bluuebunny/crossref_metadata_2025 huggingface dataset:
β1,2-Xylosyltransferase Cxt1p Is Solely Responsible for Xylose Incorporation into
Cryptococcus neoformans
Glycosphingolipids
Authors: Castle Sherry A. , Owuor Elizabeth A. , Thompson Stephanie H. , Garnsey Michelle R. , Klutts J. Stacey , Doering Tamara L. , Levery Steven B.
Published: August 2008

The Manα1,3(Xylβ1,2)Manα structural motif is common to both capsular polysaccharides of
Cryptococcus neoformans
and to cryptococcal glycosphingolipids. Comparative analysis of glycosphingolipid structural profiles in wild-type and mutant strains showed that the Xylβ1,2-transferase (Cxt1p) that participates in capsular polysaccharide biosynthesis is also the sole transferase responsible for adding xylose to
C. neoformans
glycosphingolipids.
Regulation of CorA Mg
2+
Channel Function Affects the Virulence of
Salmonella enterica
Serovar Typhimurium
Authors: Papp-Wallace Krisztina M. , Maguire Michael E.
Published: August 2008

The CorA Mg
2+
channel is the primary source of intracellular Mg
2+
in
Salmonella enterica
serovar Typhimurium. In another study, we found that a strain lacking
corA
was attenuated in mice and also defective for invasion and replication within Caco-2 epithelial cells (K. M. Papp-Wallace, M. Nartea, D. G. Kehres, S. Porwollik, M. McClelland, S. J. Libby, F. C. Fang, and M. E. Maguire, J. Bacteriol. 190:6517-6523, 2008). Therefore, we further examined
Salmonella
interaction with Caco-2 epithelial cells. Inhibiting CorA acutely or chronically with a high concentration of a selective inhibitor, Co(III) hexaammine, had no effect on
S. enterica
serovar Typhimurium invasion of Caco-2 epithelial cells. Complementing the
corA
mutation with
corA
from various species rescued the invasion defect only if the complementing allele was functional and if it was evolutionarily similar to
S. enterica
serovar Typhimurium CorA. One explanation for these results could be that regulation of CorA function is needed for optimal virulence. Further experiments examining
corA
transcription, CorA protein content, CorA transport, and cell Mg
2+
content indicated that both CorA expression and CorA function are differentially regulated. Moreover, the rates of Mg
2+
influx via CorA are not closely correlated with either protein levels or Mg
2+
content. We conclude that loss of the CorA protein disrupts a regulatory network(s) with the ultimate phenotype of decreased virulence. This conclusion is compatible with the microarray results in our other study, which showed that loss of
corA
resulted in changes in transcription (and protein expression) in multiple metabolic pathways (Papp-Wallace et al., J. Bacteriol. 190:6517-6523, 2008). Further study of the regulation of CorA expression and function provides an opportunity to dissect the complexity of Mg
2+
homeostasis and its ties to virulence within the bacterium.
Transition State Regulator AbrB Inhibits Transcription of
Bacillus amyloliquefaciens
FZB45 Phytase through Binding at Two Distinct Sites Located within the Extended
phyC
Promoter Region
Authors: Makarewicz Oliwia , Neubauer Svetlana , Preusse Corinna , Borriss Rainer
Published: August 2008

We have previously identified the
phyC
gene of
Bacillus amyloliquefaciens
FZB45, encoding extracellular phytase, as a member of the PhoP regulon, which is expressed only during phosphate starvation. Its σ
A
-dependent promoter is positively and negatively regulated by the phosphorylated PhoP response regulator in a phosphate-dependent manner (O. Makarewicz, S. Dubrac, T. Msadek, and R. Borriss, J. Bacteriol. 188:6953-6965, 2006). Here, we provide experimental evidence that the transcription of
phyC
underlies a second control mechanism exerted by the global transient-phase regulator protein, AbrB, which hinders its expression during exponential growth. Gel mobility shift and DNase I footprinting experiments demonstrated that AbrB binds to two different regions in the
phyC
promoter region that are separated by about 200 bp. One binding site is near the divergently orientated
yodU
gene, and the second site is located downstream of the
phyC
promoter and extends into the coding region of the
phyC
gene. Cooperative binding to the two distant binding regions is necessary for the AbrB-directed repression of
phyC
transcription. AbrB does not affect the transcription of the neighboring
yodU
gene.
A Defect in Menadione Biosynthesis Induces Global Changes in Gene Expression in
Staphylococcus aureus
Authors: Kohler Christian , von Eiff Christof , Liebeke Manuel , McNamara Peter J. , Lalk Michael , Proctor Richard A. , Hecker Michael , Engelmann Susanne
Published: August 2008

