bluuebunny/crossref_metadata_2025_split huggingface dataset:
Entianin, a Novel Subtilin-Like Lantibiotic from
Bacillus subtilis
subsp.
spizizenii
DSM 15029
T
with High Antimicrobial Activity
Authors: Fuchs Sebastian W. , Jaskolla Thorsten W. , Bochmann Sophie , Kötter Peter , Wichelhaus Thomas , Karas Michael , Stein Torsten , Entian Karl-Dieter 
Published: January 2011

ABSTRACT

Lantibiotics, such as nisin and subtilin, are lanthionine-containing peptides that exhibit antimicrobial as well as pheromone-like autoinducing activity. Autoinduction is specific for each lantibiotic, and reporter systems for nisin and subtilin autoinduction are available. In this report, we used the previously reported subtilin autoinduction bioassay in combination with mass spectrometric analyses to identify the novel subtilin-like lantibiotic entianin from
Bacillus subtilis
subsp.
spizizenii
DSM 15029
T
. Linearization of entianin using Raney nickel-catalyzed reductive cleavage enabled, for the first time, the use of tandem mass spectrometry for the fast and efficient determination of an entire lantibiotic primary structure, including posttranslational modifications. The amino acid sequence determined was verified by DNA sequencing of the
etnS
structural gene, which confirmed that entianin differs from subtilin at 3 amino acid positions. In contrast to
B. subtilis
ATCC 6633, which produces only small amounts of unsuccinylated subtilin,
B. subtilis
DSM 15029
T
secretes considerable amounts of unsuccinylated entianin. Entianin was very active against several Gram-positive pathogens, such as
Staphylococcus aureus
and
Enterococcus faecalis.
The growth-inhibiting activity of succinylated entianin (S-entianin) was much lower than that of unsuccinylated entianin: a 40-fold higher concentration was required for inhibition. For succinylated subtilin (S-subtilin), a concentration 100-fold higher than that of unsuccinylated entianin was required to inhibit the growth of a
B. subtilis
test strain. This finding was in accordance with a strongly reduced sensing of cellular envelope stress provided by S-entianin relative to that of entianin. Remarkably, S-entianin and S-subtilin showed considerable autoinduction activity, clearly demonstrating that autoinduction and antibiotic activity underlie different molecular mechanisms.
Stress Survival Islet 1 (SSI-1) Survey in
Listeria monocytogenes
Reveals an Insert Common to
Listeria innocua
in Sequence Type 121
L. monocytogenes
Strains
Authors: Hein Ingeborg , Klinger Sonja , Dooms Maxime , Flekna Gabriele , Stessl Beatrix , Leclercq Alexandre , Hill Colin , Allerberger Franz , Wagner Martin 
Published: January 2011

ABSTRACT

Listeria monocytogenes
strains (
n
= 117) were screened for the presence of stress survival islet 1 (SSI-1). SSI-1
+
strains (32.5%) belonged mainly to serotypes 1/2c, 3b, and 3c. All sequence type 121 (ST-121) strains included (
n
= 7) possessed homologues to
Listeria innocua
genes
lin0464
and
lin0465
instead of SSI-1.
A New Wine
Saccharomyces cerevisiae
Killer Toxin (Klus), Encoded by a Double-Stranded RNA Virus, with Broad Antifungal Activity Is Evolutionarily Related to a Chromosomal Host Gene
Authors: Rodríguez-Cousiño Nieves , Maqueda Matilde , Ambrona Jesús , Zamora Emiliano , Esteban Rosa , Ramírez Manuel 
Published: January 2011

