bluuebunny/crossref_metadata_2025_split huggingface dataset:
An Essential Role ofS-Adenosyl-l-Methionine:l-MethionineS-Methyltransferase in Selenium Volatilization by Plants. Methylation of Selenomethionine to Selenium-Methyl-l-Selenium- Methionine, the Precursor of Volatile Selenium
Authors: Tagmount Abderrahmane , Berken Antje , Terry Norman 
Published: October 2002

AbstractSelenium (Se) phytovolatilization, the process by which plants metabolize various inorganic or organic species of Se (e.g. selenate, selenite, and Se-methionine [Met]) into gaseous Se forms (e.g. dimethylselenide), is a potentially important means of removing Se from contaminated environments. Before attempting to genetically enhance the efficiency of Se phytovolatilization, it is essential to elucidate the enzymatic pathway involved and to identify its rate-limiting steps. The present research tested the hypothesis thatS-adenosyl-l-Met:l-MetS-methyltransferase (MMT) is the enzyme responsible for the methylation of Se-Met to Se-methyl Se-Met (SeMM). To this end, we identified and characterized an Arabidopsis T-DNA mutant knockout for MMT. The lack of MMT in the Arabidopsis T-DNA mutant plant resulted in an almost complete loss in its capacity for Se volatilization. Using chemical complementation with SeMM, the presumed enzymatic product of MMT, we restored the capacity of the MMT mutant to produce volatile Se. Overexpressing MMT from Arabidopsis in Escherichia coli, which is not known to have MMT activity, produced up to 10 times more volatile Se than the untransformed strain when both were supplied with Se-Met. Thus, our results provide in vivo evidence that MMT is the key enzyme catalyzing the methylation of Se-Met to SeMM.
Characterization of SP1, a Stress-Responsive, Boiling-Soluble, Homo-Oligomeric Protein from Aspen
Authors: Wang Wang-Xia , Pelah Dan , Alergand Tal , Shoseyov Oded , Altman Arie 
Published: October 2002

Abstract
sp1 cDNA was isolated from aspen (Populus tremula) plants by immunoscreening an expression library using polyclonal antibodies against BspA protein. BspA, which is a boiling-stable protein, accumulates in aspen plants in response to water stress and abscisic acid application (Pelah et al., 1995). The sp1 cDNA was found to encode a 12.4-kD generally hydrophilic protein with a hydrophobic C terminus, which is different from the BspA protein and was termed SP1 (stable protein 1). Northern-blot analysis revealed that sp1 encodes a small mRNA (about 0.6 kb) that is expressed in aspen plants under non-stress conditions and is accumulated after salt, cold, heat, and desiccation stress, and during the recovery from stress. The SP1 detected in plants remained soluble upon boiling, migrated both as a 12.4-kD band and a much higher mass of 116 kD on a 17% (w/v) Tricine-sodium dodecyl sulfate-polyacrylamide gel. Comparative protease digestion patterns, amino acid analyses, and the N-terminal sequences of the 12.4- and 116-kD proteins revealed that SP1 is homo-oligomeric. Furthermore, gel filtration chromatography analysis indicated that SP1 exists in aspen plants as a complex, composed of 12 subunits of 12.4 kD. A large number of sequences deduced from expressed sequence tags and genomic sequences of other organisms with unknown function show high homology to SP1. Thus, SP1 may represent a new protein family. Here, we present the first report on this putative protein family: the cloning, isolation, and characterization of SP1, a stress-responsive, boiling-soluble, oligomeric protein.
Hydrogen Peroxide Activates Cell Death and Defense Gene Expression in Birch
Authors: Pellinen Riikka I. , Korhonen Minna-Sisko , Tauriainen Airi A. , Palva E. Tapio , Kangasjärvi Jaakko 
Published: October 2002

Abstract
The function of hydrogen peroxide (H2O2) as a signal molecule regulating gene expression and cell death induced by external stresses was studied in birch (Betula pendula). Ozone (O3),Pseudomonas syringae pv syringae(Pss), and wounding all induced cell death of various extents in birch leaves. This was temporally preceded and closely accompanied by H2O2 accumulation at, and especially surrounding, the lesion sites. O3 andPss, along with an artificial H2O2 producing system glucose (Glc)/Glc oxidase, elicited elevated mRNA levels corresponding to genes encoding reactive oxygen species detoxifying enzymes, Pal,Ypr10, and mitochondrial phosphate translocator 1. In addition to the regulation of gene expression, Glc/Glc oxidase also induced endogenous H2O2 production in birch leaves, accompanied by cell death that resembled O3 andPss damage. Wound-induced gene expression differed from that induced by O3 and Pss. Thus, it appears that at least two separate defense pathways can be activated in birch leaves by stress factors, even though the early H2O2 accumulation response is common among them all.
An Arabidopsis Mutant Defective in Jasmonate Response Is Allelic to the Auxin-Signaling Mutant axr1
Authors: Tiryaki Iskender , Staswick Paul E. 
Published: October 2002

