bluuebunny/crossref_metadata_2025_split huggingface dataset:
A member of the Whirly family is a multifunctional RNA- and DNA-binding protein that is essential for chloroplast biogenesis
Authors: Prikryl Jana , Watkins Kenneth P. , Friso Giulia , van Wijk Klaas J. , Barkan Alice 
Published: August 2008

Abstract
‘Whirly’ proteins comprise a plant-specific protein family whose members have been described as DNA-binding proteins that influence nuclear transcription and telomere maintenance, and that associate with nucleoids in chloroplasts and mitochondria. We identified the maize WHY1 ortholog among proteins that coimmunoprecipitate with CRS1, which promotes the splicing of the chloroplast atpF group II intron. ZmWHY1 localizes to the chloroplast stroma and to the thylakoid membrane, to which it is tethered by DNA. Genome-wide coimmunoprecipitation assays showed that ZmWHY1 in chloroplast extract is associated with DNA from throughout the plastid genome and with a subset of plastid RNAs that includes atpF transcripts. Furthermore, ZmWHY1 binds both RNA and DNA in vitro. A severe ZmWhy1 mutant allele conditions albino seedlings lacking plastid ribosomes; these exhibit the altered plastid RNA profile characteristic of ribosome-less plastids. Hypomorphic ZmWhy1 mutants exhibit reduced atpF intron splicing and a reduced content of plastid ribosomes; aberrant 23S rRNA metabolism in these mutants suggests that a defect in the biogenesis of the large ribosomal subunit underlies the ribosome deficiency. However, these mutants contain near normal levels of chloroplast DNA and RNAs, suggesting that ZmWHY1 is not directly required for either DNA replication or for global plastid transcription.
The triple helix: 50 years later, the outcome
Authors: Duca Maria , Vekhoff Pierre , Oussedik Kahina , Halby Ludovic , Arimondo Paola B. 
Published: August 2008

Abstract
Triplex-forming oligonucleotides constitute an interesting DNA sequence-specific tool that can be used to target cleaving or cross-linking agents, transcription factors or nucleases to a chosen site on the DNA. They are not only used as biotechnological tools but also to induce modifications on DNA with the aim to control gene expression, such as by site-directed mutagenesis or DNA recombination. Here, we report the state of art of the triplex-based antigene strategy 50 years after the discovery of such a structure, and we show the importance of the actual applications and the main challenges that we still have ahead of us.
Formation of an RNA polymerase II preinitiation complex on an RNA promoter derived from the hepatitis delta virus RNA genome
Authors: Abrahem Abrahem , Pelchat Martin 
Published: August 2008

Abstract
Although RNA polymerases (RNAPs) are able to use RNA as template, it is unknown how they recognize RNA promoters. In this study, we used an RNA fragment derived from the hepatitis delta virus (HDV) genome as a model to investigate the recognition of RNA promoters by RNAP II. Inhibition of the transcription reaction using an antibody specific to the largest subunit of RNAP II and the direct binding of purified RNAP II to the RNA promoter confirmed the involvement of RNAP II in the reaction. RNA affinity chromatography established that an active RNAP II preinitiation complex forms on the RNA promoter and indicated that this complex contains the core RNAP II subunit and the general transcription factors TFIIA, TFIIB, TFIID, TFIIE, TFIIF, TFIIH and TFIIS. Binding assays demonstrated the direct binding of the TATA-binding protein and suggested that this protein is required to nucleate the RNAP II complex on the RNA promoter. Our findings provide a better understanding of the events leading to RNA promoter recognition by RNAP II.
AtCHX13 Is a Plasma Membrane K+ Transporter
Authors: Zhao Jian , Cheng Ning-Hui , Motes Christy M. , Blancaflor Elison B. , Moore Miranda , Gonzales Naomi , Padmanaban Senthilkumar , Sze Heven , Ward John M. , Hirschi Kendal D. 
Published: August 2008

