bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sanitation practices that inhibit reproduction of Monosporascus cannonballus in melon roots left in the field after crop termination
Authors: Radewald K. C. , Ferrin D. M. , Stanghellini M. E. 
Published: November 2004

Ascospores of Monosporascus cannonballus function as primary inoculum for infection of melon roots. Previous studies demonstrated that pathogen reproduction (i.e. ascospore production) occurs on infected melon roots primarily after the crop has been terminated. Therefore, the key to maintaining low soil population densities of the pathogen is to destroy the hyphae of the pathogen in infected roots as soon as possible after crop termination, thereby inhibiting ascospore production. Results from a 3‐year field study demonstrated that, relative to the nontreated controls, an immediate postharvest application of metam sodium (applied via the drip irrigation system at 187 L ha−1) or cultivation (which lifts roots onto the surface of the soil for rapid desiccation) significantly inhibited pathogen reproduction in infected melon roots, as shown by the number of roots subsequently bearing perithecia. Additionally, ascospore populations in plots that received either the metam sodium or cultivation treatment were significantly lower (P < 0·05) than populations in the nontreated control plots at the end of the 3‐year study. These results demonstrated the efficacy of these postharvest treatments in the inhibition of pathogen reproduction and retardation of inoculum build‐up in soil.
Effect of soil amendments, intercropping and planting time in combination on the severity of cassava bacterial blight and yield in two ecozones of West Africa
Authors: Zinsou V. , Wydra K. , Ahohuendo B. , Hau B. 
Published: November 2004

The severity of cassava bacterial blight at two sites in the forest‐savanna transition (FST) and dry savanna (DS) zones of West Africa were studied by assessing the effects of: (i) shift of planting date; (ii) potassium fertilizer application and mulching; (iii) intercropping cassava with sorghum or cowpea vs. cassava monoculture; and (iv) the combination of these measures. Disease severity of bacterial blight in two genotypes was generally reduced by 20–60% by late planting, without a negative effect on cassava root yield, in monocropping systems in most treatments in the FST zone (reduction in four treatments, and increase in two treatments, out of 19) and the DS zone (two of eight treatments in 1 year). Late planting led to crop failure in the DS zone in the second year. Intercropping cassava with sorghum reduced bacterial blight severity significantly, up to 80% at normal (all treatments) and late planting time (three out of six treatments) in the FST zone, and in some treatments (four out of seven) at normal planting in the DS zone. Intercropping of cassava with cowpea in the DS zone also reduced disease severity. Cassava‐sorghum intercropping generally had no effect on root yield compared with cassava monocropping at both planting times in the FST zone and provided an additional harvest of the intercrop, while yield was affected by intercropping in the DS zone at late, and in some treatments (three out of seven) at normal, planting time. Mulching and potassium treatment had no effect on disease severity, but increased or decreased root yield in some treatments in both sites. Analysis of combined data showed that cropping system, year, site, and site combined with planting date were the highest significant determinants of variation in bacterial blight development.
Eradication of plant pathogens and nematodes during composting: a review
Authors: Noble R. , Roberts S. J. 
Published: November 2004

The effects of temperature–time combinations and other sanitizing factors during composting on 64 plant pathogenic fungi, plasmodiophoromycetes, oomycetes, bacteria, viruses and nematodes were reviewed. In most cases pathogen survival was determined by bioassays of unknown sensitivity and minimum detection limits of 5% infection or more. For 33 out of 38 fungal and oomycete pathogens, all seven bacterial pathogens and nine nematodes, and three out of nine plant viruses, a peak temperature of 64–70°C and duration of 21 days, were sufficient to reduce numbers to below the detection limits of the tests used. Shorter periods and/or lower temperatures than those quoted in these tests may be satisfactory for eradication, but they were not always examined in detail in composting systems. Plasmodiophora brassicae (clubroot of Brassica spp.), Fusarium oxysporum f.sp. lycopersici (tomato wilt) and Macrophomina phaseolina (dry root rot) were more temperature‐tolerant, as they survived a peak compost temperature of at least 62°C (maximum 74°C) and a composting duration of 21 days. Synchytrium endobioticum (potato wart disease) survived in water at 60°C for 2 h, but was not examined in compost. For Tobacco mosaic virus (TMV), peak compost temperatures in excess of 68°C and composting for longer than 20 days were needed to reduce numbers below detection limits. However, TMV and Tomato mosaic virus (TomMV) were inactivated over time in compost, even at temperatures below 50°C. Temperatures in excess of 60°C were achieved in different composting systems, with a wide range of organic feedstocks. The potential survival of plant pathogens in cooler zones of compost, particularly in systems where the compost is not turned, has not been quantified. This may be an important risk factor in composting plant wastes.
Cladistic revision of talitroidean amphipods (Crustacea, Gammaridea), with a proposal of a new classification
Authors: Serejo Cristiana S. 
Published: November 2004