Abstract
A screen for Arabidopsis mutants that were insensitive to methyl jasmonate (MeJA) in an assay for seedling root growth yielded only alleles of previously isolated mutants jar1 andcoi1, with one exception. Mapping of the locus and morphological characterization of the new mutant suggested it might be allelic to axr1, which had not previously been reported to show resistance to MeJA. The F1 from a cross of the new mutant with axr1-3 did not show complementation, confirming that these are the same genes. The new allele is calledaxr1-24. In addition to MeJA and indole-3-acetic acid (IAA), axr1-24 had decreased sensitivity to 1-aminocyclopropane-1-carboxylic acid, 6-benzylamino-purine, epi-brassinolide, and abscisic acid. Both axr1-24 and the previously characterized axr1-3 allele were shown to be susceptible to the opportunistic pathogen Pythium irregulare, a trait found in other jasmonate response mutants, including jar1-1. The double mutantjar1-1/axr1-3 was more resistant to inhibition of root growth by MeJA and was more susceptible to P. irregulare infection than either single mutant, suggesting these genes might act in independent response pathways. In contrast, resistance to IAA in the double mutant was not different fromaxr1-3. Northern-blot analysis showed that IAA induced the jasmonate-responsive lipoxygenase 2,AOS, and AtVSP gene transcripts and induction was strongly impaired in axr1-3. However, transcript induction by MeJA was only minimally affected inaxr1-3. This study demonstrates that in addition to auxin signaling, the AXR1 locus is involved in MeJA response, providing a mechanistic link between jasmonate and auxin-signaling pathways.
Identification and Biochemical Characterization of Mutants in the Proanthocyanidin Pathway in Arabidopsis
Authors: Abrahams Sharon , Tanner Gregory J. , Larkin Philip J. , Ashton Anthony R. 
Published: October 2002

Abstract
Proanthocyanidin (PA), or condensed tannin, is a polymeric flavanol that accumulates in a number of tissues in a wide variety of plants. In Arabidopsis, we found that PA precursors (detected histochemically using OsO4) accumulate in the endothelial cell layer of the seed coat from the two-terminal cell stage of embryo development onwards. To understand how PA is made, we screened mature seed pools of T-DNA-tagged Arabidopsis lines to identify mutants defective in the synthesis of PA and found six tds(tannin-deficient seed) complementation groups defective in PA synthesis. Mutations in these loci disrupt the amount (tds1, tds2, tds3,tds5, and tds6) or location and amount of PA (tds4) in the endothelial cell layer. The PA intermediate epicatechin has been identified in wild type and mutantstds1, tds2, tds3, andtds5 (which do not produce PA) and tds6(6% of wild-type PA), whereas tds4 (2% of wild-type PA) produces an unidentified dimethylaminocinnamaldehyde-reacting compound, indicating that the mutations may be acting on genes beyond leucoanthocyanidin reductase, the first enzymatic reduction step dedicated to PA synthesis. Two other mutants were identified, an allele of tt7, which has a spotted pattern of PA deposition and produces only 8% of the wild-type level of type PA as propelargonidin, and an allele of tt8 producing no PA. Spotted patterns of PA deposition observed in seed of mutants tds4 andtt7-3 result from altered PA composition and distribution in the cell. Our mutant screen, which was not exhaustive, suggests that the cooperation of many genes is required for successful PA accumulation.
Transcription Profiling of the Early Gravitropic Response in Arabidopsis Using High-Density Oligonucleotide Probe Microarrays,
Authors: Moseyko Nick , Zhu Tong , Chang Hur-Song , Wang Xun , Feldman Lewis J. 
Published: October 2002