Both the high-resolution two-dimensional protein gel electrophoresis technique and full-genome DNA microarrays were used for identification of
Staphylococcus aureus
genes whose expression was changed by a mutation in
menD
. Because the electron transport chain is interrupted, the mutant should be unable to use oxygen and nitrate as terminal electron acceptors. Consistent with this, a mutation in
menD
was found to cause a gene expression pattern typically detected under anaerobic conditions in wild-type cells: proteins involved in glycolytic as well as in fermentation pathways were upregulated, whereas tricarboxylic acid (TCA) cycle enzymes were significantly downregulated. Moreover, the expression of genes encoding enzymes for nitrate respiration and the arginine deiminase pathway was strongly increased in the mutant strain. These results indicate that the
menD
mutant, just as the site-directed
S. aureus hemB
mutant, generates ATP from glucose or fructose mainly by substrate phosphorylation and might be defective in utilizing a variety of carbon sources, including TCA cycle intermediates and compounds that generate ATP only via electron transport phosphorylation. Of particular interest is that there are also differences in the gene expression patterns between
hemB
and
menD
mutants. While some anaerobically active enzymes were present in equal amounts in both strains (Ldh1, SACOL2535), other classically anaerobic enzymes seem to be present in higher amounts either in the
hemB
mutant (e.g., PflB, Ald1, IlvA1) or in the
menD
mutant (
arc
operon). Only genes involved in nitrate respiration and the
ald1
operon seem to be additionally regulated by a depletion of oxygen in the
hemB
and/or
menD
mutant.
X-Ray Absorption Spectroscopy as a Probe of Microbial Sulfur Biochemistry: the Nature of Bacterial Sulfur Globules Revisited
Authors: George Graham N. , Gnida Manuel , Bazylinski Dennis A. , Prince Roger C. , Pickering Ingrid J.
Published: August 2008

The chemical nature of the sulfur in bacterial sulfur globules has been the subject of controversy for a number of years. Sulfur K-edge X-ray absorption spectroscopy (XAS) is a powerful technique for probing the chemical forms of sulfur in situ, but two groups have used it with very different conclusions. The root of the controversy lies with the different detection strategies used by the two groups, which result in very different spectra. This paper seeks to resolve the controversy. We experimentally demonstrate that the use of transmittance detection for sulfur K-edge XAS measurements is highly prone to spectroscopic distortions and that much of the published work on sulfur bacteria is very likely based on distorted data. We also demonstrate that all three detection methods used for X-ray absorption experiments yield essentially identical spectra when the measurements are carried out under conditions where no experimental distortions are expected. Finally, we turn to the original question—the chemical nature of bacterial sulfur. We examine isolated sulfur globules of
Allochromatium vinosum
and intact cells of a strain of magnetotactic coccus and show that XAS indicates the presence of a chemical form of sulfur resembling S
8
.
The
Vibrio cholerae
Hybrid Sensor Kinase VieS Contributes to Motility and Biofilm Regulation by Altering the Cyclic Diguanylate Level
Authors: Martinez-Wilson Hector F. , Tamayo Rita , Tischler Anna D. , Lazinski David W. , Camilli Andrew
Published: August 2008

Phosphorelay systems are important mediators of signal transduction during bacterial adaptation to new environments. Previously we described the
vieSAB
operon, encoding a putative three-protein component phosphorelay involved in regulating
Vibrio cholerae
virulence gene expression. At least part of the regulatory activity of VieSAB is exerted through the cyclic diguanylate (c-di-GMP)-degrading activity of the putative response regulator VieA. So far no direct evidence that VieSAB encodes a phosphorelay system exists. In addition, the role VieS plays in modulating VieA activity remains unclear. To address these questions, we expressed and purified VieA and a soluble cytoplasmic portion of VieS and used them in autophosphorylation and phosphotransfer assays. These assays showed that VieS has kinase activity in vitro and is able to selectively phosphorylate VieA. A phenotypic comparison revealed that deletion of
vieS
results in increased biofilm production comparable to that seen for deletion of
vieA
, whereas motility was decreased only slightly in the Δ
vieS
mutant compared to the profound defect observed in a Δ
vieA
mutant. We also found that the Δ
vieS
strain has a lower level of
vieA
transcript and, similar to a Δ
vieA
mutant, an increased intracellular level of c-di-GMP. Further analysis using site-directed
vieA
mutants showed that some of the phenotypes observed were due to the phosphorylation status of VieA. The evidence presented in this report is the first to link VieS and VieA biochemically and genetically, lending support to the hypothesis that these proteins function together in a signaling system.
The Pangenome Structure ofEscherichia coli: Comparative Genomic Analysis ofE. coliCommensal and Pathogenic Isolates
Authors: Rasko David A. , Rosovitz M. J. , Myers Garry S. A. , Mongodin Emmanuel F. , Fricke W. Florian , Gajer Pawel , Crabtree Jonathan , Sebaihia Mohammed , Thomson Nicholas R. , Chaudhuri Roy , Henderson Ian R. , Sperandio Vanessa , Ravel Jacques
Published: August 2008

Whole-genome sequencing has been skewed toward bacterial pathogens as a consequence of the prioritization of medical and veterinary diseases. However, it is becoming clear that in order to accurately measure genetic variation within and between pathogenic groups, multiple isolates, as well as commensal species, must be sequenced. This study examined the pangenomic content ofEscherichia coli. Six distinctE. colipathovars can be distinguished using molecular or phenotypic markers, but only two of the six pathovars have been subjected to any genome sequencing previously. Thus, this report provides a seminal description of the genomic contents and unique features of three unsequenced pathovars, enterotoxigenicE. coli, enteropathogenicE. coli, and enteroaggregativeE. coli. We also determined the first genome sequence of a human commensalE. coliisolate,E. coliHS, which will undoubtedly provide a new baseline from which workers can examine the evolution of pathogenicE. coli. Comparison of 17E. coligenomes, 8 of which are new, resulted in identification of ∼2,200 genes conserved in all isolates. We were also able to identify genes that were isolate and pathovar specific. Fewer pathovar-specific genes were identified than anticipated, suggesting that each isolate may have independently developed virulence capabilities. Pangenome calculations indicate thatE. coligenomic diversity represents an open pangenome model containing a reservoir of more than 13,000 genes, many of which may be uncharacterized but important virulence factors. This comparative study of the speciesE. coli, while descriptive, should provide the basis for future functional work on this important group of pathogens.
Characterization of the
traD
Operon of Naphthalene-Catabolic Plasmid NAH7: a Host-Range Modifier in Conjugative Transfer
Authors: Miyazaki Ryo , Ohtsubo Yoshiyuki , Nagata Yuji , Tsuda Masataka
Published: August 2008

