: Sordariomycetes, order: Phyllachorales, genus: Verticillium.Host range and disease symptoms:  Over 200 mainly dicotyledonous species including herbaceous annuals, perennials and woody species are host to Verticillium diseases. As Verticillium symptoms can vary between hosts, there are no unique symptoms that belong to all plants infected by this fungus. Disease symptoms may comprise wilting, chlorosis, stunting, necrosis and vein clearing. Brown vascular discoloration may be observed in stem tissue cross‐sections.Pathogenicity:  Verticillium spp. have been reported to produce cell‐wall‐degrading enzymes and phytotoxins that all have been implicated in symptom development. Nevertheless, evidence for a crucial role of toxins in pathogenicity is inconsistent and therefore not generally accepted. Microsclerotia and melanized mycelium play an important role in the disease cycle as they are a major inoculum source and are the primary long‐term survival structures.Resistance:  Different defence responses in the prevascular and the vascular stage of Verticillium wilt diseases determine resistance. Although resistance physiology is well established, the molecular processes underlying this physiology remain largely unknown. Resistance against Verticillium largely depends on the isolation of the fungus in contained parts of the xylem tissues followed by subsequent elimination of the fungus. Although genetic resistance has been described in several plant species, only one resistance locus against Verticillium has been cloned to date.Useful website:  http://cbr‐rbc.nrc‐cnrc.gc.ca/services/cogeme/
In vivo and in vitro studies of Chlamydia trachomatis TrpR:DNA interactions
Authors: Carlson John H. , Wood Heidi , Roshick Christine , Caldwell Harlan D. , McClarty Grant 
Published: January 2006

SummaryWe previously reported that Chlamydia trachomatis expresses the genes encoding tryptophan synthase (trpBA) and the tryptophan repressor (trpR). Here we employ primer extension analysis to identify the transcriptional origins of both trpR and trpBA, allowing for the identification of the putative operator sequences for both trpR and trpBA. Moreover we demonstrate that native recombinant chlamydial TrpR binds to the predicted operator sequence upstream of trpR. A restriction endonuclease protection assay was designed and used to demonstrate that 5‐fluorotryptophan was the only tryptophan analogue capable of activating binding of native recombinant chlamydial TrpR to its operator. Additionally, 5‐fluorotryptophan was the only analogue that repressed expression of trpBA at a level analogous to l‐tryptophan itself. Based on these findings, a mutant selection protocol was designed and a C. trachomatis isolate containing a frameshift mutation in trpR was isolated. This chlamydial mutant synthesizes a truncated TrpR protein that cannot regulate expression of trpBA and trpR in response to changes in tryptophan levels. These findings provide the first genetic proof that TrpR acts as a negative regulator of transcription in C. trachomatis.
The toxbox: specific DNA sequence requirements for activation of Vibrio cholerae virulence genes by ToxT
Authors: Withey Jeffrey H. , DiRita Victor J. 
Published: January 2006

SummaryThe Gram‐negative, curved rod Vibrio cholerae causes the severe diarrhoeal disease cholera. The two major virulence factors produced by V. cholerae during infection are the cholera toxin (CT) and the toxin‐coregulated pilus (TCP). Transcription of the genes encoding both CT and the components of the TCP is directly activated by ToxT, a transcription factor in the AraC/XylS family. ToxT binds upstream of the ctxAB genes, encoding CT, and upstream of tcpA, the first gene in a large operon encoding the components of the TCP. The DNA sequences upstream of ctxAB and tcpA that contain ToxT binding sites do not have any significant similarity other than being AT‐rich. Extensive site‐directed mutagenesis was performed on the region upstream of tcpA previously shown to be protected by ToxT, and we identified specific base pairs important for activation of tcpA transcription by ToxT. This genetic approach was complemented by copper‐phenanthroline footprinting experiments that showed protection by ToxT of the base pairs identified as most important for transcription activation in the mutagenesis experiments. Based on this new information and on previous work, we propose the presence of a ToxT‐binding motif – the ‘toxbox’– in promoters regulated by ToxT. At tcpA, two toxbox elements are present in a direct repeat configuration and both are required for activation of transcription by ToxT. The identity of only a few of the base pairs within the toxbox is important for activation by ToxT, and we term these the core toxbox elements. Lastly, we examined ToxT binding to a mutant having 5 bp inserted between the two toxboxes at tcpA and found that occupancy of both binding sites is retained regardless of the positions of the binding sites relative to each other on the face of the DNA. This suggests that ToxT binds independently as a monomer to each toxbox in the tcpA direct repeat, in accordance with what we observed previously with the inverted repeat ToxT sites between acfA and acfD.
A novel polar surface polysaccharide from Rhizobium leguminosarum binds host plant lectin
Authors: Laus Marc C. , Logman Trudy J. , Lamers Gerda E. , Van Brussel Anton A. N. , Carlson Russell W. , Kijne Jan W. 
Published: January 2006