Abstract
Studies of plant tropisms, the directed growth toward or away from external stimuli such as light and gravity, began more than a century ago. Yet biochemical, physiological, and especially molecular mechanisms of plant tropic responses remain for the most part unclear. We examined expression of 8,300 genes during early stages of the gravitropic response using high-density oligonucleotide probe microarrays. Approximately 1.7% of the genes represented on the array exhibited significant expression changes within the first 30 min of gravity stimulation. Among gravity-induced genes were a number of genes previously implicated to be involved in gravitropism. However, a much larger number of the identified genes have not been previously associated with gravitropism. Because reorientation of plants may also expose plants to mechanical perturbations, we also compared the effects of a gentle mechanical perturbation on mRNA levels during the gravity response. It was found that approximately 39% of apparently gravity-regulated genes were also regulated by the mechanical perturbation caused by plant reorientation. Our study revealed the induction of complex gene expression patterns as a consequence of gravitropic reorientation and points to an interplay between the gravitropic and mechanical responses and to the extreme sensitivity of plants to even very gentle mechanical perturbations.
Mineralogy of complex Co-Ni-Bi vein mineralization, Bieber deposit, Spessart, Germany
Authors: Wagner T. , Lorenz J. 
Published: October 2002

AbstractPost-Variscan vein-type Co-Ni-Bi ores of the Bieber deposit, Spessart mountains, Germany, which are related to the Permian Kupferschiefer, have been investigated by ore microscopy, X-ray powder diffraction and electron-probe microanalysis. The samples contain a variety of ore minerals, notably skutterudite, native bismuth, cobaltite, alloclasite, niccolite, maucherite, gersdorffite, rammelsbergite/pararammelsbergite, safflorite, loellingite and emplectite. The ores display structures indicative of multiple brecciation and complex zoned arsenide assemblages. Three sequential stages of deposition are identified, which are (1) the Cu stage, (2) the main Co-Ni-Bi stage, and (3) the late stage. The arsenide minerals, notably skutterudite, diarsenides and sulpharsenides, show a large range of compositional variation in Co-Ni-Fe space. A relatively limited number of skutterudite and diarsenide compositions lie outside the compositional fields established in the literature. Skutterudite and diarsenides are characterized by a significant substitution of As by S up to 0.44 a.p.f.u. and 0.31 a.p.f.u., respectively, which is larger than the range previously reported for these minerals. Sulpharsenide compositions can be grouped into three populations, which conform to cobaltian arsenopyrite, cobaltite and gersdorffite. They display highly variable As/S ratios between 0.95:1.00 and 1.29:0.73, consistent with experimental data. Estimates of the formation temperatures, based on the presence of dendritic native bismuth and emplectite, are in the range 100–300°C, similar to different post-Variscan mineralization styles widespread in Central Europe. Comparison of the Co-Ni-Bi vein assemblage with the framework of available paragenetic information and radiometric age data for regional mineralization events indicates an age of mineralization of ~150–160 Ma for the Bieber deposit.
Short deletion within the blood group Dombrock locus causing a Donull phenotype
Authors: Lucien Nicole , Celton Jean-Louis , Pennec Pierre-Yves Le , Cartron Jean-Pierre , Bailly Pascal 
Published: October 2002

Abstract
A new alteration of the blood group DO*A allele was identified in a female Donull donor from Reunion Island with allo– anti-DO3 in her serum; her parents are consanguineous. Because the amplification of the DO transcript failed, each exon and intron–exon junction from the DO gene were examined. After polymerase chain reaction (PCR) amplification and sequencing, the only deviation from the wild-type DO*A allele sequence was an 8-nucleotide deletion (nt 343-350) within exon 2. This short deletion generates a premature stop codon and encodes a truncated protein lacking the predicted functional motif of the adenosine diphosphate–ribosyltransferase enzyme and the glycosyl-phosphatidylinositol anchor motif essential for RBC membrane attachment. An allele-specific PCR to detect the DO(Δ8nt) deletion was developed.
Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) acts as a regulator of B-cell development, B-cell antigen receptor (BCR)–mediated activation, and autoimmune disease
Authors: Wilkinson Ray , Lyons A. Bruce , Roberts Donna , Wong Mae-Xhum , Bartley Paul A. , Jackson Denise E. 
Published: October 2002

AbstractPlatelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) is an immunoglobulin–immunoreceptor tyrosine-based inhibitory motif (Ig-ITIM) superfamily member that recruits and activates protein-tyrosine phosphatases, SHP-1 and SHP-2, through its intrinsic ITIMs. PECAM-1–deficient (PECAM-1−/− ) mice exhibit a hyperresponsive B-cell phenotype, increased numbers of B-1 cells, reduced B-2 cells, and develop autoantibodies. In the periphery, there are reduced mature recirculating B-2 cells and increased B-1a cells within the peritoneal cavity. In addition, PECAM-1−/− B cells display hyperproliferative responses to lipopolysaccharide and anti-IgM stimulation and showed enhanced kinetics in their intracellular Ca++ response following IgM cross-linking. PECAM-1−/− mice showed increased serum levels of IgM with elevated IgG isotypes and IgA antidinitrophenol antibody in response to the T-independent antigen, dinitrophenol-Ficoll. Finally, PECAM-1−/− mice developed antinuclear antibodies and lupuslike autoimmune disease with age.
Plasmodium falciparum cysteine protease falcipain-2 cleaves erythrocyte membrane skeletal proteins at late stages of parasite development
Authors: Hanspal Manjit , Dua Meenakshi , Takakuwa Yuichi , Chishti Athar H. , Mizuno Akiko 
Published: October 2002

