bluuebunny/crossref_metadata_2025_split huggingface dataset:
The RcsCDB Signaling System and Swarming Motility inSalmonella entericaSerovar Typhimurium: Dual Regulation of Flagellar and SPI-2 Virulence Genes
Authors: Wang Qingfeng , Zhao Yifang , McClelland Michael , Harshey Rasika M. 
Published: September 2007

ABSTRACTThe Rcs phosphorelay is a multicomponent signaling system that positively regulates colanic acid synthesis and negatively regulates motility and virulence. We have exploited a spontaneously isolated mutant, IgaA(T191P), that is nearly maximally activated for the Rcs system to identify a vast set of genes that respond to the stimulation, and we report new regulatory properties of this signaling system inSalmonella entericaserovar Typhimurium. Microarray data show that the Rcs system normally functions as a positive regulator of SPI-2 and other genes important for the growth ofSalmonellain macrophages, although when highly activated the system completely represses the SPI-1/SPI-2 virulence, flagellar, and fimbrial biogenesis pathways. The auxiliary protein RcsA, which works with RcsB to positively regulate colanic acid and other target genes, not only stimulates but also antagonizes the positive regulation of many genes in theigaAmutant. We show that RcsB represses motility through the RcsB box in the promoter region of the master operonflhDCand that RcsA is not required for this regulation. Curiously, RcsB selectively stimulates expression of the flagellar type 3 secretion genesfliPQR; an RcsAB box located downstream offliRinfluences this regulation. We show that excess colanic acid impairs swimming and inhibits swarming motility, consistent with the inverse regulation of the two pathways by the Rcs system.
Dynamics ofEscherichia coliChromosome Segregation during Multifork Replication
Authors: Nielsen Henrik J. , Youngren Brenda , Hansen Flemming G. , Austin Stuart 
Published: September 2007

ABSTRACTSlowly growingEscherichia colicells have a simple cell cycle, with replication and progressive segregation of the chromosome completed before cell division. In rapidly growing cells, initiation of replication occurs before the previous replication rounds are complete. At cell division, the chromosomes contain multiple replication forks and must be segregated while this complex pattern of replication is still ongoing. Here, we show that replication and segregation continue in step, starting at the origin and progressing to the replication terminus. Thus, early-replicated markers on the multiple-branched chromosomes continue to separate soon after replication to form separate protonucleoids, even though they are not segregated into different daughter cells until later generations. The segregation pattern follows the pattern of chromosome replication and does not follow the cell division cycle. No extensive cohesion of sister DNA regions was seen at any growth rate. We conclude that segregation is driven by the progression of the replication forks.
Genetic Dissection of the Divergent Activities of the Multifunctional Membrane Sensor BglF
Authors: Monderer-Rothkoff Galya , Amster-Choder Orna 
Published: September 2007

ABSTRACTBglF catalyzes β-glucoside phosphotransfer across the cytoplasmic membrane inEscherichia coli. In addition, BglF acts as a sugar sensor that controls expression of β-glucoside utilization genes by reversibly phosphorylating the transcriptional antiterminator BglG. Thus, BglF can exist in two opposed states: a nonstimulated state that inactivates BglG by phosphorylation and a sugar-stimulated state that activates BglG by dephosphorylation and phosphorylates the incoming sugar. Sugar phosphorylation and BglG (de)phosphorylation are both catalyzed by the same residue, Cys24. To investigate the coordination and the structural requirements of the opposing activities of BglF, we conducted a genetic screen that led to the isolation of mutations that shift the balance toward BglG phosphorylation. We show that some of the mutants that are impaired in dephosphorylation of BglG retained the ability to catalyze the concurrent activity of sugar phosphotransfer. These mutations map to two regions in the BglF membrane domain that, based on their predicted topology, were suggested to be implicated in activity. Using in vivo cross-linking, we show that a glycine in the membrane domain, whose substitution impaired the ability of BglF to dephosphorylate BglG, is spatially close to the active-site cysteine located in a hydrophilic domain. This residue is part of a newly identified motif conserved among β-glucoside permeases associated with RNA-binding transcriptional antiterminators. The phenotype of the BglF mutants could be suppressed by BglG mutants that were isolated by a second genetic screen. In summary, we identified distinct sites in BglF that are involved in regulating phosphate flow via the common active-site residue in response to environmental cues.
Distribution of Centromere-LikeparSSites in Bacteria: Insights from Comparative Genomics
Authors: Livny Jonathan , Yamaichi Yoshiharu , Waldor Matthew K. 
Published: September 2007