Pseudomonas putida
G7 carries a naphthalene-catabolic and self-transmissible plasmid, NAH7, which belongs to the IncP-9 incompatibility group. Adjacent to the putative origin of conjugative transfer (
oriT
) of NAH7 are three genes,
traD
,
traE
, and
traF
, whose functions and roles in conjugation were previously unclear. These three genes were transcribed monocistronically and thus were designated the
traD
operon. Mutation of the three genes in the
traD
operon resulted in 10- to 10
5
-fold decreases in the transfer frequencies of the plasmids from
Pseudomonas
to
Pseudomonas
and
Escherichia coli
and from
E. coli
to
E. coli
. On the other hand, the
traD
operon was essential for the transfer of NAH7 from
E. coli
to
Pseudomonas
strains. These results indicated that the
traD
operon is a host-range modifier in the conjugative transfer of NAH7. The TraD, TraE, and TraF proteins were localized in the cytoplasm, periplasm, and membrane, respectively, in strain G7 cells. Our use of a bacterial two-hybrid assay system showed that TraE interacted in vivo with other essential components for conjugative transfer, including TraB (coupling protein), TraC (relaxase), and MpfH (a channel subunit in the mating pair formation system).
Isorenieratene Biosynthesis in Green Sulfur Bacteria Requires the Cooperative Actions of Two Carotenoid Cyclases
Authors: Maresca Julia A. , Romberger Steven P. , Bryant Donald A.
Published: August 2008

The cyclization of lycopene to γ- or β-carotene is a major branch point in the biosynthesis of carotenoids in photosynthetic bacteria. Four families of carotenoid cyclases are known, and each family includes both mono- and dicyclases, which catalyze the formation of γ- and β-carotene, respectively. Green sulfur bacteria (GSB) synthesize aromatic carotenoids, of which the most commonly occurring types are the monocyclic chlorobactene and the dicyclic isorenieratene. Recently, the
cruA
gene, encoding a conserved hypothetical protein found in the genomes of all GSB and some cyanobacteria, was identified as a lycopene cyclase. Further genomic analyses have found that all available fully sequenced genomes of GSB encode an ortholog of
cruA
. Additionally, the genomes of all isorenieratene-producing species of GSB encode a
cruA
paralog, now named
cruB
. The
cruA
gene from the chlorobactene-producing GSB species
Chlorobaculum tepidum
and both
cruA
and
cruB
from the brown-colored, isorenieratene-producing GSB species
Chlorobium phaeobacteroides
strain DSM 266
T
were heterologously expressed in lycopene- and neurosporene-producing strains of
Escherichia coli
, and the
cruB
gene of
Chlorobium clathratiforme
strain DSM 5477
T
was also heterologously expressed in
C. tepidum
by inserting the gene at the
bchU
locus. The results show that CruA is probably a lycopene monocyclase in all GSB and that CruB is a γ-carotene cyclase in isorenieratene-producing species. Consequently, the branch point for the synthesis of mono- and dicyclic carotenoids in GSB seems to be the modification of γ-carotene, rather than the cyclization of lycopene as occurs in cyanobacteria.
Dual Promoters Control Expression of theBacillus anthracisVirulence Factor AtxA
Authors: Bongiorni Cristina , Fukushima Tatsuya , Wilson Adam C. , Chiang Christina , Mansilla M. Cecilia , Hoch James A. , Perego Marta
Published: August 2008

The AtxA virulence regulator ofBacillus anthracisis required for toxin and capsule gene expression. AtxA is a phosphotransferase system regulatory domain-containing protein whose activity is regulated by phosphorylation/dephosphorylation of conserved histidine residues. Here we report that transcription of theatxAgene occurs from two independent promoters, P1 (previously described by Dai et al. [Z. Dai, J. C. Sirard, M. Mock, and T. M. Koehler, Mol. Microbiol.16:1171-1181, 1995]) and P2, whose transcription start sites are separated by 650 bp. Both promoters have −10 and −35 consensus sequences compatible with recognition by σA-containing RNA polymerase, and neither promoter depends on the sporulation sigma factor SigH. The dual promoter activity and the extended untranslated mRNA suggest that as-yet-unknown regulatory mechanisms may act on this region to influence the level of AtxA in the cell.
The CorA Mg2+Channel Is Required for the Virulence ofSalmonella entericaSerovar Typhimurium
Authors: Papp-Wallace Krisztina M. , Nartea Margaret , Kehres David G. , Porwollik Steffen , McClelland Michael , Libby Stephen J. , Fang Ferric C. , Maguire Michael E.
Published: August 2008

CorA is the primary Mg2+channel inSalmonella entericaserovar Typhimurium. AcorAmutant is attenuated in mice and defective for invasion of and replication within epithelial cells. Microarray studies show that several virulence effectors are repressed in acorAmutant strain, which ultimately manifests itself as a decrease in virulence.
The Stable, Functional Core of DdrA from
Deinococcus radiodurans
R1 Does Not Restore Radioresistance In Vivo
Authors: Harris Dennis R. , Ngo Khanh V. , Cox Michael M.
Published: August 2008

