bluuebunny/crossref_metadata_2025_split huggingface dataset:
The spatial legacy of introduction:Celastrus orbiculatusin the southern Appalachians, USA
Authors: Albright Thomas P. , Anderson Dean P. , Keuler Nicholas S. , Pearson Scott M. , Turner Monica G. 
Published: September 2009

Summary1. A variety of abiotic, biotic, human and historic variables related to environmental suitability and propagule pressure determine the distribution of invasive plants in a landscape. Understanding the role of these variables for invasive species is challenging because environmental variables are often correlated, many invaders have broad ecological niches, and invasive distributions are often highly dynamic.2. We examined the role of environmental variables at multiple spatial scales on the distribution of an invasive vineCelastrus orbiculatus(Celastraceae) in the southern Appalachians, USA. Using existing and newly collected occurrence data, we constructed spatial generalized linear mixed models ofC. orbiculatusoccurrence in the whole region as well as the areas nearest (established zone) and farthest (pioneer zone) from the purported introduction locus.3. For the entire study region, distance from the introduction locus and terrain slope were negatively related to the probability of occurrence ofC. orbiculatus. The model was highly discriminatory, with an area under the receiver‐operating characteristic curve of 0·91.4. Distance from introduction locus and slope were also important in the models for the pioneer and established zones respectively.5. The pioneer zone model also indicated a negative relationship with elevation and the established zone model indicated a positive relationship with local topographic position, but these models were less discriminatory.6. Synthesis and applications. Distance from introduction locus was the most powerful variable examined, suggesting an enduring legacy of introduction for the current distribution ofC. orbiculatus.The varying results in the three zones highlight the importance of accounting for both introduction history and uneven propagule pressure in studies of observed invasive species distributions. The observed relationships with distance and elevation suggest that land managers should prepare forC. orbiculatusto expand its distribution in the region over time and with a warming climate.
SaPI mutations affecting replication and transfer and enabling autonomous replication in the absence of helper phage
Authors: Úbeda Carles , Maiques Elisa , Barry Peter , Matthews Avery , Tormo María Ángeles , Lasa Íñigo , Novick Richard P. , Penadés José R. 
Published: September 2009

SummaryThe SaPIs are chromosomal islands in staphylococci and other Gram‐positive bacteria that carry genes for superantigens, virulence factors, resistance and certain metabolic functions. They have intimate relationships with certain temperate phages involving phage‐induced excision, replication and efficient packaging in special small‐headed infective phage‐like particles, resulting in very high transfer frequencies. They generally contain 18–22 ORFs. We have systematically inactivated each of these ORFs and determined their functional groupings. In other reports, we have shown that five are involved in excision/integration, replication and packaging. In this report, we summarize the mutational analysis and focus on two key ORFs involved in regulation of the SaPI excision–replication–packaging cycle vis‐à‐vis phage induction. These two genes are divergently transcribed and define the major transcriptional organization of the SaPI genome. One of them, stl, encodes a master repressor, possibly analogous to the standard cI phage repressor. Mutational inactivation of this gene results in SaPI excision and replication in the absence of any inducing phage. This replicated SaPI DNA is not packaged; however, since the capsid components are provided by the helper phage. We have not yet ascertained any specific function for the second putative regulatory gene, though it is highly conserved among the SaPIs.
Activation of the Cpx regulon destabilizes the F plasmid transfer activator, TraJ, via the HslVU protease in Escherichia coli
Authors: Lau‐Wong Isabella C. , Locke Troy , Ellison Michael J. , Raivio Tracy L. , Frost Laura S. 
Published: September 2009

SummaryThe Escherichia coli CpxAR two‐component signal transduction system senses and responds to extracytoplasmic stress. The cpxA101* allele was previously found to reduce F plasmid conjugation by post‐transcriptional inactivation of the positive activator TraJ. Microarray analysis revealed upregulation of the protease–chaperone pair, HslVU, which was shown to degrade TraJ in an E. coli C600 cpxA101* background. Double mutants of cpxA101* and hslV or hslU restored TraJ and F conjugation to wild‐type levels. The constitutive overexpression of nlpE, an outer membrane lipoprotein that induces the Cpx stress response, also led to HslVU‐mediated degradation of TraJ and repression of F transfer. However, Cpx‐mediated TraJ degradation appears to be growth phase‐dependent, as induction of nlpE in mid‐log phase cells did not appreciably alter TraJ levels. Further, His6‐TraJ was sensitive to HslVU degradation in vitro only when it was purified from cells overexpressing nlpE. Thus, TraJ appears to become resistant to HslVU during normal growth, with this resistance mapping to the F transfer region. Extracytoplasmic stress prevents this modification of TraJ, leaving it susceptible to HslVU. Thus, the CpxAR stress response indirectly controls the synthesis of the F mating apparatus, a complex transenvelope type IV secretion system, by degrading TraJ.
Small mobile sequences in bacteria display diverse structure/function motifs
Authors: Delihas Nicholas 
Published: September 2009