ABSTRACTPartitioning of low-copy-number plasmids to daughter cells often depends on ParA and ParB proteins acting on centromere-likeparSsites. Similar chromosome-encodedparloci likely also contribute to chromosome segregation. Here, we used bioinformatic approaches to search for chromosomalparSsites in 400 prokaryotic genomes. Although the consensus sequence matrix used to search forparSsites was derived from two gram-positive species, putativeparSsites were identified on the chromosomes of 69% of strains from all branches of bacteria. Strains that were not found to containparSsites clustered among relatively few branches of the prokaryotic evolutionary tree. In the vast majority of cases,parSsites were identified in origin-proximal regions of chromosomes. The widespread conservation ofparSsites across diverse bacteria suggests thatparloci evolved very early in the evolution of bacterial chromosomes and that the absence ofparS,parA, and/orparBin certain strains likely reflects the loss of one of more of these loci much later in evolution. Moreover, the highly conserved origin-proximal position ofparSsuggestsparloci are primarily devoted to regulating processes that involve the origin region of bacterial chromosomes. In species containing multiple chromosomes, theparSsites found on secondary chromosomes diverge significantly from those found on their primary chromosomes, suggesting that chromosome segregation of multipartite genomes requires distinct replicon-specificparloci. Furthermore,parSsites on secondary chromosomes are not well conserved among different species, suggesting that the evolutionary histories of secondary chromosomes are more diverse than those of primary chromosomes.
The
Myxococcus xanthus
Developmental Program Can Be Delayed by Inhibition of DNA Replication
Authors: Rosario Christopher J. , Singer Mitchell 
Published: September 2007

ABSTRACT

Under conditions of nutrient deprivation,
Myxococcus xanthus
undergoes a developmental process that results in the formation of a fruiting body containing environmentally resistant myxospores. We have shown that myxospores contain two copies of the genome, suggesting that cells must replicate the genome prior to or during development. To further investigate the role of DNA replication in development, a temperature-sensitive
dnaB
mutant, DnaB
A116V
, was isolated from
M. xanthus
. Unlike what happens in
Escherichia coli dnaB
mutants, where DNA replication immediately halts upon a shift to a nonpermissive temperature, growth and DNA replication of the
M. xanthus
mutant ceased after one cell doubling at a nonpermissive temperature, 37°C. We demonstrated that at the nonpermissive temperature the DnaB
A116V
mutant arrested as a population of 1
n
cells, implying that these cells could complete one round of the cell cycle but did not initiate new rounds of DNA replication. In developmental assays, the DnaB
A116V
mutant was unable to develop into fruiting bodies and produced fewer myxospores than the wild type at the nonpermissive temperature. However, the mutant was able to undergo development when it was shifted to a permissive temperature, suggesting that cells had the capacity to undergo DNA replication during development and to allow the formation of myxospores.
Molecular Typing of a Suspected Cluster of
Nocardia farcinica
Infections by Use of Randomly Amplified Polymorphic DNA, Pulsed-Field Gel Electrophoresis, and Amplified Fragment Length Polymorphism Analyses
Authors: Kalpoe J. S. , Templeton K. E. , Horrevorts A. M. , Endtz H. P. , Kuijper E. J. , Bernards A. T. , Klaassen C. H. W. 
Published: October 2007

ABSTRACT

Randomly amplified polymorphic DNA (RAPD), pulsed-field gelelectrophoresis (PFGE), and amplified fragment length polymorphism (AFLP) analyses were used to investigate a possible outbreak of
Nocardia farcinica
. RAPD and PFGE analyses yielded irreproducible and unsatisfactory results, respectively. AFLP analysis seem to be a promising and welcome addition for molecular analysis of
Nocardia
isolates.
Mycobacterium avium
Subspecies
paratuberculosis
Infection in Cases of Irritable Bowel Syndrome and Comparison with Crohn's Disease and Johne's Disease: Common Neural and Immune Pathogenicities
Authors: Scanu Antonio M. , Bull Tim J. , Cannas Sara , Sanderson Jeremy D. , Sechi Leonardo A. , Dettori Giuseppe , Zanetti Stefania , Hermon-Taylor John 
Published: October 2007