AbstractPlasmodium falciparum–derived cysteine protease falcipain-2 cleaves host erythrocyte hemoglobin at acidic pH and specific components of the membrane skeleton at neutral pH. Analysis of stage-specific expression of these 2 proteolytic activities of falcipain-2 shows that hemoglobin-hydrolyzing activity is maximum in early trophozoites and declines rapidly at late stages, whereas the membrane skeletal protein hydrolyzing activity is markedly increased at the late trophozoite and schizont stages. Among the erythrocyte membrane skeletal proteins, ankyrin and protein 4.1 are cleaved by native and recombinant falcipain-2 near their C-termini. To identify the precise peptide sequence at the hydrolysis site of protein 4.1, we used a recombinant construct of protein 4.1 as substrate followed by MALDI-MS analysis of the cleaved product. We show that falcipain-2–mediated cleavage of protein 4.1 occurs immediately after lysine 437, which lies within a region of the spectrin–actin-binding domain critical for erythrocyte membrane stability. A 16-mer peptide containing the cleavage site completely inhibited the enzyme activity and blocked falcipain-2–induced fragmentation of erythrocyte ghosts. Based on these results, we propose that falcipain-2 cleaves hemoglobin in the acidic food vacuole at the early trophozoite stage, whereas it cleaves specific components of the red cell skeleton at the late trophozoite and schizont stages. It is the proteolysis of skeletal proteins that causes membrane instability, which, in turn, facilitates parasite release in vivo.
Allogeneic bone marrow transplantation: cure for familial Mediterranean fever
Authors: Milledge John , Shaw Peter J. , Mansour Albert , Williamson Sarah , Bennetts Bruce , Roscioli Tony , Curtin Julie , Christodoulou John 
Published: October 2002

Abstract
We describe data on a 7-year-old girl with congenital dyserythropoietic anemia (CDA), who also had familial Mediterranean fever (FMF). Repeated transfusions required since the age of 6 months to treat her CDA led to iron overload and a persistently high ferritin level. Her relapsing FMF made effective iron chelation therapy very difficult. Consequently, at the age of 4 years, she underwent allogeneic, sibling bone marrow transplantation (BMT). During conditioning for her BMT, symptoms of FMF, including splenomegaly, arthritis, and recurrent abdominal pain, began to resolve and she was gradually weaned off colchicine. Now, 2 years after the transplantation, she remains free from FMF symptomatology and is off all immunosuppressants. This case demonstrates that symptoms of FMF can be alleviated by the therapy used during allogeneic BMT. In this patient it is likely that the missing factor in FMF is now being provided by granulocytes derived from the stem cells within transplanted bone marrow.
Functional analysis of human hematopoietic repopulating cells mobilized with granulocyte colony-stimulating factor alone versus granulocyte colony-stimulating factor in combination with stem cell factor
Authors: Hess David A. , Levac Krysta D. , Karanu Francis N. , Rosu-Myles Michael , White Martin J. , Gallacher Lisa , Murdoch Barbara , Keeney Michael , Ottowski Pamela , Foley Ronan , Chin-Yee Ian , Bhatia Mickie 
Published: October 2002