ABSTRACT

Wine
Saccharomyces cerevisiae
strains producing a new killer toxin (Klus) were isolated. They killed all the previously known
S. cerevisiae
killer strains, in addition to other yeast species, including
Kluyveromyces lactis
and
Candida albicans
. The Klus phenotype is conferred by a medium-size double-stranded RNA (dsRNA) virus,
Saccharomyces
cerevisiae
virus Mlus (ScV-Mlus), whose genome size ranged from 2.1 to 2.3 kb. ScV-Mlus depends on ScV-L-A for stable maintenance and replication. We cloned and sequenced Mlus. Its genome structure is similar to that of M1, M2, or M28 dsRNA, with a 5′-terminal coding region followed by two internal A-rich sequences and a 3′-terminal region without coding capacity. Mlus positive strands carry
cis
-acting signals at their 5′ and 3′ termini for transcription and replication similar to those of killer viruses. The open reading frame (ORF) at the 5′ portion codes for a putative preprotoxin with an N-terminal secretion signal, potential Kex2p/Kexlp processing sites, and N-glycosylation sites. No sequence homology was found either between the Mlus dsRNA and M1, M2, or M28 dsRNA or between Klus and the K1, K2, or K28 toxin. The Klus amino acid sequence, however, showed a significant degree of conservation with that of the product of the host chromosomally encoded ORF YFR020W of unknown function, thus suggesting an evolutionary relationship.
Autoregulation of Nodulation Interferes with Impacts of Nitrogen Fertilization Levels on the Leaf-Associated Bacterial Community in Soybeans
Authors: Ikeda Seishi , Anda Mizue , Inaba Shoko , Eda Shima , Sato Shusei , Sasaki Kazuhiro , Tabata Satoshi , Mitsui Hisayuki , Sato Tadashi , Shinano Takuro , Minamisawa Kiwamu 
Published: January 2011

ABSTRACT

The diversities leaf-associated bacteria on nonnodulated (Nod
−
), wild-type nodulated (Nod
+
), and hypernodulated (Nod
++
) soybeans were evaluated by clone library analyses of the 16S rRNA gene. To analyze the impact of nitrogen fertilization on the bacterial leaf community, soybeans were treated with standard nitrogen (SN) (15 kg N ha
−1
) or heavy nitrogen (HN) (615 kg N ha
−1
) fertilization. Under SN fertilization, the relative abundance of
Alphaproteobacteria
was significantly higher in Nod
−
and Nod
++
soybeans (82% to 96%) than in Nod
+
soybeans (54%). The community structure of leaf-associated bacteria in Nod
+
soybeans was almost unaffected by the levels of nitrogen fertilization. However, differences were visible in Nod
−
and Nod
++
soybeans. HN fertilization drastically decreased the relative abundance of
Alphaproteobacteria
in Nod
−
and Nod
++
soybeans (46% to 76%) and, conversely, increased those of
Gammaproteobacteria
and
Firmicutes
in these mutant soybeans. In the
Alphaproteobacteria
, cluster analyses identified two operational taxonomic units (OTUs) (
Aurantimonas
sp. and
Methylobacterium
sp.) that were especially sensitive to nodulation phenotypes under SN fertilization and to nitrogen fertilization levels. Arbuscular mycorrhizal infection was not observed on the root tissues examined, presumably due to the rotation of paddy and upland fields. These results suggest that a subpopulation of leaf-associated bacteria in wild-type Nod
+
soybeans is controlled in similar ways through the systemic regulation of autoregulation of nodulation, which interferes with the impacts of N levels on the bacterial community of soybean leaves.
Tracking Glideosome-Associated Protein 50 Reveals the Development and Organization of the Inner Membrane Complex of Plasmodium falciparum
Authors: Yeoman Jeffrey A. , Hanssen Eric , Maier Alexander G. , Klonis Nectarios , Maco Bohumil , Baum Jake , Turnbull Lynne , Whitchurch Cynthia B. , Dixon Matthew W. A. , Tilley Leann 
Published: January 2011

ABSTRACT

The most deadly of the human malaria parasites,
Plasmodium falciparum
, has different stages specialized for invasion of hepatocytes, erythrocytes, and the mosquito gut wall. In each case, host cell invasion is powered by an actin-myosin motor complex that is linked to an inner membrane complex (IMC) via a membrane anchor called the glideosome-associated protein 50 (PfGAP50). We generated
P. falciparum
transfectants expressing green fluorescent protein (GFP) chimeras of PfGAP50 (PfGAP50-GFP). Using immunoprecipitation and fluorescence photobleaching, we show that C-terminally tagged PfGAP50-GFP can form a complex with endogenous copies of the linker protein PfGAP45 and the myosin A tail domain-interacting protein (MTIP). Full-length PfGAP50-GFP is located in the endoplasmic reticulum in early-stage parasites and then redistributes to apical caps during the formation of daughter merozoites. In the final stage of schizogony, the PfGAP50-GFP profile extends further around the merozoite surface. Three-dimensional (3D) structured illumination microscopy reveals the early-stage IMC as a doubly punctured flat ellipsoid that separates to form claw-shaped apposed structures. A GFP fusion of PfGAP50 lacking the C-terminal membrane anchor is misdirected to the parasitophorous vacuole. Replacement of the acid phosphatase homology domain of PfGAP50 with GFP appears to allow correct trafficking of the chimera but confers a growth disadvantage.
Depletion of Mitochondrial Acyl Carrier Protein in Bloodstream-Form Trypanosoma brucei Causes a Kinetoplast Segregation Defect
Authors: Clayton April M. , Guler Jennifer L. , Povelones Megan L. , Gluenz Eva , Gull Keith , Smith Terry K. , Jensen Robert E. , Englund Paul T. 
Published: January 2011