Summary Rhizobium bacteria produce different surface polysaccharides which are either secreted in the growth medium or contribute to a capsule surrounding the cell. Here, we describe isolation and partial characterization of a novel high molecular weight surface polysaccharide from a strain of Rhizobium leguminosarum that nodulates Pisum sativum (pea) and Vicia sativa (vetch) roots. Carbohydrate analysis showed that the polysaccharide consists for 95% of mannose and glucose, with minor amounts of galactose and rhamnose. Lectin precipitation analysis revealed high binding affinity of pea and vetch lectin for this polysaccharide, in contrast to the other known capsular and extracellular polysaccharides of this strain. Expression of the polysaccharide was independent of the presence of a Sym plasmid or the nod gene inducer naringenin. Incubation of R. leguminosarum with labelled pea lectin showed that this polysaccharide is exclusively localized on one of the poles of the bacterial cell. Vetch roots incubated with rhizobia and labelled pea lectin revealed that this bacterial pole is involved in attachment to the root surface. A mutant strain deficient in the production of this polysaccharide was impaired in attachment and root hair infection under slightly acidic conditions, in contrast to the situation at slightly alkaline conditions. Our data are consistent with the hypothesis that rhizobia can use (at least) two mechanisms for docking at the root surface, with use of a lectin–glycan mechanism under slightly acidic conditions.
Antibiotics and the ribosome
Authors: Tenson Tanel , Mankin Alexander 
Published: January 2006

SummaryThe ribosome is one of the main antibiotic targets in the cell. Recent years brought important insights into the mode of interaction of antibiotics with the ribosome and mechanisms of antibiotic action. Ribosome crystallography provided a detailed view of the interactions between antibiotics and rRNA. Advances in biochemical techniques let us better understand how the binding of small organic molecules can interfere with functions of an enzyme four orders of magnitude larger than the inhibitor. These and other achievements paved the way for the development of new ribosome‐targeting antibiotics, some of which have already entered medical practice. The recent progress, problems and new directions of research of ribosome‐targeting antibiotics are discussed in this review.
Bed forms in bimodal sand–gravel sediments: laboratory and field analysis
Authors: KUHNLE R. A. , HORTON J. K. , BENNETT S. J. , BEST J. L. 
Published: January 2006

AbstractBed forms were studied in Goodwin Creek and a laboratory flume channel. The bed sediment of the field site and flume had median diameters of 8·3 (modes of 0·4, 22·6 mm) and 1·82 mm (modes of 0·5, 5·6 mm), respectively. The laboratory and field channels had similar values of bimodal parameters, ratios of flow depth to median bed material diameter, and ratios of shear stress to critical shear stress and were judged to be comparable in the transport of bed load sediment and the resulting bed forms. Three groupings of bed forms from the laboratory flume experiments (ripple‐like bed forms, bed load sheets, low‐relief bed waves) were identified using the height and period of the bed forms. For the range of flow depths and discharges investigated in the flume, bed forms became higher and longer with increasing bed shear stress. Bed forms from Goodwin Creek were similar to those from the flume with comparable ratios between bed form length, height, and flow depth. The bed forms in the flume provide a positive link between rate and size fluctuations measured in the field and the bed forms. The smaller bed forms identified were sediment starved and are not considered to be dunes, while the largest bed forms in which all of the bed material sizes were mobilized in the field and laboratory were judged to be dunes.
Reduced inbreeding depression due to historical inbreeding in Drosophila melanogaster: evidence for purging
Authors: Swindell W. R. , Bouzat J. L. 
Published: January 2006