ABSTRACT

Mycobacterium avium
subsp.
paratuberculosis
causes Johne's disease, a systemic infection and chronic inflammation of the intestine that affects many species, including primates. Infection is widespread in livestock, and human populations are exposed. Johne's disease is associated with immune dysregulation, with involvement of the enteric nervous system overlapping with features of irritable bowel syndrome in humans. The present study was designed to look for an association between
Mycobacterium avium
subsp.
paratuberculosis
infection and irritable bowel syndrome. Mucosal biopsy specimens from the ileum and the ascending and descending colon were obtained from patients with irritable bowel syndrome attending the University of Sassari, Sassari, Sardinia, Italy. Crohn's disease and healthy control groups were also included.
Mycobacterium avium
subsp.
paratuberculosis
was detected by IS
900
PCR with amplicon sequencing. Data on the potential risk factors for human exposure to these pathogens and on isolates from Sardinian dairy sheep were also obtained.
Mycobacterium avium
subsp.
paratuberculosis
was detected in 15 of 20 (75%) patients with irritable bowel syndrome, 3 of 20 (15%) healthy controls, and 20 of 23 (87%) people with Crohn's disease (
P
= 0.0003 for irritable bowel syndrome patients versus healthy controls and
P
= 0.0000 for Crohn's disease patients versus healthy controls). One subject in each group had a conserved single-nucleotide polymorphism at position 247 of IS
900
that was also found in isolates from seven of eight dairy sheep. There was a significant association (
P
= 0.0018) between
Mycobacterium avium
subsp.
paratuberculosis
infection and the consumption of hand-made cheese.
Mycobacterium avium
subsp.
paratuberculosis
is a candidate pathogen in the causation of a proportion of cases of irritable bowel syndrome as well as in Crohn's disease.
Emergence of Usutu Virus in Hungary
Authors: Bakonyi Tamás , Erdélyi Károly , Ursu Krisztina , Ferenczi Emőke , Csörgő Tibor , Lussy Helga , Chvala Sonja , Bukovsky Christiane , Meister Tanja , Weissenböck Herbert , Nowotny Norbert 
Published: October 2007

ABSTRACT

In 2001, Usutu virus (USUV), a mosquito-borne flavivirus of the Japanese encephalitis virus serogroup related to West Nile virus and previously restricted to sub-Saharan Africa, emerged in wild and zoo birds in and around Vienna, Austria. In order to monitor the spread of the infection, a dead bird surveillance program was established in Austria and in neighboring Hungary. In Hungary, 332 dead birds belonging to 52 species were tested for USUV infection between 2003 and 2006. In the first 2 years, all birds investigated were negative. In August 2005, however, USUV was detected in organ samples of a blackbird (
Turdus merula
), which was found dead in Budapest, Hungary, by reverse transcription-PCR, immunohistochemistry, and in situ hybridization. In July and August 2006, a further six dead blackbirds tested positive for USUV, and the virus was isolated from organ samples of one bird. These birds were also found in urban areas of Budapest. The nearly complete genomic sequence of one Hungarian USUV strain was determined; it was found to share 99.9% identity with the strain that has been circulating in Austria since 2001. This result indicates that the USUV strain responsible for the blackbird die-off in Budapest most likely spread from Austria to Hungary instead of being independently introduced from Africa.
Human Seminal Plasma Abrogates the Capture and Transmission of Human Immunodeficiency Virus Type 1 to CD4
+
T Cells Mediated by DC-SIGN
Authors: Sabatté Juan , Ceballos Ana , Raiden Silvina , Vermeulen Mónica , Nahmod Karen , Maggini Julián , Salamone Gabriela , Salomón Horacio , Amigorena Sebastian , Geffner Jorge 
Published: October 2007

ABSTRACT

Dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN) is expressed by dendritic cells (DCs) at mucosal surfaces and appears to play an important role in the dissemination of human immunodeficiency virus type 1 (HIV-1) infection. DC-SIGN binds HIV-1 gp120 and efficiently transmits the virus to T CD4
+
cells, which become the center of viral replication. Semen represents the main vector for HIV-1 dissemination worldwide. In the present study we show that human seminal plasma (SP), even when used at very high dilutions (1:10
4
to 1:10
5
), markedly inhibits the capture and transmission of HIV-1 to T CD4
+
cells mediated by both DCs and B-THP-1-DC-SIGN cells. In contrast, SP does not inhibit the capture of HIV-1 by DC-SIGN-negative target cells, such as the T-cell line SupT-1, monocytes, and activated peripheral blood mononuclear cells. The SP inhibitor has a high molecular mass (>100 kDa) and directly interacts with DC-SIGN-positive target cells but not with HIV-1. Moreover, the inhibitor binds to concanavalin A, suggesting that it contains high-mannose N-linked carbohydrates. Of note, using biotin-labeled SP we found that the binding of SP components to DCs was abrogated by mannan, while their interaction with B-THP-1 cells was almost completely dependent on the expression of DC-SIGN. Since epithelium integrity is often compromised after vaginal or anal intercourse, as well as in the presence of ulcerative-sexually transmitted diseases, our results support the notion that components of the SP might be able to access to the subepithelium, inhibiting the recognition of HIV-1 gp120 by DC-SIGN-positive DCs.
Contribution of Endocytic Motifs in the Cytoplasmic Tail of Herpes Simplex Virus Type 1 Glycoprotein B to Virus Replication and Cell-Cell Fusion
Authors: Beitia Ortiz de Zarate Igor , Cantero-Aguilar Lilia , Longo Magalie , Berlioz-Torrent Clarisse , Rozenberg Flore 
Published: October 2007