SummarySmall repeat sequences in bacterial genomes, which represent non‐autonomous mobile elements, have close similarities to archaeon and eukaryotic miniature inverted repeat transposable elements. These repeat elements are found in both intergenic and intragenic chromosomal regions, and contain an array of diverse motifs. These can include DNA sequences containing an integration host factor binding site and a proposed DNA methyltransferase recognition site, transcribed RNA secondary structural motifs, which are involved in mRNA regulation, and translated open reading frames found fused to other open reading frames. Some bacterial mobile element fusions are in evolutionarily conserved protein and RNA genes. Others might represent or lead to creation of new protein genes. Here we review the remarkable properties of these small bacterial mobile elements in the context of possible beneficial roles resulting from random insertions into the genome.
DivS, a novel SOS‐inducible cell‐division suppressor in Corynebacterium glutamicum
Authors: Ogino Hidetaka , Teramoto Haruhiko , Inui Masayuki , Yukawa Hideaki 
Published: September 2009

SummaryDNA damage‐induced SOS response elicits the induction of cell‐division suppressor as well as DNA repair genes. In Gram‐positive bacteria, cell‐division suppressor genes, so far characterized from Bacillus subtilis (yneA) and Mycobacterium tuberculosis (rv2719c), share limited homology, but are both located in the vicinity of lexA on their respective genomes. Using this proximity to lexA, Corynebacterium glutamicum R divS (cgR1759) was identified as an SOS‐inducible cell‐division suppressor in this study. The amino acid sequence of DivS showed no homology to that of YneA and Rv2719c. divS expression was markedly induced by DNA‐damaging mitomycin C treatment in wild‐type cells, but not in its ΔrecA mutant cells, which are unable to induce the SOS response. Wild‐type C. glutamicum R cells exposed to DNA‐damaging mitomycin C exhibited elongated morphology that, using green fluorescent protein–FtsZ fusion protein, was attributed to defects in FtsZ ring assembly. Cells defective in FtsZ ring assembly were subsequently incapable of septum wall synthesis. In the presence of mitomycin C, divS mutant cells did not exhibit this elongated morphology, whereas cells overexpressing divS were elongated and abnormally branched.
The membrane‐integrated transcriptional activator CadC of Escherichia coli senses lysine indirectly via the interaction with the lysine permease LysP
Authors: Tetsch Larissa , Koller Christiane , Haneburger Ina , Jung Kirsten 
Published: September 2009

SummaryIn an acidic (pH 5.8) and lysine‐rich environment Escherichia coli induces expression of the cadBA operon which encodes CadA, catalysing the decarboxylation of lysine to cadaverine, and CadB, the lysine/cadaverine antiporter. cadBA expression is dependent on CadC, a membrane‐integrated transcriptional activator which belongs to the ToxR‐like protein family and directly binds to the DNA in the cadBA promoter region. Here we describe that CadC senses the extracellular lysine not directly but indirectly requiring the interplay with the lysine permease LysP. Biochemical analyses of isolated CadC or the periplasmic domain of CadC (CadC188–512) revealed an unexpectedly low affinity for lysine, making it unlikely that CadC is a direct sensor for this substrate. Moreover, CadC hybrid proteins, in which the transmembrane domain or single amino acids were replaced, supported lysine‐independent cadBA expression but retained a pH‐dependent regulation. These CadC mutants were resistant to the effect of an overproduction of LysP, which represses cadBA expression in wild‐type cells. Our results suggest a model according to which CadC is inactivated by an interaction with LysP at a low external lysine concentration. When lysine is abundantly available, the interaction between LysP and CadC is released, and CadC becomes susceptible to activation by low pH.
ppGpp and DksA likely regulate the activity of the extracytoplasmic stress factor σE in Escherichia coli by both direct and indirect mechanisms
Authors: Costanzo Alessandra , Nicoloff Herve , Barchinger Sarah E. , Banta Amy B. , Gourse Richard L. , Ades Sarah E. 
Published: September 2009