Abstract
An important issue in conservation biology and the study of evolution is the extent to which inbreeding depression can be reduced or reversed by natural selection. If the deleterious recessive alleles causing inbreeding depression can be ‘purged’ by natural selection, outbred populations that have a history of inbreeding are expected to be less susceptible to inbreeding depression. This expectation, however, has not been realized in previous laboratory experiments. In the present study, we used Drosophila melanogaster as a model system to test for an association between inbreeding history and inbreeding depression. We created six ‘purged’ populations from experimental lineages that had been maintained at a population size of 10 male–female pairs for 19 generations. We then measured the inbreeding depression that resulted from one generation of full-sib mating in the purged populations and in the original base population. The magnitude of inbreeding depression in the purged populations was approximately one-third of that observed in the original base population. In contrast to previous laboratory experiments, therefore, we found that inbreeding depression was reduced in populations that have a history of inbreeding. The large purging effects observed in this study may be attributable to the rate of historical inbreeding examined, which was slower than that considered in previous experiments.
Possible role of excitotoxicity in the pathogenesis of glaucoma
Authors: Casson Robert J 
Published: February 2006

AbstractExcitotoxicity describes the process of neuronal injury by excess stimulation of amino acid receptors. This form of insult was first described in the retina, and subsequently has been shown to be an important component of the pathogenesis of ischaemic and traumatic injury in the central nervous system. Furthermore, there is increasing evidence that excitotoxicity is involved in several chronic neurological conditions, and anti‐excitotoxic treatment has already been approved for some of these conditions. A large‐scale trial is currently underway that will determine the efficacy of an anti‐excitotoxic drug (memantine) in the management of glaucoma. This review provides an overview of neurotransmission and the mechanisms of excitotoxicity. The evidence for excitotoxicity as a component of certain neurological diseases, including glaucoma, is discussed.
Use of packaged entrees as part of a weight‐loss diet in overweight men: an 8‐week randomized clinical trial
Authors: Hannum S. M. , Carson L. A. , Evans E. M. , Petr E. L. , Wharton C. M. , Bui L. , Erdman J. W. 
Published: February 2006

Aim:  This study assessed the efficacy of a weight‐loss diet by using packaged portion‐controlled entrees vs. a self‐selected diet based on the United States Department of Agriculture Food Guide Pyramid (FGP).Methods:  Sixty healthy overweight men (body mass index (BMI) 26–42 kg/m2; aged 24–60 years) were randomized into two groups for an 8‐week intervention. Group E consumed two portion‐controlled entrees daily, plus recommended servings from the FGP. Group P consumed a self‐selected diet consisting of a recommended number of servings from the FGP. Diets were designed to be isocaloric (1700 kcal) and identical in macronutrient composition (55% carbohydrate, 25% protein and 20% fat). Participants were instructed to make no changes in physical activity levels. Each group was blinded to the protocol of the other group, and received separate diet instructions, but no behavioural or diet counselling. Outcomes included weight, BMI, body composition by dual energy X‐ray absorptiometry, waist and hip circumference, blood pressure (BP), fasting blood lipids, glucose, insulin and C‐reactive protein.Results:  Fifty‐one men completed the study. The portion‐control group E (n = 25) experienced greater decreases in weight (−7.4 ± 3.1 vs. −5.1 ± 4.0 kg), BMI (−2.4 ± 1.0 vs. −1.6 ± 1.3 kg/m2), fat mass (−3.6 ± 1.8 vs. −2.5 ± 1.8 kg), waist circumference (−6.6 ± 3.3 vs. −4.3 ± 2.9 cm) and diastolic BP (−6.0 ± 7.2 vs. + 0.2 ± 10.1 mmHg) than group P (n = 26) (p < 0.05). Consumption of a packaged entree diet resulted in greater losses of weight and fat mass, and reduced BP.Conclusions:  Use of packaged entrees as part of a weight‐loss diet is an effective means of achieving portion control and enhancing losses of weight and fat mass in overweight men.
A role for mixed lineage kinases in granule cell apoptosis induced by cytoskeletal disruption
Authors: Müller Georg Johannes , Geist Marie Aavang , Veng Lone Merete , Willesen Mette Georgi , Johansen Flemming Fryd , Leist Marcel , Vaudano Elisabetta 
Published: January 2006