This paper reports the results of a cladistic analysis of the Talitroidea s.l., which includes about 400 species, in 96 genera distributed in 10 families. The analysis was performed using paup and was based on a character matrix of 34 terminal taxa and 43 morphological characters. Four most parsimonious trees were obtained with 175 steps (CI = 0.617, RI = 0.736). A strict consensus tree was calculated and the following general conclusions were reached. The superfamily Talitroidea is elevated herein as infraorder Talitrida, which is subdivided into three main branches: a small clade formed by Kuria and Micropythia (the Kurioidea), and two larger groups maintained as distinct superfamilies (Phliantoidea, including six families, and Talitroidea s.s., including four). Within the Talitroidea s.s., the following taxonomic changes are proposed: Hyalellidae and Najnidae are synonymized with Dogielinotidae, and treated as subfamilies; a new family rank is proposed for the Chiltoniinae.
Characterization of a novel Neisseria meningitidis Fur and iron‐regulated operon required for protection from oxidative stress: utility of DNA microarray in the assignment of the biological role of hypothetical genes
Authors: Grifantini Renata , Frigimelica Elisabetta , Delany Isabel , Bartolini Erika , Giovinazzi Serena , Balloni Sergio , Agarwal Sarika , Galli Giuliano , Genco Caroline , Grandi Guido 
Published: November 2004

SummaryWe have previously shown that in the human pathogen Neisseria meningitidis group B (MenB) more than 200 genes are regulated in response to growth with iron. Among the Fur‐dependent, upregulated genes identified by microarray analysis was a putative operon constituted by three genes, annotated as NMB1436, NMB1437 and NMB1438 and encoding proteins with so far unknown function. The operon was remarkably upregulated in the presence of iron and, on the basis of gel retardation analysis, its regulation was Fur dependent. In this study, we have further characterized the role of iron and Fur in the regulation of the NMB1436–38 operon and we have mapped the promoter and the Fur binding site. We also demonstrate by mutant analysis that the NMB1436–38 operon is required for protection of MenB to hydrogen peroxide‐mediated killing. By using both microarray analysis and S1 mapping, we demonstrate that the operon is not regulated by oxidative stress signals. We also show that the deletion of the NMB1436–38 operon results in an impaired capacity of MenB to survive in the blood of mice using an adult mouse model of MenB infection. Finally, we show that the NMB1436–38 deletion mutant exhibits increased susceptibility to the killing activity of polymorphonuclears (PMNs), suggesting that the ‘attenuated’ phenotype is mediated in part by the increased sensitivity to reactive oxygen species‐producing cells. This study represents one of the first examples of the use of DNA microarray to assign a biological role to hypothetical genes in bacteria.
RNA‐guided nucleotide modification of ribosomal and non‐ribosomal RNAs in Archaea
Authors: Ziesche Sonia M. , Omer Arina D. , Dennis Patrick P. 
Published: November 2004