DdrA protein binds to and protects 3′ DNA ends and is essential for preserving the genome integrity of
Deinococcus radiodurans
following treatment by gamma radiation in an environment lacking nutrients. Limited proteolysis was used to identify a stable and functional protein core, designated DdrA157, consisting of the first 157 residues of the protein. In vitro, the biochemical differences between wild-type and mutant proteins were modest. DdrA exhibits a strong bias in binding DNA with 3′ extensions but not with 5′ extensions. The mutant DdrA157 exhibited a greater affinity for 5′ DNA ends but still bound to 3′ ends more readily. However, when we replaced the wild-type
ddrA
gene with the mutant gene for
ddrA157
, the resulting
D. radiodurans
strain became almost as sensitive to gamma radiation as the
ddrA
knockout strain. These results suggest that while the stable protein core DdrA157 is functional for DNA binding and protection assays in vitro, the carboxyl terminus is required for important functions in vivo. The C terminus may therefore be required for protein or DNA interactions or possibly as a regulatory region for DNA binding or activities not yet identified.
Phage-Associated Mutator Phenotype in Group A Streptococcus
Authors: Scott Julie , Thompson-Mayberry Prestina , Lahmamsi Stephanie , King Catherine J. , McShan W. Michael
Published: August 2008

Defects in DNA mismatch repair (MMR) occur frequently in natural populations of pathogenic and commensal bacteria, resulting in a mutator phenotype. We identified a unique genetic element in
Streptococcus pyogenes
strain SF370 that controls MMR via a dynamic process of prophage excision and reintegration in response to growth. In
S. pyogenes
,
mutS
and
mutL
are organized on a polycistronic mRNA under control of a common promoter. Prophage SF370.4 is integrated between the two genes, blocking expression of the downstream gene (
mutL
) and resulting in a mutator phenotype. However, in rapidly growing cells the prophage excises and replicates as an episome, allowing
mutL
to be expressed. Excision of prophage SF370.4 and expression of MutL mRNA occur simultaneously during early logarithmic growth when cell densities are low; this brief window of MutL gene expression ends as the cell density increases. However, detectable amounts of MutL protein remain in the cell until the onset of stationary phase. Thus, MMR in
S. pyogenes
SF370 is functional in exponentially growing cells but defective when resources are limiting. The presence of a prophage integrated into the 5′ end of
mutL
correlates with a mutator phenotype (10
−7
to 10
−8
mutation/generation, an approximately a 100-fold increase in the rate of spontaneous mutation compared with prophage-free strains [10
−9
to 10
−10
mutation/generation]). Such genetic elements may be common in
S. pyogenes
since 6 of 13 completed genomes have related prophages, and a survey of 100 strains found that about 20% of them are positive for phages occupying the SF370.4
attP
site. The dynamic control of a major DNA repair system by a bacteriophage is a novel method for achieving the mutator phenotype and may allow the organism to respond rapidly to a changing environment while minimizing the risks associated with long-term hypermutability.
Studies on lipoic acid uptake by bacteria. III. Intracellular distribution of enzymes
Authors: Oh Yong K. , Leach Franklin R.
Published: August 2008

Because the lipoic acid activating systems catalyze reactions which are formally expected for an energy-dependent transport system, an examination of their cellular distribution was made. The pyruvate: lipoate oxidoreductase (acceptor-acetylating) complex (E.C. No. 1.2.4.1) and the lipoic acid activating system in both S. faecalis 10 C1 and E. coli (Crookes strain) were found entirely in the membrane supernatant solution preparations (soluble enzymes). NADH oxidase was located in the solubilized membrane preparation, suggesting that the membrane preparations were representative, and glucose-6-phosphate dehydrogenase was found almost exclusively in the soluble fraction. It appears unlikely from distribution studies that the enzyme(s) of the lipoic acid activating system are involved in the transport of the lipoic acid into the cell.
Preparation of stable noninfective influenza virus antigens for typing by hemagglutination–inhibition
Authors: Polley John R.
Published: August 2008

For use in the hemagglutination–inhibition test, influenza virus antigens in the form of (a) untreated and inactivated allantoic fluids and (b) untreated and inactivated purified virus suspensions were compared. The inactivation procedures used were formaldehyde treatment and gamma irradiation. It was found that there was no significant difference in the potency and specificity of the purified virus antigens but that the formaldehyde-treated allantoic fluids lost potency during this process. The inactivated antigens can be lyophilized for stable storage and, after reconstitution, can be used in the diagnostic laboratory without risk of infection or interference with isolation procedures. For ease and speed of treatment, gamma irradiation is superior to treatment with formaldehyde.
Characterization of a cytoplasmic fraction from Sindbis virus-infected cultures
Authors: Dobos P. , Faulkner P.
Published: August 2008

The rate of formation and properties of a viral-specific cytoplasmic fraction which sediments at 140 S and is produced in Sindbis-infected BHK cells have been studied. The fraction contains 42 S infectious viral ribonucleic acid (RNA) and it accumulates in infected cells. The rate of formation of 140 S material is similar to the rate of release of Sindbis virions from cells. The 140 S particle is not infectious under conditions where infectivity of virions or infectious RNA may be demonstrated. These properties agree with the concept that the 140 S particle is a nucleocapsid precursor of the virion. A second cytoplasmic fraction which sediments at 65 S contains viral-specific but non-infectious RNA.
Coproporphyria excretion by Rhizobium meliloti
Authors: Hendry G. S. , Jordan D. C.
Published: August 2008