AbstractMicrotubule disruption by colchicine induces apoptosis in selected neuronal populations. However, little is known about the upstream death signalling events mediating the neurotoxicity. We investigated first whether colchicine‐induced granule cell apoptosis activates the c‐Jun N‐terminal kinase (JNK) pathway. Cultured murine cerebellar granule cells were exposed to 1 µmcolchicine for 24 h. Activation of the JNK pathway was detected by western blotting as well as immunocytochemistry using antibodies against phospho‐c‐Jun (p‐c‐Jun). Next, adult male rats were injected intracerebroventricularly with colchicine (10 µg), and JNK pathway activation in dentate granule cells (DGCs) was detected by antibodies against p‐c‐Jun. The second part of the study tested the involvement of mixed lineage kinases (MLK) as upstream activators of the JNK pathway in colchicine toxicity, using CEP‐1347, a potent MLK inhibitor.In vitro, significant inhibition of the JNK pathway, activated by colchicine, was achieved by 100–300 nmCEP‐1347, which blocked both activation of cell death proteases and apoptosis. Moreover, CEP‐1347 markedly delayed neurite fragmentation and cell degeneration.In vivo, CEP‐1347 (1 mg/kg) significantly prevented p‐c‐jun increase following injection of colchicine, and enhanced survival of DGCs. We conclude that colchicine‐induced neuronal apoptosis involves the JNK/MLK pathway, and that protection of granule cells can be achieved by MLK inhibition.
Histamine protects against NMDA‐induced necrosis in cultured cortical neurons through H2 receptor/cyclic AMP/protein kinase A and H3 receptor/GABA release pathways
Authors: Dai Haibin , Zhang Zhongmiao , Zhu Yongpin , Shen Yao , Hu Weiwei , Huang Yuwen , Luo Jianhong , Timmerman Henk , Leurs Rob , Chen Zhong 
Published: January 2006

AbstractUsing histamine and the H3 receptor antagonist thioperamide, the roles of histamine receptors in NMDA‐induced necrosis were investigated in rat cultured cortical neurons. Within 3 h of intense NMDA insult, most neurons died by necrosis. Histamine reversed the neurotoxicity in a concentration‐dependent manner and showed peak protection at a concentration of 10−7 m. This protection was antagonized by the H2 receptor antagonists cimetidine and zolantidine but not by the H1 receptor antagonists pyrilamine and diphenhydramine. In addition, the selective H2 receptor agonist amthamine mimicked the protection by histamine. This action was prevented by cimetidine but not by pyrilamine. 8‐Bromo‐cAMP also mimicked the effect of histamine. In contrast, both the adenylyl cyclase inhibitor 9‐(tetrahydro‐2‐furanyl)‐9H‐purine‐6‐amine and the cAMP‐dependent protein kinase inhibitor N‐[2‐(p‐bromocinnamylamino) ethyl]‐5‐isoquinolinesulfonamide reversed the protection by histamine. Thioperamide also attenuated NMDA‐induced excitotoxicity, which was reversed by the H3 receptor agonist (R)‐α‐methylhistamine but not by pyrilamine and cimetidine. In addition, the protection by thioperamide was inhibited by the GABAA receptor antagonists picrotoxin and bicuculline. Further study demonstrated that the protection by thioperamide was due to increased GABA release in NMDA‐stimulated samples. These results indicate that not only the H2 receptor/cAMP/cAMP‐dependent protein kinase pathway but also the H3 receptor/GABA release pathway can attenuate NMDA‐induced neurotoxicity.
Shift in the ratio of three‐repeat tau and four‐repeat tau mRNAs in individual cholinergic basal forebrain neurons in mild cognitive impairment and Alzheimer's disease
Authors: Ginsberg Stephen D. , Che Shaoli , Counts Scott E. , Mufson Elliott J. 
Published: January 2006