ABSTRACT
Like other eukaryotes, trypanosomes have an essential type II fatty acid synthase in their mitochondrion. We have investigated the function of this synthase in bloodstream-form parasites by studying the effect of a conditional knockout of acyl carrier protein (ACP), a key player in this fatty acid synthase pathway. We found that ACP depletion not only caused small changes in cellular phospholipids but also, surprisingly, caused changes in the kinetoplast. This structure, which contains the mitochondrial genome in the form of a giant network of several thousand interlocked DNA rings (kinetoplast DNA [kDNA]), became larger in some cells and smaller or absent in others. We observed the same pattern in isolated networks viewed by either fluorescence or electron microscopy. We found that the changes in kDNA size were not due to the disruption of replication but, instead, to a defect in segregation. kDNA segregation is mediated by the tripartite attachment complex (TAC), and we hypothesize that one of the TAC components, a differentiated region of the mitochondrial double membrane, has an altered phospholipid composition when ACP is depleted. We further speculate that this compositional change affects TAC function, and thus kDNA segregation.
A Processive Glycosyltransferase Involved in Glycolipid Synthesis during Phosphate Deprivation in
Mesorhizobium loti
Authors: Devers Emanuel A. , Wewer Vera , Dombrink Isabel , Dörmann Peter , Hölzl Georg 
Published: January 2011

ABSTRACT

Natural habitats are often characterized by a low availability of phosphate. In plants and many bacteria, phosphate deficiency causes different physiological responses, including the replacement of phosphoglycerolipids in the membranes with nonphosphorous lipids. We describe here a processive glycosyltransferase (Pgt) in
Mesorhizobium loti
(
Rhizobiales
) involved in the synthesis of di- and triglycosyldiacylglycerols (DGlycD and TGlycD) during phosphate deprivation. Cells of the corresponding Δ
pgt
deletion mutant are deficient in DGlycD and TGlycD. Additional Pgt-independent lipids accumulate in
Mesorhizobium
after phosphate starvation, including diacylglyceryl trimethylhomoserine (DGTS) and ornithine lipid (OL). The accumulation of the nonphosphorous lipids during phosphate deprivation leads to the reduction of phosphoglycerolipids from 90 to 50%. Nodulation experiments of
Mesorhizobium
wild type and the Δ
pgt
mutant with its host plant,
Lotus japonicus
, revealed that DGlycD and TGlycD are not essential for nodulation under phosphate-replete or -deficient conditions. Lipid measurements showed that the Pgt-independent lipids including OL and DGTS accumulate to higher proportions in the Δ
pgt
mutant and therefore might functionally replace DGlycD and TGlycD during phosphate deprivation.
Mesenchymal stem cells in infantile haemangioma
Authors: Itinteang Tinte , Vishvanath Anasuya , Day Darren J , Tan Swee T 
Published: January 2011

BackgroundFibro-fatty deposition commonly occurs during involution of infantile haemangioma (IH). Mesenchymal stem cells have been identified in this tumour and have been proposed to be recruited from the bone marrow and/or adjacent niches, and then give rise to the fibro-fatty tissue. The authors have recently demonstrated that the capillary endothelium of proliferating IH co-expresses primitive mesodermal, mesenchymal and neural crest markers and proposed that this same endothelium has the ability to give rise to cells of mesenchymal lineage that constitute the fibro-fatty deposition.MethodsImmunohistochemistry and real-time RT-PCR were used to further characterise proliferating IHs and haemangioma explant-derived cells (HaemEDCs).ResultsThe authors have further confirmed expression of the mesenchymal-associated proteins including preadipocyte factor-1, a mesenchymal differentiation inhibition-associated cytokine. The HaemEDCs could be differentiated into osteoblasts and adipocytes, indicating their functional potential for terminal differentiation.DiscussionThe collective expression of neural crest, mesenchymal and mesenchymal differentiation inhibition-associated proteins on the endothelium of proliferating IH suggests that the cells in the capillary endothelium within the lesion possess the ability to undergo terminal mesenchymal differentiation during the proliferating phase, but are inhibited from doing so.
Variational-Like Inclusions and Resolvent Equations Involving Infinite Family of Set-Valued Mappings
Authors: Ahmad Rais , Dilshad Mohd 
Published: January 2011