Strains of Rhizobium meliloti were found to excrete coproporphyrin into the growth medium. Maximum excretion in a modified Dudman's medium containing arginine occurred at a shaker speed of at least 98 oscillations/min (2 in. travel) and at Fe3+ and biotin concentrations of 1 μg/ml and 1 μg/l respectively. No consistent differences in coproporphyrin excretion were noted among strains differing in their ability to form active, nitrogen-fixing root nodules on their leguminous host plant.
Variations de la croissance de la coquille, et de la structure d'âge du bivalve Macoma balthica (L.) dans une population intertidale de l'estuaire du Saint-Laurent (Québec)
Authors: Vincent Bruno , Brassard Claude , Harvey Michel
Published: August 2008

Greater annual shell growth rate and increased mortality are observed in Macoma balthica (L.) with an increase of immersion time in the intertidal zone of the St. Lawrence estuary. There is also a greater annual growth rate in tidal pools, and sediment temperature alone may explain spatial variations in spring and annual growth. Reciprocal transfers of specimens between upper (0.8 m above mean water level) and lower (1.2 m below mean water level) tidal level result in enhanced shell growth for individuals of the upper level transferred to the lower level. There is no corresponding change of shell growth rate for individuals of the lower level. This genotypic difference in short-term physiological responses to environmental changes may be the result of different selective pressures associated with habitat temporal heterogeneity. An opportunistic strategy is associated with the more terrestrial and unpredictable environment (upper tidal level) and a more specialized strategy accompanied by low phenotypic variability is associated with the more marine and stable environment (lower tidal level).
Mise en évidence d'une activité neurohormonale inhibitrice de la vitellogenèse chez l'amphipode Orchestia gammarella
Authors: Blanchet-Tournier M. F.
Published: August 2008

The presence of an additional brain in female Orchestia gammarella induces the inhibition of yolky oocyte growth followed by their lysis. The graft, deprived of external influences, secretes a factor resembling vitellogenesis-inhibiting hormone. Oocytes undergoing primary vitellogenesis also appear to be target cells of vitellogenesis-inhibiting hormone.
Similarity of spring population densities of the island beach vole (Microtus breweri), 1972–1986
Authors: Tamarin Robert H. , Adler Gregory H. , Sheridan Marita , Zwicker Ken
Published: August 2008

The beach vole (Microtus breweri) population on Muskeget Island was intensively trapped from 1972 until 1977 and has been monitored annually since then. Using two criteria for cyclicity, we confirmed that the population is acyclic. The sex ratio did not deviate substantially from a 1:1 ratio. Twenty percent of animals had a forehead blaze. From 1972 to 1977, when trapped throughout the year, these values increased during the breeding season. For the year as a whole there were 1.33 male voles per female and a blaze frequency among the animals of 40.8%.
Interaction of Apanteles fumiferanae (Hymenoptera: Braconidae) and Nosema fumiferanae (Microsporidia) parasitizing spruce budworm, Choristoneura fumiferana (Lepidoptera: Tortricidae)
Authors: Nealis V. G. , Smith S. M.
Published: August 2008

The relationship between a braconid parasitoid, Apanteles fumiferanae, and a microsporidian pathogen, Nosema fumiferanae, two larval parasites frequently coincident in the spruce budworm, Choristoneura fumiferana, was examined in the laboratory. When Apanteles was reared in spruce budworm infected with high levels of Nosema (i.e., more than 20 × 106 spores/mg dry weight), there was a slight reduction in the within-host rate of development of larval female Apanteles, but survival, within-cocoon rate of development, cocoon weight, and adult longevity were not affected. There was no evidence that any stage of Apanteles was infected with spores of Nosema. A few adult female parasitoids were found to carry spores of Nosema on their integuments but it is unlikely that Apanteles is an important vector of the microsporidian. We conclude that these natural enemies of budworm do not interact significantly in their common host. The implications for population dynamics of the spruce budworm and mass rearing of Apanteles are discussed.
CD GRAMMAR SYSTEMS WITH REGULAR START CONDITIONS
Authors: FREUND RUDOLF , OSWALD MARION
Published: August 2008

We consider cooperating distributed grammar systems with the components working in different derivation modes as well as with regular sets as additional start conditions for the components. With the classical derivation modes ≤ k and = k as well as with the internally hybrid mode (≥ ℓ∧ ≤ k) we obtain a characterization of the family of recursively enumerable languages even with only one component, with the derivation modes *, t, and ≥ k as well as with the internally hybrid mode (t∧ ≥ k) two components working in the same mode and only one common regular set for both components yield computational completeness. For the internally hybrid modes (t∧ ≤ k) and (t∧ = k) we only obtain languages of finite index, but combining one component working in one of these modes (t∧ ≤ k) and (t∧ = k) with a component working in one of the modes * and ≥ k we again obtain a characterization of the family of recursively enumerable languages.
A REGULARITY CONDITION FOR CONTEXT-FREE GRAMMARS
Authors: PALANO BEATRICE
Published: August 2008

We define a complexity measure on context-free grammars called end. Roughly speaking, for a context-free grammar G, endG(n) measures the distance of variables from the ends of sentential forms along the derivations of words in L(G) of length n. We prove in a constructive way the regularity of L(G)wheneverendG(n)is constant. Yet, we improve on this by showing that ifL(G)is nonregular thenendG(n) = Ω∞( log n). We establish the optimality of such bound. Finally, we show that, in case of unambiguous context-free grammars, the end lower bound for generating nonregular languages turns out to be linear.
THE FINITE TILING PROBLEM IS UNDECIDABLE IN THE HYPERBOLIC PLANE
Authors: MARGENSTERN MAURICE
Published: August 2008