ABSTRACT

The use of endocytic pathways by viral glycoproteins is thought to play various functions during viral infection. We previously showed in transfection assays that herpes simplex virus type 1 (HSV-1) glycoprotein B (gB) is transported from the cell surface back to the
trans
-Golgi network (TGN) and that two motifs of gB cytoplasmic tail, YTQV and LL, function distinctly in this process. To investigate the role of each of these gB trafficking signals in HSV-1 infection, we constructed recombinant viruses in which each motif was rendered nonfunctional by alanine mutagenesis. In infected cells, wild-type gB was internalized from the cell surface and concentrated in the TGN. Disruption of YTQV abolished internalization of gB during infection, whereas disruption of LL induced accumulation of internalized gB in early recycling endosomes and impaired its return to the TGN. The growth of both recombinants was moderately diminished. Moreover, the fusion phenotype of cells infected with the gB recombinants differed from that of cells infected with the wild-type virus. Cells infected with the YTQV-mutated virus displayed reduced cell-cell fusion, whereas giant syncytia were observed in cells infected with the LL-mutated virus. Furthermore, blocking gB internalization or impairing gB recycling to the cell surface, using drugs or a transdominant negative form of Rab11, significantly reduced cell-cell fusion. These results favor a role for endocytosis in virus replication and suggest that gB intracellular trafficking is involved in the regulation of cell-cell fusion.
RNA Editing of the Human Herpesvirus 8 Kaposin Transcript Eliminates Its Transforming Activity and Is Induced during Lytic Replication
Authors: Gandy Sharon Z. , Linnstaedt Sarah D. , Muralidhar Sumitra , Cashman Kathleen A. , Rosenthal Leonard J. , Casey John L. 
Published: October 2007

ABSTRACT
Human herpesvirus 8 is the etiologic agent associated with Kaposi's sarcoma and primary effusion lymphoma (PEL). The K12 RNA, which produces as many as three variants of the kaposin protein, as well as a microRNA, is the most abundant transcript expressed in latent Kaposi's sarcoma-associated herpesvirus infection, and yet it is also induced during lytic replication. The portion of the transcript that includes the microRNA and the kaposin A sequence has been shown to have tumorigenic potential. Genome coordinate 117990, which is within this transcript, has been found to be heterogeneous, primarily in RNAs but also among viral DNA sequences. This sequence heterogeneity affects an amino acid in kaposins A and C and the microRNA. The functional effects of this sequence heterogeneity have not been studied, and its origin has not been definitively settled; both RNA editing and heterogeneity at the level of the viral genome have been proposed. Here, we show that transcripts containing A at position 117990 are tumorigenic, while those with G at this position are not. Using a highly sensitive quantitative assay, we observed that, in PEL cells under conditions where more than 60% of cDNAs derived from K12 RNA transcripts have G at coordinate 117990, there is no detectable G in the viral DNA sequence at this position, only A. This result is consistent with RNA editing by one of the host RNA adenosine deaminases (ADARs). Indeed, we observed that purified human ADAR1 efficiently edits K12 RNA in vitro. Remarkably, the amount of editing correlated with the replicative state of the virus; editing levels were nearly 10-fold higher in cells treated to induce lytic viral replication. These results suggest that RNA editing controls the function of one segment of the kaposin transcript, such that it has transforming activity during latent replication and possibly another, as-yet-undetermined, function during lytic replication.
Adhesion Molecule Interactions Facilitate Human Immunodeficiency Virus Type 1-Induced Virological Synapse Formation between T Cells
Authors: Jolly Clare , Mitar Ivonne , Sattentau Quentin J. 
Published: October 2007