SummaryOne of the major signalling pathways responsible for intercompartmental communication between the cell envelope and cytoplasm in Escherichia coli is mediated by the alternative sigma factor, σE. σE has been studied primarily for its role in response to the misfolding of outer membrane porins. This response is essentially reactionary; cells are stressed, porin folding is disrupted, and the response is activated. σE can also be activated following starvation for a variety of nutrients by the alarmone ppGpp. This response is proactive, as σE is activated in the absence of any obvious damage to the cell envelope sensed by the stress signalling pathway. Here we examine the mechanism of regulation of σE by ppGpp. ppGpp has been proposed to activate at least two alternative sigma factors, σN and σS, indirectly by altering the competition for core RNA polymerase between the alternative sigma factors and the housekeeping sigma factor, σ70. In vivo experiments with σE are consistent with this model. However, ppGpp and its cofactor DksA can also activate transcription by EσEin vitro, suggesting that the effects of ppGpp on σE activity are both direct and indirect.
Single amino acid substitutions in either YhjD or MsbA confer viability to 3‐deoxy‐d‐manno‐oct‐2‐ulosonic acid‐depleted Escherichia coli
Authors: Mamat Uwe , Meredith Timothy C. , Aggarwal Parag , Kühl Annika , Kirchhoff Paul , Lindner Buko , Hanuszkiewicz Anna , Sun Jennifer , Holst Otto , Woodard Ronald W. 
Published: September 2009

SummaryThe Escherichia coli K‐12 strain KPM22, defective in synthesis of 3‐deoxy‐d‐manno‐oct‐2‐ulosonic acid (Kdo), is viable with an outer membrane (OM) composed predominantly of lipid IVA, a precursor of lipopolysaccharide (LPS) biosynthesis that lacks any glycosylation. To sustain viability, the presence of a second‐site suppressor was proposed for transport of lipid IVA from the inner membrane (IM), thus relieving toxic side‐effects of lipid IVA accumulation and providing sufficient amounts of LPS precursors to support OM biogenesis. We now report the identification of an arginine to cysteine substitution at position 134 of the conserved IM protein YhjD in KPM22 that acts as a compensatory suppressor mutation of the lethal ΔKdo phenotype. Further, the yhjD400 suppressor allele renders the LPS transporter MsbA dispensable for lipid IVA transmembrane trafficking. The independent derivation of a series of non‐conditional KPM22‐like mutants from the Kdo‐dependent parent strain TCM15 revealed a second class of suppressor mutations localized to MsbA. Proline to serine substitutions at either residue 18 or 50 of MsbA relieved the Kdo growth dependence observed in the isogenic wild‐type strain. The possible impact of these suppressor mutations on structure and function are discussed by means of a computationally derived threading model of MsbA.
Deletion of the archaeal histone in Methanosarcina mazei Gö1 results in reduced growth and genomic transcription
Authors: Weidenbach Katrin , Glöer Jens , Ehlers Claudia , Sandman Kathleen , Reeve John N. , Schmitz Ruth A. 
Published: September 2009

SummaryHMm is the only archaeal histone in Methanosarcina mazei Göl and recombinant HMm, synthesized by expression of MM1825 in Escherichia coli, has been purified and confirmed to have the DNA binding and compaction properties characteristic of an archaeal histone. Insertion of a puromycin resistance conferring cassette (pac) into MM1825 was not lethal but resulted in mutants (M. mazei MM1825::pac) that have impaired ability to grow on methanol and trimethylamine. Loss of HMm also resulted in increased sensitivity to UV light and decreased transcript levels for ∼25% of all M. mazei genes. For most genes, the transcript decrease was 3‐ to 10‐fold, but transcripts of MM483 (small heat‐shock protein), MM1688 (trimethylamine:corrinoid methyl transferase) and MM3195 (transcription regulator), were reduced 100‐, 100‐ and 25‐fold, respectively, in M. mazei MM1825::pac cells. Transcripts of only five adjacent genes that appear to constitute an aromatic amino acid biosynthetic operon were elevated in M. mazei MM1825::pac cells. Complementary synthesis of HMm from a plasmid transformed into M. mazei MM1825::pac restored wild‐type growth and transcript levels.
Compensation for the loss of the conserved membrane targeting sequence of FtsA provides new insights into its function
Authors: Shiomi Daisuke , Margolin William 
Published: September 2009