AbstractWe study variational-like inclusions involving infinite family of set-valued mappings and their equivalence with resolvent equations. It is established that variational-like inclusions in real Banach spaces are equivalent to fixed point problems. This equivalence is used to suggest an iterative algorithm for solving resolvent equations. Some examples are constructed.
6-Thioguanine Reactivates Epigenetically Silenced Genes in Acute Lymphoblastic Leukemia Cells by Facilitating Proteasome-mediated Degradation of DNMT1
Authors: Yuan Bifeng , Zhang Jing , Wang Hongxia , Xiong Lei , Cai Qian , Wang Tina , Jacobsen Steven , Pradhan Sriharsa , Wang Yinsheng 
Published: January 2011

Abstract
Thiopurines including 6-thioguanine (SG), 6-mercaptopurine, and azathioprine are effective anticancer agents with remarkable success in clinical practice, especially in effective treatment of acute lymphoblastic leukemia (ALL). SG is understood to act as a DNA hypomethylating agent in ALL cells, however, the underlying mechanism leading to global cytosine demethylation remains unclear. Here we report that SG treatment results in reactivation of epigenetically silenced genes in T leukemia cells. Bisulfite genomic sequencing revealed that SG treatment universally elicited demethylation in the promoters and/or first exons of the genes that were reactivated. SG treatment also attenuated the expression of histone lysine-specific demethylase 1 (LSD1), thereby stimulating lysine methylation of the DNA methylase DNMT1 and triggering its degradation via the ubiquitin-proteasomal pathway. Taken together, our findings reveal a previously uncharacterized but vital mechanistic link between SG treatment and DNA hypomethylation. Cancer Res; 71(5); 1904–11. ©2011 AACR.
KRASMutation Is Associated with Lung Metastasis in Patients with Curatively Resected Colorectal Cancer
Authors: Tie Jeanne , Lipton Lara , Desai Jayesh , Gibbs Peter , Jorissen Robert N. , Christie Michael , Drummond Katharine J. , Thomson Benjamin N.J. , Usatoff Valery , Evans Peter M. , Pick Adrian W. , Knight Simon , Carne Peter W.G. , Berry Roger , Polglase Adrian , McMurrick Paul , Zhao Qi , Busam Dana , Strausberg Robert L. , Domingo Enric , Tomlinson Ian P.M. , Midgley Rachel , Kerr David , Sieber Oliver M. 
Published: January 2011

AbstractPurpose: Oncogene mutations contribute to colorectal cancer development. We searched for differences in oncogene mutation profiles between colorectal cancer metastases from different sites and evaluated these as markers for site of relapse.Experimental Design: One hundred colorectal cancer metastases were screened for mutations in 19 oncogenes, and further 61 metastases and 87 matched primary cancers were analyzed for genes with identified mutations. Mutation prevalence was compared between (a) metastases from liver (n = 65), lung (n = 50), and brain (n = 46), (b) metastases and matched primary cancers, and (c) metastases and an independent cohort of primary cancers (n = 604). Mutations differing between metastasis sites were evaluated as markers for site of relapse in 859 patients from the VICTOR trial.Results: In colorectal cancer metastases, mutations were detected in 4 of 19 oncogenes: BRAF (3.1%), KRAS (48.4%), NRAS (6.2%), and PIK3CA (16.1%). KRAS mutation prevalence was significantly higher in lung (62.0%) and brain (56.5%) than in liver metastases (32.3%; P = 0.003). Mutation status was highly concordant between primary cancer and metastasis from the same individual. Compared with independent primary cancers, KRAS mutations were more common in lung and brain metastases (P &lt; 0.005), but similar in liver metastases. Correspondingly, KRAS mutation was associated with lung relapse (HR = 2.1; 95% CI, 1.2 to 3.5, P = 0.007) but not liver relapse in patients from the VICTOR trial.Conclusions: KRAS mutation seems to be associated with metastasis in specific sites, lung and brain, in colorectal cancer patients. Our data highlight the potential of somatic mutations for informing surveillance strategies. Clin Cancer Res; 17(5); 1122–30. ©2011 AACR.
Novel Chemosensitive Single-Nucleotide Polymorphism Markers to Targeted Regimens in Metastatic Colorectal Cancer
Authors: Kim Jin C. , Kim Seon Y. , Cho Dong H. , Ha Ye J. , Choi Eun Y. , Kim Chan W. , Roh Seon A. , Kim Tae W. , Ju Hyoungseok , Kim Yong S. 
Published: January 2011