AbstractMolecular mechanisms underlying tauopathy remain undetermined. In the current study, single cell gene expression profiling was coupled with custom‐designed cDNA array analysis to evaluate tau expression and other cytoskeletal elements within individual neuronal populations in patients with no cognitive impairment (NCI), mild cognitive impairment (MCI), and Alzheimer's disease (AD). Results revealed a shift in the ratio of three‐repeat tau (3Rtau) to four‐repeat tau (4Rtau) mRNAs within individual human cholinergic basal forebrain (CBF) neurons within nucleus basalis (NB) and CA1 hippocampal neurons during the progression of AD, but not during normal aging. A shift in 3Rtau to 4Rtau may precipitate a cascade of events in the selective vulnerability of neurons, ultimately leading to frank neurofibrillary tangle (NFT) formation in tauopathies including AD.
The BH3‐only protein Puma is both necessary and sufficient for neuronal apoptosis induced by DNA damage in sympathetic neurons
Authors: Wyttenbach Andreas , Tolkovsky Aviva M. 
Published: January 2006

AbstractDNA damage activates apoptosis in several neuronal populations and is an important component of neuropathological conditions. While it is well established that neuronal apoptosis, induced by DNA damage, is dependent on the key cell death regulators p53 and Bax, it is unknown which proteins link the p53 signal to Bax. Using rat sympathetic neurons as an in vitro model of neuronal apoptosis, we show that cytosine arabinoside is a DNA damaging drug that induces the expression of the BH3‐only pro‐apoptotic genes Noxa, Puma and Bim. Increased expression occurred after p53 activation, measured by its phosphorylation at serine 15, but prior to the conformational change of Bax at the mitochondria, cytochrome c (cyt c) release and apoptosis. Hence Noxa, Puma and Bim could potentially link p53 to Bax. We directly tested this hypothesis by the use of nullizygous mice. We show that Puma, but not Bim or Noxa, is a crucial mediator of DNA damage‐induced neuronal apoptosis. Despite the powerful pro‐apoptotic effects of overexpressed Puma in Bax‐expressing neurons, Bax nullizygous neurons were resistant to Puma‐induced death. Therefore, Puma provides the critical link between p53 and Bax, and is both necessary and sufficient to mediate DNA damage‐induced apoptosis of sympathetic neurons.
Ethanol inhibits L1 cell adhesion molecule activation of mitogen‐activated protein kinases
Authors: Tang Ningfeng , He Min , O'Riordan Mary Ann , Farkas Chloe , Buck Kevin , Lemmon Vance , Bearer Cynthia F. 
Published: January 2006

AbstractInhibition of the functions of L1 cell adhesion molecule (L1) by ethanol has been implicated in the pathogenesis of the neurodevelopmental aspects of the fetal alcohol syndrome (FAS). Ethanol at pharmacological concentrations has been shown to inhibit L1‐mediated neurite outgrowth of rat post‐natal day 6 cerebellar granule cells (CGN). Extracellular signal‐related kinases (ERK) 1/2 activation occurs following L1 clustering. Reduction in phosphoERK1/2 by inhibition of mitogen‐activated protein kinase kinase (MEK) reduces neurite outgrowth of cerebellar neurons. Here, we examine the effects of ethanol on L1 activation of ERK1/2, and whether this activation occurs via activation of fibroblast growth factor receptor 1 (FGFR1). Ethanol at 25 mm markedly inhibited ERK1/2 activation by both clustering L1 with cross‐linked monoclonal antibodies, or by L1‐Fc chimeric proteins. Clustering L1 with subsequent ERK1/2 activation did not result in tyrosine phosphorylation of the FGFR1. In addition, inhibition of FGFR1 tyrosine kinase blocked basic fibroblast growth factor (bFGF) activation of ERK1/2, but did not affect activation of ERK1/2 by clustered L1. We conclude that ethanol disrupts the signaling pathway between L1 clustering and ERK1/2 activation, and that this occurs independently of the FGFR1 pathway in cerebellar granule cells.