SummaryArchaea use ribonucleoprotein (RNP) machines similar to those found in the eukaryotic nucleolus to methylate ribose residues in nascent ribosomal RNA. The archaeal complex required for this 2′‐O‐ribose‐methylation consists of the C/D box sRNA guide and three proteins, the core RNA‐binding aL7a protein, the aNop56 protein and the methyltransferase aFib protein. These RNP machines were reconstituted in vitro from purified recombinant components, and shown to have methylation activity when provided with a simple target oligonucleotide, complementary to the sRNA guide sequence. To obtain a better understanding of the versatility and specificity of this reaction, the activity of reconstituted particles on more complex target substrates, including 5S RNA, tRNAGln and ‘double target’ oligonucleotides that exhibit either direct or reverse complementarity to both the D′ and D box guides, has been examined. The natural 5S and tRNAGln substrates were efficiently methylated in vitro, as long as the complementarity between guide and target was about 10 base pairs in length, and lacked mismatches. Maximal activity of double guide sRNAs required that both methylation sites be present in cis on the target RNA.
Identification of host‐specific colonization factors of Salmonella enterica serovar Typhimurium
Authors: Morgan Eirwen , Campbell June D. , Rowe Sonya C. , Bispham Jennie , Stevens Mark P. , Bowen Alison J. , Barrow Paul A. , Maskell Duncan J. , Wallis Timothy S. 
Published: November 2004

SummaryThe severity of infections caused by Salmonella enterica serovar Typhimurium varies depending on the host species. Numerous virulence genes have been identified in S. Typhimurium, largely from studies in mice, but their roles in infections of other species remain unclear. In the most comprehensive survey of its kind, through the use of signature‐tagged mutagenesis of S. Typhimurium we have identified mutants that were unable to colonize calf intestines, mutants unable to colonize chick intestines and mutants unable to colonize both species. The type three secretion systems encoded on Salmonella pathogenicity islands (SPIs) 1 and 2 were required for efficient colonization of cattle. However, disruption of these secretion systems only caused a minor defect in S. Typhimurium colonization of chicks. Transposon insertions in SPI‐4 compromised S. Typhimurium colonization of cattle, but not chicks. This is the first data confirming a role for SPI‐4 in pathogenesis. We have also been able to ascribe a role in colonization for cell surface polysaccharides, cell envelope proteins, and many ‘housekeeping’ genes and genes of unknown function. We conclude that S. Typhimurium uses different strategies to colonize calves and chicks. This has major implications for vaccine design.
In vivo effect of inactivation of ribosome recycling factor – fate of ribosomes after unscheduled translation downstream of open reading frame
Authors: Hirokawa Go , Inokuchi Hachiro , Kaji Hideko , Igarashi Kazuei , Kaji Akira 
Published: November 2004

SummaryThe post‐termination ribosomal complex is disassembled by ribosome recycling factor (RRF) and elongation factor G. Without RRF, the ribosome is not released from mRNA at the termination codon and reinitiates translation downstream. This is called unscheduled translation. Here, we show that at the non‐permissive temperature of a temperature‐sensitive RRF strain, RRF is lost quickly, and some ribosomes reach the 3′ end of mRNA. However, instead of accumulating at the 3′ end of mRNA, ribosomes are released as monosomes. Some ribosomes are transferred to transfer‐messenger RNA from the 3′ end of mRNA. The monosomes thus produced are able to translate synthetic homopolymer but not natural mRNA with leader and canonical initiation signal. The pellet containing ribosomes appears to be responsible for rapid but reversible inhibition of most but not all of protein synthesis in vivo closely followed by decrease of cellular RNA and DNA synthesis.
Enolase in the RNA degradosome plays a crucial role in the rapid decay of glucose transporter mRNA in the response to phosphosugar stress in Escherichia coli
Authors: Morita Teppei , Kawamoto Hiroshi , Mizota Taisei , Inada Toshifumi , Aiba Hiroji 
Published: November 2004

SummaryThe ptsG mRNA encoding the major glucose transporter is rapidly degraded in an RNase E‐dependent manner in response to the accumulation of glucose 6‐P or fructose 6‐P when the glycolytic pathway is blocked at its early steps in Escherichia coli. RNase E, a major endonuclease, is associated with polynucleotide phosphorylase (PNPase), RhlB helicase and a glycolytic enzyme, enolase, which bind to its C‐terminal scaffold region to form a multienzyme complex called the RNA degradosome. The role of enolase within the RNase E‐based degradosome in RNA decay has been totally mysterious. In this article, we demonstrate that the removal of the scaffold region of RNase E suppresses the rapid degradation of ptsG mRNA in response to the metabolic stress without affecting the expression of ptsG mRNA under normal conditions. We also demonstrate that the depletion of enolase but not the disruption of pnp or rhlB eliminates the rapid degradation of ptsG mRNA. Taken together, we conclude that enolase within the degradosome plays a crucial role in the regulation of ptsG mRNA stability in response to a metabolic stress. This is the first instance in which a physiological role for enolase in the RNA degradosome has been demonstrated. In addition, we show that PNPase and RhlB within the degradosome cooperate to eliminate short degradation intermediates of ptsG mRNA.
A novel sensor kinase–response regulator hybrid regulates type III secretion and is required for virulence in Pseudomonas aeruginosa
Authors: Laskowski Michelle A. , Osborn Ellice , Kazmierczak Barbara I. 
Published: November 2004