Abstract
Purpose: Methods for predicting individual responsiveness to targeted chemotherapy are urgently needed, considering the frequent resistance and extremely high cost.
Experimental Design: A chemosensitive single-nucleotide polymorphism (SNP) discovery schema is presented that utilizes (i) genome-wide SNP screening with a human SNP array and an in vitro chemosensitivity assay in 118 colorectal cancers, (ii) clinical association analysis in the other 98 patients who had received chemotherapy for metastatic cancer, and (iii) biological utility assessment using cell viability assays of transfected colorectal cancer (CRC) cells.
Results: Nine SNPs related to bevacizumab and cetuximab regimen sensitivity were chosen during screening. Overall responses for bevacizumab regimens revealed that patients carrying the TT genotype at ANXA11 rs1049550 or at least one G allele at LINS1 rs11247226 seemed greater chemosensitive than those carrying at least one C allele or the AA genotype, respectively (P &lt; 0.05). For cetuximab regimens, patients carrying the GG genotype at DFNB31 rs2274159 or LIFR rs3729740 seemed greater chemosensitive than those carrying at least one A allele (P = 0.025 and P = 0.07). Cytotoxicity analyses showed that all RKO and HCT116 CRC clones transfected with the G allele at LIFR rs3729740 and the C allele at ISX rs361863 were more sensitive to cetuximab regimens than those with the A and T allele, respectively (P ≤ 0.001–0.024).
Conclusions: Chemosensitive SNP markers were identified using a novel three-step process. The candidate marker LIFR rs3729740 and possibly ISX rs361863 will hopefully predict responsive patients to cetuximab regimens, although further validation is needed in large cohorts. Clin Cancer Res; 17(5); 1200–9. ©2011 AACR.
Quantification of Ventricular Resynchronization Reserve by Radionuclide Phase Analysis in Heart Failure Patients
Authors: Dauphin Raphael , Nonin Emilie , Bontemps Laurence , Vincent Madeleine , Pinel Alain , Bonijoly Serge , Barborier Denis , Ribier Arnaud , Mestre Fernandes Christine , Bert-Marcaz Patrick , Itti Roland , Chevalier Philippe 
Published: January 2011

Background—
Phase analysis, developed to assess dyssynchrony from ECG-gated radionuclide ventriculography, has shown promising results. We hypothesized that quantifying the cardiac resynchronization reserve, that is, the extent of response to cardiac resynchronization therapy (CRT), by radionuclide imaging could potentially identify patients who are best suited for CRT.

Methods and Results—
Seventy-four patients ages 64.8±10.1 years were prospectively studied from July 2004 to July 2006, of whom 62.2% and 37.8%, respectively, were in New York Heart Association class 3 and 4. Mean QRS width was 173±25 ms. ECG-gated radionuclide ventriculography to quantify interventricular and intraventricular dyssynchrony was performed at baseline with and without CRT and at the 3-month follow-up visit. Amino-terminal-pro-brain natriuretic peptide (NT-pro-BNP) levels were also determined at baseline and at 3 months. During a mean follow-up of 10.1±7.6 months, there were 37 (50%) clinical events that defined the nonresponder group, including cardiac death or readmission for worsening heart failure. In multivariate Cox model analysis, higher NT-pro-BNP blood levels were associated with a significant increase in the risk for event (hazard ratio=1.085 for a 100 pg/L increase in NT-pro-BNP; 95% confidence interval, 1.014 to 1.161). Each 10° elevation in intraventricular dyssynchrony was associated with a decrease in the risk of events (hazard ratio=0.456, 95% confidence interval, 0.304 to 0.683). Receiver operating characteristic curve analysis demonstrated that an interventricular dyssynchrony cutoff value of 25.5° for intraventricular synchrony yielded 91.4% sensitivity and 84.4% specificity for predicting a good response to CRT.

Conclusions—
The quantification of interventricular dyssynchrony with radionuclide phase analysis suggests that early postimplantation interventricular dyssynchrony may provide identification of CRT responders.