In this paper, we consider the finite tiling problem which was proved undecidable in the Euclidean plane by Jarkko Kari, see [5]. Here, we prove that the same problem for the hyperbolic plane is also undecidable.
PROPERTIES AND CONSTRUCTION OF UNIQUE MAXIMAL FACTORIZATION FAMILIES FOR STRINGS
Authors: DAYKIN DAVID E. , DAYKIN JACQUELINE W.
Published: August 2008

We say a family [Formula: see text] of strings over an alphabet is an UMFF if every string has a unique maximal factorization over [Formula: see text]. Foundational work by Chen, Fox and Lyndon established properties of the Lyndon circ-UMFF, which is based on lexicographic ordering. Commencing with the circ-UMFF related to V-order, we then proved analogous factorization families for a further 32 Block-like binary orders. Here we distinguish between UMFFs and circ-UMFFs, and then study the structural properties of circ-UMFFs. These properties give rise to the complete construction of any circ-UMFF. We prove that any circ-UMFF is a totally ordered set and a factorization over it must be monotonic. We define atom words and initiate a study of u, v-atoms. Applications of circ-UMFFs arise in string algorithmics.
Hepatic regulation of fatty acid synthase by insulin and T3: evidence for T3genomic and nongenomic actions
Authors: Radenne Anne , Akpa Murielle , Martel Caroline , Sawadogo Sabine , Mauvoisin Daniel , Mounier Catherine
Published: August 2008

Fatty acid synthase (FAS) is a key enzyme of hepatic lipogenesis responsible for the synthesis of long-chain saturated fatty acids. This enzyme is mainly regulated at the transcriptional level by nutrients and hormones. In particular, glucose, insulin, and T3increase FAS activity, whereas glucagon and saturated and polyunsaturated fatty acids decrease it. In the present study we show that, in liver, T3and insulin were able to activate FAS enzymatic activity, mRNA expression, and gene transcription. We localized the T3response element (TRE) that mediates the T3genomic effect, on the FAS promoter between −741 and −696 bp that mediates the T3genomic effect. We show that both T3and insulin regulate FAS transcription via this sequence. The TRE binds a TR/RXR heterodimer even in the absence of hormone, and this binding is increased in response to T3and/or insulin treatment. The use of H7, a serine/threonine kinase inhibitor, reveals that a phosphorylation mechanism is implicated in the transcriptional regulation of FAS in response to both hormones. Specifically, we show that T3is able to modulate FAS transcription via a nongenomic action targeting the TRE through the activation of a PI 3-kinase-ERK1/2-MAPK-dependent pathway. Insulin also targets the TRE sequence, probably via the activation of two parallel pathways: Ras/ERK1/2 MAPK and PI 3-kinase/Akt. Finally, our data suggest that the nongenomic actions of T3and insulin are probably common to several TREs, as we observed similar effects on a classical DR4 consensus sequence.
Cardiac hypertrophy is associated with altered thioredoxin and ASK-1 signaling in a mouse model of menopause
Authors: Ebrahimian Talin , Sairam M. Ram , Schiffrin Ernesto L. , Touyz Rhian M.
Published: August 2008

Oxidative stress is implicated in menopause-associated hypertension and cardiovascular disease. The role of antioxidants in this process is unclear. We questioned whether the downregulation of thioredoxin (TRX) is associated with oxidative stress and the development of hypertension and target-organ damage (cardiac hypertrophy) in a menopause model. TRX is an endogenous antioxidant that also interacts with signaling molecules, such as apoptosis signal-regulated kinase 1 (ASK-1), independently of its antioxidant function. Aged female wild-type (WT) and follitropin receptor knockout (FORKO) mice (20–24 wk), with hormonal imbalances, were studied. Mice were infused with ANG II (400 ng·kg−1·min−1; 14 days). Systolic blood pressure was increased by ANG II in WT (166 ± 8 vs. 121 ± 5 mmHg) and FORKO (176 ± 7 vs. 115 ± 5 mmHg; P < 0.0001; n = 9/group) mice. In ANG II-infused FORKO mice, cardiac mass was increased by 42% ( P < 0.001). This was associated with increased collagen content and augmented ERK1/2 phosphorylation (2-fold). Cardiac TRX expression and activity were decreased by ANG II in FORKO but not in WT ( P < 0.01) mice. ASK-1 expression, cleaved caspase III content, and Bax/Bcl-2 content were increased in ANG II-infused FORKO ( P < 0.05). ANG II had no effect on cardiac NAD(P)H oxidase activity or on O2•−levels in WT or FORKO. Cardiac ANG II type 1 receptor expression was similar in FORKO and WT. These findings indicate that in female FORKO, ANG II-induced cardiac hypertrophy and fibrosis are associated with the TRX downregulation and upregulation of ASK-1/caspase signaling. Our data suggest that in a model of menopause, protective actions of TRX may be blunted, which could contribute to cardiac remodeling independently of oxidative stress and hypertension.
Fasudil inhibits the myogenic response in the fetal pulmonary circulation
Authors: Tourneux Pierre , Chester Marc , Grover Theresa , Abman Steven H.
Published: August 2008