AbstractUsing in vitro progenitor assays, serum-free in vitro cultures, and the nonobese diabetic/severe combined immune-deficient (NOD/SCID) ecotropic murine virus knockout xenotransplantation model to detect human SCID repopulating cells (SRCs) with multilineage reconstituting function, we have characterized and compared purified subpopulations harvested from the peripheral blood (PB) of patients receiving granulocyte colony-stimulating factor (G-CSF) alone or in combination with stem cell factor (SCF). Mobilized G-CSF plus SCF PB showed a 2-fold increase in total mononuclear cell content and a 5-fold increase in CD34-expressing cells depleted for lineage-marker expression (CD34+Lin−) as compared with patients treated with G-CSF alone. Functionally, G-CSF plus SCF–mobilized CD34+CD38−Lin−cells contained a 2-fold enhancement in progenitor frequency as compared with G-CSF–mobilized subsets. Despite enhanced cellularity and progenitor capacity, G-CSF plus SCF mobilization did not increase the frequency of SRCs as determined by limiting dilution analysis by means of unfractionated PB cells. Purification of SRCs from these sources demonstrated that as few as 1000 CD34+CD38−Lin− cells from G-CSF–mobilized PB contained SRC capacity while G-CSF plus SCF–mobilized CD34+CD38−Lin−cells failed to repopulate at doses up to 500 000 cells. In addition, primitive CD34−CD38−AC133+Lin−cells derived from G-CSF plus SCF–mobilized PB were capable of differentiation into CD34-expressing cells, while the identical subfractions from G-CSF PB were unable to produce CD34+cells in serum-free cultures. Our study defines qualitative and quantitative distinctions among subsets of primitive cells mobilized by means of G-CSF plus SCF versus G-CSF alone, and therefore has implications for the utility of purified repopulating cells from these sources.
Human cytomegalovirus inhibits maturation and impairs function of monocyte-derived dendritic cells
Authors: Moutaftsi Magdalena , Mehl Anja M. , Borysiewicz Leszek K. , Tabi Zsuzsanna 
Published: October 2002

AbstractDendritic cells (DCs) play a pivotal role in the generation of virus-specific cytotoxic T-cell responses, but some viruses can render DCs inefficient in stimulating T cells. We studied whether infection of DCs with human cytomegalovirus (HCMV) results in a suppression of DC function which may assist HCMV in establishing persistence. The effect of HCMV infection on the phenotype and function of monocyte-derived DCs and on their ability to mature following infection with an endothelial cell–adapted clinical HCMV isolate were studied. HCMV infection induced no maturation of DCs; instead, it efficiently down-regulated the expression of surface major histocompatibility complex (MHC) class I, CD40, and CD80 molecules. Slight down-regulation of MHC class II and CD86 molecules was also observed. Lipopolysaccharide (LPS)–induced maturation of infected DCs was strongly inhibited, as indicated by lower levels of surface expression of MHC class I, class II, costimulatory, and CD83 molecules. The down-regulation or inhibition of these surface markers occurred only in HCMV antigen-positive DCs. DCs produced no interleukin 12 (IL-12) and only low levels of tumor necrosis factor alpha (TNF-α) upon HCMV infection. Furthermore, cytokine production upon stimulation with LPS or CD40L was significantly impaired. Inhibition of cytokine production did not depend on viral gene expression as UV-irradiated HCMV resulted in the same effect. Proliferation and cytotoxicity of T cells specific to a recall antigen presented by DCs were also reduced when DCs were HCMV infected. This study shows that HCMV inhibits DC function, revealing a powerful viral strategy to delay or prevent the generation of virus-specific cytotoxic T cells.
Presence of a mobilizable intracellular pool of hepatocyte growth factor in human polymorphonuclear neutrophils
Authors: Grenier Alain , Chollet-Martin Sylvie , Crestani Bruno , Delarche Charlotte , El Benna Jamel , Boutten Anne , Andrieu Valérie , Durand Geneviève , Gougerot-Pocidalo Marie-Anne , Aubier Michel , Dehoux Monique 
Published: October 2002

AbstractHepatocyte growth factor (HGF), a heparin-binding factor, is synthesized as a single-chain inactive precursor (pro-HGF), which is converted by proteolysis to an active heterodimer (mature HGF). HGF has pleiotropic activities and has been implicated in the regulation of mitogenesis, motogenesis, and morphogenesis of epithelial and endothelial cells. As polymorphonuclear neutrophils (PMNs) secrete numerous cytokines involved in the modulation of local inflammation, we investigated their ability to produce HGF. We found that HGF was stored in secretory vesicles and in gelatinase/specific granules. This intracellular stock was rapidly mobilized by degranulation when neutrophils were stimulated with phorbol myristate acetate or N-formylmethionyl-leucyl-phenylalanine. Cycloheximide did not affect the release of HGF. Moreover, HGF messenger RNA and protein expression was found in bone marrow myeloid cells, suggesting that HGF synthesis likely occurs during PMN maturation. In mature circulating PMNs, intracellular HGF was in the pro-HGF form, whereas the HGF secreted by degranulation was the mature form. Furthermore, PMNs pretreated with diisopropyl fluorophosphate only released the pro-HGF form, suggesting that PMN-derived serine protease(s) are involved in the proteolytic process. We also obtained evidence that secreted mature HGF binds PMN-derived glycosaminoglycans (probably heparan sulfate). These findings suggest that PMNs infiltrating damaged tissues may modulate local wound healing and repair through the production of HGF, a major mediator of tissue regeneration.