SummaryThe type III secretion system (TTSS) of Pseudomonas aeruginosa is induced by contact with eukaryotic cells and by growth in low‐calcium media. We have identified a protein, RtsM, that is necessary for expression of the TTSS genes in P. aeruginosa. RtsM possesses both histidine kinase and response regulator domains common to two‐component signalling proteins, as well as a large predicted periplasmic domain and seven transmembrane domains. Deletion of rtsM resulted in a defect in production and secretion of the type III effectors. Northern blot analysis revealed that mRNAs encoding the effectors ExoT and ExoU are absent in the ΔrtsM strain under TTSS‐inducing conditions. Using transcriptional fusions, we demonstrated that RtsM is required for transcription of the operons encoding the TTSS effectors and apparatus in response to calcium limitation or to host cell contact. The operon encoding the TTSS regulator ExsA does not respond to calcium limitation, but the basal transcription rate of this operon was lower in ΔrtsM than in the wild‐type parent, PA103. The defect in TTSS effector production and secretion of ΔrtsM could be complemented by overexpressing ExsA or Vfr, two transcriptional activators involved in TTSS regulation. ΔrtsM was markedly less virulent than PA103 in a murine model of acute pneumonia, demonstrating that RtsM is required in vivo. We propose that RtsM is a sensor protein at the start of a signalling cascade that induces expression of the TTSS in response to environmental signals.
Functional dependence on calcineurin by variants of the Saccharomyces cerevisiae vacuolar Ca2+/H+ exchanger Vcx1p
Authors: Pittman Jon K. , Cheng Ning‐Hui , Shigaki Toshiro , Kunta Madhurababu , Hirschi Kendal D. 
Published: November 2004

SummaryThe Ca2+‐dependent protein phosphatase calcineurin is an important regulator of ion transporters from many organisms, including the Saccharomyces cerevisiae vacuolar Ca2+/H+ exchanger Vcx1p. In yeast and plants, cation/H+ exchangers are important in shaping cytosolic Ca2+ levels involved in signal transduction and providing tolerance to potentially toxic concentrations of cations such as Ca2+, Mn2+ and Cd2+. Previous genetic evidence suggested Vcx1p is negatively regulated by calcineurin. By utilizing direct transport measurements into vacuolar membrane vesicles, we demonstrate that Vcx1p is a low‐affinity Ca2+ transporter and may also function in Cd2+ transport, but cannot transport Mn2+. Furthermore, direct Ca2+ transport by Vcx1p is calcineurin sensitive. Using a yeast growth assay, a mutant allele of VCX1 (VCX1‐S204A/L208P), termed VCX1‐M1, was previously found to confer strong Mn2+ tolerance. Here we demonstrate that this Mn2+ tolerance is independent of the Ca2+/Mn2+‐ATPase Pmr1p and results from Mn2+‐specific vacuolar transport activity of Vcx1‐M1p. This Mn2+ transport by Vcx1‐M1p is calcineurin dependent, although the localization of Vcx1‐M1p to the vacuole appears to be calcineurin independent. Additionally, we demonstrate that mutation of L208P alone is enough to confer calcineurin‐dependent Mn2+ tolerance. This study demonstrates that calcineurin can positively regulate the transport of cations by VCX1‐M1p.
Direct and indirect transcriptional activation of virulence genes by an AraC‐like protein, PerA from enteropathogenic Escherichia coli
Authors: Porter Megan E. , Mitchell Paul , Roe Andrew J. , Free Andrew , Smith David G. E. , Gally David L. 
Published: November 2004