SummaryThe bacterial actin homologue FtsA has a conserved C‐terminal membrane targeting sequence (MTS). Deletion or point mutations in the MTS, such as W408E, were shown previously to inactivate FtsA function and inhibit cell division. Because FtsA binds to the tubulin‐like FtsZ protein that forms the Z ring, it is thought that the MTS of FtsA is required, along with the transmembrane protein ZipA, to assemble the Z ring and anchor it to the cytoplasmic membrane. Here, we show that despite its reduced membrane binding, FtsA‐W408E could localize to the Z ring and recruit the late cell division protein FtsI, but was defective in self‐interaction and recruitment of FtsN, another late cell division protein. These defects could be suppressed by a mutation that stimulates membrane association of FtsA‐W408E, or by expressing a tandem FtsA‐W408E. Remarkably, the FtsA MTS could be completely replaced with the transmembrane domain of MalF and remain functional for cell division. We propose that FtsA function in cell division depends on additive effects of membrane binding and self‐interaction, and that the specific requirement of an amphipathic helix for tethering FtsA to the membrane can be bypassed.
Common CCR 5 Polymorphism in Stroke The CCR 5 Δ32 Polymorphism Differentiates Cardioembolism from Other Aetiologies of Ischaemic Cerebrovascular Diseases
Authors: Nikolaos K. , Ioanna M. , Vasilios K. , Jan H. , Konstantinos K. 
Published: September 2009

AbstractInflammation is involved in the development of atherosclerosis. The CC chemokine receptor 5 (CCR5) initiates chemotaxis and modulates the inflammation secondary to atherosclerosis and related vascular diseases. The CCR5 Δ32 polymorphism influences the expression of CCR5 on the cell surface. The purpose of this study was to examine the effect of the Δ32 polymorphism in ischaemic cerebrovascular disease (ICVD). The CCR5 Δ32 polymorphism was genotyped in 1462 individuals: 562 ischaemic stroke (IS), 97 transient ischaemic attack (TIA) and in 803 healthy controls. All 659 ICVD patients were categorized according to the Trial of Org 10172 in Acute Stroke Treatment aetiological classification. The investigated subtypes were large artery atherosclerosis (LAA), cardioembolism (CE), small artery occlusion (SAO) and cryptogenic disease (CRYPT). Genotyping was performed with the TaqMan polymerase chain reaction. The Δ32 allele was less frequent in CE patients compared with LAA (OR, 0.4; 95% CI, 0.24–0.79; P = 0.008), SAO (OR, 0.5; 95% CI, 0.29–0.84; P = 0.01), CRYPT (OR, 0.5; 95% CI, 0.28–0.82; P = 0.008) and controls (OR, 0.5; 95% CI, 0.36–0.82; P = 0.002). Multiple logistic regression analysis showed that the Δ32 allele is associated with a lower risk for cardioembolic ICVD (OR 0.5; 95% CI, 0.28–0.75; P = 0.002) when compared with ICVD of other causes. The Δ32 polymorphism of CCR5 may differentiate cardioembolism from the remaining causes of ICVD.
New Alternative Vaccine Component Against Mycobacterium Tuberculosis– Heat Shock Protein 16.3 or its T‐Cell Epitope
Authors: Shi C. , Zhang H. , Zhang T. , Wang X. , Bai B. , Zhao Y. , Zhang C. , Xu Z. 
Published: September 2009

AbstractHeat shock protein 16.3 (Hsp16.3) of Mycobacterium tuberculosis (MTB) containing T‐cell and B‐cell epitopes not only plays an important role in the survival of MTB against macrophages, but also has great potential to be used to develop new TB vaccines. In order to study whether Hsp16.3 can be replaced with its T‐cell epitope for producing a vaccine against TB, we expressed and purified Hsp16.3 protein of MTB H37Rv strain and confirmed by immunoblotting. The immune responses and protection against the H37Rv induced by Hsp16.3 protein were compared with its T‐cell epitope synthetic peptide in mice. The results showed that both Hsp16.3 and its synthetic peptide induced significantly stronger specific antibodies than the classical TB vaccine–BCG (bacillus Calmette‐Guérin). Compared with BCG, the stimulation index in the splenolymphocyte proliferation of both recombinant protein and its synthetic peptide were remarkably enhanced, but the levels of IFN‐γ release were lower. Dramatic reduction in the numbers of MTB colony forming units (CFU) in the spleens and lungs was observed in the mice immunized with Hsp16.3 or its synthetic peptide. The protection provided by Hsp16.3 or its synthetic peptide in the lungs was equivalent to that provided by BCG. Both Hsp16.3 and its T‐cell epitope are effective components and Hsp16.3 can be replaced with its T‐cell epitope while developing the vaccine against TB, without requiring the complicated procedure of expressing and purifying Hsp16.3.
Does our Current Understanding of Immune Tolerance, Autoimmunity, and Immunosuppressive Mechanisms Facilitate the Design of Efficient Cancer Vaccines?
Authors: Sioud M. 
Published: September 2009