In addition to high pulmonary vascular resistance (PVR) and low pulmonary blood flow, the fetal pulmonary circulation is characterized by mechanisms that oppose vasodilation. Past work suggests that high myogenic tone contributes to high PVR and may contribute to autoregulation of blood flow in the fetal lung. Rho-kinase (ROCK) can mediate the myogenic response in the adult systemic circulation, but whether high ROCK activity contributes to the myogenic response and modulates time-dependent vasodilation in the developing lung circulation are unknown. We studied the effects of fasudil, a ROCK inhibitor, on the hemodynamic response during acute compression of the ductus arteriosus (DA) in chronically prepared, late-gestation fetal sheep. Acute DA compression simultaneously induces two opposing responses: 1) blood flow-induced vasodilation through increased shear stress that is mediated by NO release and 2) stretch-induced vasoconstriction (i.e., the myogenic response). The myogenic response was assessed during acute DA compression after treatment with Nω-nitro-l-arginine, an inhibitor of nitric oxide synthase, to block flow-induced vasodilation and unmask the myogenic response. Intrapulmonary fasudil infusion (100 μg over 10 min) did not enhance flow-induced vasodilation during brief DA compression but reduced the myogenic response by 90% ( P < 0.05). During prolonged DA compression, fasudil prevented the time-dependent decline in left pulmonary artery blood flow at 2 h (183 ± 29 vs. 110 ± 11 ml/min with and without fasudil, respectively; P < 0.001). We conclude that high ROCK activity opposes pulmonary vasodilation in utero and that the myogenic response maintains high PVR in the normal fetal lung through ROCK activation.
Proteasome inhibition decreases cardiac remodeling after initiation of pressure overload
Authors: Hedhli Nadia , Lizano Paulo , Hong Chull , Fritzky Luke F. , Dhar Sunil K. , Liu Huasheng , Tian Yimin , Gao Shumin , Madura Kiran , Vatner Stephen F. , Depre Christophe
Published: August 2008

We tested the possibility that proteasome inhibition may reverse preexisting cardiac hypertrophy and improve remodeling upon pressure overload. Mice were submitted to aortic banding and followed up for 3 wk. The proteasome inhibitor epoxomicin (0.5 mg/kg) or the vehicle was injected daily, starting 2 wk after banding. At the end of the third week, vehicle-treated banded animals showed significant ( P < 0.05) increase in proteasome activity (PA), left ventricle-to-tibial length ratio (LV/TL), myocyte cross-sectional area (MCA), and myocyte apoptosis compared with sham-operated animals and developed signs of heart failure, including increased lung weight-to-TL ratio and decreased ejection fraction. When compared with that group, banded mice treated with epoxomicin showed no increase in PA, a lower LV/TL and MCA, reduced apoptosis, stabilized ejection fraction, and no signs of heart failure. Because overload-mediated cardiac remodeling largely depends on the activation of the proteasome-regulated transcription factor NF-κB, we tested whether epoxomicin would prevent this activation. NF-κB activity increased significantly upon overload, which was suppressed by epoxomicin. The expression of NF-κB-dependent transcripts, encoding collagen types I and III and the matrix metalloprotease-2, increased ( P < 0.05) after banding, which was abolished by epoxomicin. The accumulation of collagen after overload, as measured by histology, was 75% lower ( P < 0.05) with epoxomicin compared with vehicle. Myocyte apoptosis increased by fourfold in hearts submitted to aortic banding compared with sham-operated hearts, which was reduced by half upon epoxomicin treatment. Therefore, we propose that proteasome inhibition after the onset of pressure overload rescues ventricular remodeling by stabilizing cardiac function, suppressing further progression of hypertrophy, repressing collagen accumulation, and reducing myocyte apoptosis.
Mechanisms of atrial fibrillation termination by rapidly unbinding Na+ channel blockers: insights from mathematical models and experimental correlates
Authors: Comtois Philippe , Sakabe Masao , Vigmond Edward J. , Munoz Mauricio , Texier Anne , Shiroshita-Takeshita Akiko , Nattel Stanley
Published: August 2008

Atrial fibrillation (AF) is the most common sustained clinical arrhythmia and is a problem of growing proportions. Recent studies have increased interest in fast-unbinding Na+ channel blockers like vernakalant (RSD1235) and ranolazine for AF therapy, but the mechanism of efficacy is poorly understood. To study how fast-unbinding INa blockers affect AF, we developed realistic mathematical models of state-dependent Na+ channel block, using a lidocaine model as a prototype, and studied the effects on simulated cholinergic AF in two- and three-dimensional atrial substrates. We then compared the results with in vivo effects of lidocaine on vagotonic AF in dogs. Lidocaine action was modeled with the Hondeghem-Katzung modulated-receptor theory and maximum affinity for activated Na+ channels. Lidocaine produced frequency-dependent Na+ channel blocking and conduction slowing effects and terminated AF in both two- and three-dimensional models with concentration-dependent efficacy (maximum ∼89% at 60 μM). AF termination was not related to increases in wavelength, which tended to decrease with the drug, but rather to decreased source Na+ current in the face of large ACh-sensitive K+ current-related sinks, leading to the destabilization of primary generator rotors and a great reduction in wavebreak, which caused primary rotor annihilations in the absence of secondary rotors to resume generator activity. Lidocaine also reduced the variability and maximum values of the dominant frequency distribution during AF. Qualitatively similar results were obtained in vivo for lidocaine effects on vagal AF in dogs, with an efficacy of 86% at 2 mg/kg iv, as well as with simulations using the guarded-receptor model of lidocaine action. These results provide new insights into the mechanisms by which rapidly unbinding class I antiarrhythmic agents, a class including several novel compounds of considerable promise, terminate AF.
Proteomic analysis of CTGF-activated lung fibroblasts: identification of IQGAP1 as a key player in lung fibroblast migration
Authors: Bogatkevich Galina S. , Ludwicka-Bradley Anna , Singleton C. Beth , Bethard Jennifer R. , Silver Richard M.
Published: August 2008