SummaryThe plasmid‐encoded Per regulatory locus of enteropathogenic Escherichia coli (EPEC) is generally considered to consist of three genes, perA, perB and perC. PerA, a member of the AraC‐like family of transcriptional regulators, is known to be an activator of its own promoter (autoactivation) as well as of the plasmid‐located bfp operon encoding bundle‐forming pili, but its role in activation of the chromosomal locus of enterocyte effacement (LEE) pathogenicity island, which confers the property of intimate adherence on EPEC, requires clarification. Here, we show that PerA is also required for activation of the master regulatory LEE operon, LEE1, but that this activation is indirect, being achieved via autoactivation of the per promoter which ensures sufficient production of the PerC protein to activate LEE1. In contrast, PerA‐dependent activation of the per and bfp promoters is direct and does not require the other Per proteins, but is modulated by the nucleoid‐associated protein H‐NS. The closely related VirF regulator from Shigella flexneri cannot substitute for PerA to activate these promoters, despite being able to bind their upstream regions in vitro. PerA can bind the per and bfp promoter fragments to form multiple complexes, while VirF forms only a single complex. Site‐directed mutagenesis of the PerA protein suggests that, like VirF, it may use both of its carboxy‐terminal helix—turn–helix motifs for DNA interaction, and may also make direct contacts with RNA polymerase. In addition, we have isolated mutations in the poorly characterized amino‐terminal domain of PerA which affect its ability to activate gene expression.
FtsK activities in Xer recombination, DNA mobilization and cell division involve overlapping and separate domains of the protein
Authors: Bigot Sarah , Corre Jacqueline , Louarn Jean‐Michel , Cornet François , Barre François‐Xavier 
Published: November 2004

Summary Escherichia coli FtsK is a multifunctional protein that couples cell division and chromosome segregation. Its N‐terminal transmembrane domain (FtsKN) is essential for septum formation, whereas its C‐terminal domain (FtsKC) is required for chromosome dimer resolution by XerCD‐dif site‐specific recombination. FtsKC is an ATP‐dependent DNA translocase. In vitro and in vivo data point to a dual role for this domain in chromosome dimer resolution (i) to directly activate recombination by XerCD‐dif and (ii) to bring recombination sites together and/or to clear DNA from the closing septum. FtsKN and FtsKC are separated by a long linker region (FtsKL) of unknown function that is highly divergent between bacterial species. Here, we analysed the in vivo effects of deletions of FtsKL and/or of FtsKC, of swaps of these domains with their Haemophilus influenzae counterparts and of a point mutation that inactivates the walker A motif of FtsKC. Phenotypic characterization of the mutants indicated a role for FtsKL in cell division. More importantly, even though Xer recombination activation and DNA mobilization both rely on the ATPase activity of FtsKC, mutants were found that can perform only one or the other of these two functions, which allowed their separation in vivo for the first time.
The Sm‐like protein Hfq regulates polyadenylation dependent mRNA decay in Escherichia coli
Authors: Mohanty Bijoy K. , Maples Valerie F. , Kushner Sidney R. 
Published: November 2004

SummaryIn Escherichia coli, the post‐transcriptional addition of poly(A) tails by poly(A) polymerase I (PAP I, pcnB) plays a significant role in cellular RNA metabolism. However, many important features of this system, including its regulation and the selection of polyadenylation sites, are still poorly understood. Here we show that the inactivation of Hfq (hfq), an abundant RNA‐binding protein, leads to the reduction in the ability of PAP I to add poly(A) tails at the 3′ termini of mRNAs containing Rho‐independent transcription terminators even though PAP I protein levels remain unchanged. Those poly(A) tails that are synthesized in the absence of Hfq are shorter in length, even in the absence of polynucleotide phosphorylase (PNPase), RNase II and RNase E. In fact, the biosynthetic activity of PNPase in the hfq single mutant is enhanced and it becomes the primary polynucleotide polymerase, adding heteropolymeric tails almost exclusively to 3′ truncated mRNAs. Surprisingly, both PNPase and Hfq co‐purified with His‐tagged PAP I under native conditions indicating a potential complex among these proteins. Immunoprecipitation experiments using PNPase‐ and Hfq‐specific antibodies confirmed the protein–protein interactions among PAP I, PNPase and Hfq. Analysis of mRNA half‐lives in hfq, ΔpcnB and hfq ΔpcnB mutants suggests that Hfq and PAP I function in the same mRNA decay pathway.