AbstractThe therapeutic use of the immune system to attack cancer cells has been a longstanding vision among tumour immunologists. However, most human tumours are poorly immunogenic and are able to invade the host immune system. Although these obstacles are clearly critical to cancer vaccine development, the induction of a strong anti‐tumour immune response may rely on the activation of high affinity T cells through a molecular mimicry mechanism which involves cross‐reactive recognition of foreign antigens mimicking the structure of tumour proteins. Taking into account the disparity in HLA molecules needed to present shared antigens; in late 1990s Stauss et al. described the possibility of generating allorestricted high affinity cytotoxic T cells against synthetic self‐peptides bound to non‐self‐MHC molecules. In addition to the strategies indicated above, the inhibition of the immunosuppressive mechanisms associated with tumour invasion of the immune system using RNA interference also offers a new approach to vaccine design. This review highlights the problem of immune tolerance, the induction of autoreactive T cells, and describes strategies to enhance tumour immunity.
Jasmonate controls late development stages of petal growth in Arabidopsis thaliana
Authors: Brioudes Florian , Joly Caroline , Szécsi Judit , Varaud Emilie , Leroux Julie , Bellvert Floriant , Bertrand Cédric , Bendahmane Mohammed 
Published: September 2009

SummaryIn Arabidopsis, four homeotic gene classes, A, B, C and E, are required for the patterning of floral organs. However, very little is known about how the activity of these master genes is translated into regulatory processes leading to specific growth patterns and the formation of organs with specific shapes and sizes. Previously we showed that the transcript variant BPEp encodes a bHLH transcription factor that is involved in limiting petal size by controlling post‐mitotic cell expansion. Here we show that the phytohormone jasmonate is required for control of BPEp expression. Expression of BPEp was negatively regulated in opr3 mutant flowers that are deficient in jasmonate synthesis. Moreover, the expression of BPEp was restored in opr3 flowers following exogenous jasmonate treatments. Expression of the second transcript variant BPEub, which originates from the same gene as BPEp via an alternative splicing event, was not affected, indicating that BPEp accumulation triggered by jasmonate occurs at the post‐transcriptional level. Consistent with these data, opr3 exhibited an increase in petal size as a result of increased cell size, as well as a modified vein pattern, phenotypes that are similar to those of the bpe‐1 mutant. Furthermore, exogenous treatments with jasmonate rescued petal phenotypes associated with loss of function of OPR3. Our data demonstrate that jasmonate signaling downstream of OPR3 is involved in the control of cell expansion and in limiting petal size, and that BPEp is a downstream target that functions as a component mediating jasmonate signaling during petal growth.
Ipsilateral café‐au‐lait macules, deafness, and pituitary microadenoma in a 35‐year‐old woman
Authors: Valdivieso Rommel 
Published: September 2009

AbstractBackground  The association between ipsilateral café‐au‐lait macules, deafness, and pituitary adenoma has not been described previously.Case report and results  A 35‐year‐old woman affected since birth with two café‐au‐lait macules, one measuring 15 × 20 cm, with an irregular shape, covering almost all of the left buttock, and the other measuring 6 × 13 cm on the front side of the left thigh, is described. For as long as the patient can remember, she has been totally deaf in the left ear, diagnosed as 100% congenital sensorineural deafness. In addition, a left‐side pituitary microadenoma was detected at the age of 31 years. She was also found to have a transitional lumbosacral vertebra, and multiple dermatofibromas and nevomelanocytic nevi.Conclusion  It is suggested that this association is not a coincidence, but is part of a neurocutaneous syndrome which has not been described previously.