ABSTRACTHuman immunodeficiency virus type 1 (HIV-1) can spread between CD4+T cells by using a virological synapse (VS). The VS assembly is a cytoskeleton-driven process dependent on HIV-1 envelope glycoprotein (Env)-receptor engagement and is hypothesized to require adhesion molecule interactions. Here we demonstrate that leukocyte function-associated antigen 1 (LFA-1), intercellular adhesion molecule 1 (ICAM-1), and ICAM-3 are enriched at the VS and that inhibition of these interactions influences conjugate formation and reduces VS assembly. Moreover, CD4+T cells deficient in LFA-1 or with modified LFA-1 function were less able to support VS assembly and cell-cell transfer of HIV-1. Thus, cognate adhesion molecule interactions at the VS are important for HIV-1 spread between T cells.
Tioman Virus, a Paramyxovirus of Bat Origin, Causes Mild Disease in Pigs and Has a Predilection for Lymphoid Tissues
Authors: Yaiw Koon Chu , Bingham John , Crameri Gary , Mungall Bruce , Hyatt Alex , Yu Meng , Eaton Bryan , Shamala Devi , Wang Lin-Fa , Thong Wong Kum 
Published: October 2007

ABSTRACT

Disease manifestation, pathology, and tissue tropism following infection with Tioman virus (TioPV), a newly isolated, bat-derived paramyxovirus, was investigated in subcutaneously (
n
= 12) and oronasally (
n
= 4) inoculated pigs. Pigs were either asymptomatic or developed pyrexia, but all of the animals produced neutralizing antibodies. The virus (viral antigen and/or genome) was detected in lymphocytes of the thymus, tonsils, spleen, lymph nodes and Peyer's patches (ileum), tonsillar epithelium, and thymic epithelioreticular cells. Virus was isolated from oral swabs but not from urine. Our findings suggest that the pig could act as an intermediate or amplifying host for TioPV and that oral secretion is a possible means of viral transmission.
Human Papillomavirus Type 16 E7 Oncoprotein Associates with the Centrosomal Component γ-Tubulin
Authors: Nguyen Christine L. , Eichwald Catherine , Nibert Max L. , Münger Karl 
Published: October 2007

ABSTRACTExpression of a high-risk human papillomavirus (HPV) E7 oncoprotein is sufficient to induce aberrant centrosome duplication in primary human cells. The resulting centrosome-associated mitotic abnormalities have been linked to the development of aneuploidy. HPV type 16 (HPV16) E7 induces supernumerary centrosomes through a mechanism that is at least in part independent of the inactivation of the retinoblastoma tumor suppressor pRb and is dependent on cyclin-dependent kinase 2 activity. Here, we show that HPV16 E7 can concentrate around mitotic spindle poles and that a small pool of HPV16 E7 is associated with centrosome fractions isolated by sucrose density gradient centrifugation. The targeting of HPV16 E7 to the centrosome, however, was not sufficient for centrosome overduplication. Nonetheless, we found that HPV16 E7 can associate with the centrosomal regulator γ-tubulin and that the recruitment of γ-tubulin to the centrosome is altered in HPV16 E7-expressing cells. Since the association of HPV16 E7 with γ-tubulin is independent of pRb, p107, and p130, our results suggest that the association with γ-tubulin contributes to the pRb/p107/p130-independent ability of HPV16 E7 to subvert centrosome homeostasis.
Allogeneic Differences in the Dependence on CD4+T-Cell Help for Virus-Specific CD8+T-Cell Differentiation
Authors: Kemball Christopher C. , Szomolanyi-Tsuda Eva , Lukacher Aron E. 
Published: October 2007

ABSTRACTCD4+T-cell help enables antiviral CD8+T cells to differentiate into fully competent memory cells and sustains CD8+T-cell-mediated immunity during persistent virus infection. We recently reported that mice of C57BL/6 and C3H strains differ in their dependence on CD28 and CD40L costimulation for long-term control of infection by polyoma virus, a persistent mouse pathogen. In this study, we asked whether mice of these inbred strains also vary in their requirement for CD4+T-cell help for generating and maintaining polyoma virus-specific CD8+T cells. CD4+T-cell-depleted C57BL/6 mice mounted a robust antiviral CD8+T-cell response during acute infection, whereas unhelped CD8+T-cell effectors in C3H mice were functionally impaired during acute infection and failed to expand upon antigenic challenge during persistent infection. Using (C57BL/6 × C3H)F1mice, we found that the dispensability for CD4+T-cell help for the H-2b-restricted polyoma virus-specific CD8+T-cell response during acute infection extends to the H-2k-restricted antiviral CD8+T cells. Our findings demonstrate that dependence on CD4+T-cell help for antiviral CD8+T-cell effector differentiation can vary among allogeneic strains of inbred mice.