Connective tissue growth factor (CTGF, CCN2) is overexpressed in lung fibroblasts isolated from patients with interstitial lung disease (ILD) and systemic sclerosis (SSc, scleroderma) and is considered to be a molecular marker of fibrosis. To understand the significance of elevated CTGF, we investigated the changes in lung fibroblast proteome in response to CTGF overexpression. Using 2-dimensional gel electrophoresis followed by in-gel proteolytic digestion and mass spectrometric analysis, we identified 13 proteins affected by CTGF. Several of the CTGF-induced proteins, such as pro-α (I) collagen and cytoskeletal proteins vinculin, moesin, and ezrin, are known to be elevated in pulmonary fibrosis, whereas 9 of 13 proteins have not been studied in pulmonary fibrosis and are, therefore, novel CTGF-responsive molecules that may have important roles in ILD. Our study demonstrates that 1 of the novel CTGF-induced proteins, IQ motif containing GTPase activating protein (IQGAP) 1, is elevated in lung fibroblasts isolated from scleroderma patients with ILD. IQGAP1 is a scaffold protein that plays a pivotal role in regulating migration of endothelial and epithelial cells. Scleroderma lung fibroblasts and normal lung fibroblasts treated with CTGF demonstrated increased rate of migration in a wound healing assay. Depletion of IQGAP1 expression by small interfering RNA inhibited CTGF-induced migration and MAPK ERK1/2 phosphorylation in lung fibroblasts. MAPK inhibitor U0126 decreased CTGF-induced cell migration and did not interfere with CTGF-induced IQGAP1 expression, suggesting that MAPK pathway is downstream of IQGAP1. These findings further implicate the importance of CTGF in lung tissue repair and fibrosis and propose that CTGF-induced migration of lung fibroblasts to the damaged tissue is mediated via IQGAP1 and MAPK signaling pathways.
Cross talk between paxillin and Rac is critical for mediation of barrier-protective effects by oxidized phospholipids
Authors: Birukova Anna A. , Alekseeva Elena , Cokic Ivan , Turner Christopher E. , Birukov Konstantin G.
Published: August 2008

We previously reported that the barrier-protective effects of oxidized 1-palmitoyl-2-arachidonoyl- sn-glycero-3-phosphocholine (OxPAPC) on pulmonary endothelial cells (ECs) delineate the role of Rac- and Cdc42-dependent mechanisms and described the involvement of the focal adhesion (FA) protein paxillin in enhancement of the EC barrier upon OxPAPC challenge. This study examined a potential role of paxillin in the feedback mechanism of Rac regulation by FAs in OxPAPC-stimulated ECs. Our results demonstrate that OxPAPC induced Rac-dependent, Rho-independent peripheral accumulation of paxillin-containing FAs and time-dependent paxillin phosphorylation. Molecular inhibition of Rac decreased association of paxillin with the Rac-specific guanine nucleotide exchange factor β-PIX. Molecular inhibition of paxillin also attenuated OxPAPC-induced enhancement of adherens junctions critical for the EC barrier-protective response, accumulation of vascular endothelial cadherin in the membrane fractions, and decreased activation of Rac and its effector p21-activated kinase (PAK1). Expression of paxillin with a mutated PAK1-dependent phosphorylation site (S273A) attenuated OxPAPC-induced PAK1 activation and the EC barrier-protective response. These results suggest that PAK1-specific paxillin phosphorylation at Ser273is critically involved in the positive-feedback regulation of the Rac-PAK1 pathway and may contribute to sustained enhancement of the EC barrier caused by oxidized phospholipids.
Complex Organization of Human Primary Motor Cortex: A High-Resolution fMRI Study
Authors: Meier Jeffrey D. , Aflalo Tyson N. , Kastner Sabine , Graziano Michael S. A.
Published: August 2008

A traditional view of the human motor cortex is that it contains an overlapping sequence of body part representations from the tongue in a ventral location to the foot in a dorsal location. In this study, high-resolution functional MRI (1.5 × 1.5 × 2 mm) was used to examine the somatotopic map in the lateral motor cortex of humans, to determine whether it followed the traditional somatotopic order or whether it contained any violations of that somatotopic order. The arm and hand representation had a complex organization in which the arm was relatively emphasized in two areas: one dorsal and the other ventral to a region that emphasized the fingers. This violation of a traditional somatotopic order suggests that the motor cortex is not merely a map of the body but is topographically shaped by other influences, perhaps including correlations in the use of body parts in the motor repertoire.
Neuronal Adaptation Caused by Sequential Visual Stimulation in the Frontal Eye Field
Authors: Mayo J. Patrick , Sommer Marc A.
Published: August 2008

Images on the retina can change drastically in only a few milliseconds. A robust description of visual temporal processing is therefore necessary to understand visual analysis in the real world. To this end, we studied subsecond visual changes and asked how prefrontal neurons in monkeys respond to stimuli presented in quick succession. We recorded the visual responses of single neurons in the frontal eye field (FEF), a prefrontal area polysynaptically removed from the retina that is involved with higher level cognition. For comparison, we also recorded from small groups of neurons in the superficial superior colliculus (supSC), an area that receives direct retinal input. Two sequential flashes of light at varying interstimulus intervals were presented in a neuron's receptive field. We found pervasive neuronal adaptation in FEF and supSC. Visual responses to the second stimulus were diminished for up to half a second after the first stimulus presentation. Adaptation required a similar amount of time to return to full responsiveness in both structures, but there was significantly more neuronal adaptation overall in FEF. Adaptation was not affected by saccades, although visual responses to single stimuli were transiently suppressed postsaccadically. Our FEF and supSC results systematically document subsecond visual adaptation in prefrontal cortex and show that this adaptation is comparable to, but stronger than, adaptation found earlier in the visual system.