AbstractPotassium (K+) homeostasis is essential for diverse cellular processes, although how various cation transporters collaborate to maintain a suitable K+ required for growth and development is poorly understood. The Arabidopsis (Arabidopsis thaliana) genome contains numerous cation:proton antiporters (CHX), which may mediate K+ transport; however, the vast majority of these transporters remain uncharacterized. Here, we show that AtCHX13 (At2g30240) has a role in K+ acquisition. AtCHX13 suppressed the sensitivity of yeast (Saccharomyces cerevisiae) mutant cells defective in K+ uptake. Uptake experiments using 86Rb+ as a tracer for K+ demonstrated that AtCHX13 mediated high-affinity K+ uptake in yeast and in plant cells with a K m of 136 and 196 μ m, respectively. Functional green fluorescent protein-tagged versions localized to the plasma membrane of both yeast and plant. Seedlings of null chx13 mutants were sensitive to K+ deficiency conditions, whereas overexpression of AtCHX13 reduced the sensitivity to K+ deficiency. Collectively, these results suggest that AtCHX13 mediates relatively high-affinity K+ uptake, although the mode of transport is unclear at present. AtCHX13 expression is induced in roots during K+-deficient conditions. These results indicate that one role of AtCHX13 is to promote K+ uptake into plants when K+ is limiting in the environment.
Two New Clock Proteins, LWD1 and LWD2, Regulate Arabidopsis Photoperiodic Flowering
Authors: Wu Jing-Fen , Wang Ying , Wu Shu-Hsing 
Published: August 2008

AbstractThe “light” signal from the environment sets the circadian clock to regulate multiple physiological processes for optimal rhythmic growth and development. One such process is the control of flowering time by photoperiod perception in plants. In Arabidopsis (Arabidopsis thaliana), the flowering time is determined by the correct interconnection of light input and signal output by the circadian clock. The identification of additional clock proteins will help to better dissect the complex nature of the circadian clock in Arabidopsis. Here, we show LIGHT-REGULATED WD1 (LWD1)/LWD2 as new clock proteins involved in photoperiod control. The lwd1lwd2 double mutant has an early-flowering phenotype, contributed by the significant phase shift of CONSTANS (CO), and, therefore, an increased expression of FLOWERING LOCUS T (FT) before dusk. Under entrainment conditions, the expression phase of oscillator (CIRCADIAN CLOCK ASSOCIATED1 [CCA1], LATE ELONGATED HYPOCOTYL [LHY], TIMING OF CAB EXPRESSION1 [TOC1], and EARLY FLOWERING4 [ELF4]) and output (GIGANTEA, FLAVIN-BINDING, KELCH REPEAT, F-BOX1, CYCLING DOF FACTOR1, CO, and FT) genes in the photoperiod pathway shifts approximately 3 h forward in the lwd1lwd2 double mutant. Both the oscillator (CCA1, LHY, TOC1, and ELF4) and output (COLD, CIRCADIAN RHYTHM, AND RNA BINDING2 and CHLOROPHYLL A/B-BINDING PROTEIN2) genes have a short period length in the lwd1lwd2 double mutant. Our data imply that LWD1/LWD2 proteins function in close proximity to or within the circadian clock for photoperiodic flowering control.
Singlet Oxygen Is the Major Reactive Oxygen Species Involved in Photooxidative Damage to Plants
Authors: Triantaphylidès Christian , Krischke Markus , Hoeberichts Frank Alfons , Ksas Brigitte , Gresser Gabriele , Havaux Michel , Van Breusegem Frank , Mueller Martin Johannes 
Published: August 2008

Abstract
Reactive oxygen species act as signaling molecules but can also directly provoke cellular damage by rapidly oxidizing cellular components, including lipids. We developed a high-performance liquid chromatography-electrospray ionization-tandem mass spectrometry-based quantitative method that allowed us to discriminate between free radical (type I)- and singlet oxygen (1O2; type II)-mediated lipid peroxidation (LPO) signatures by using hydroxy fatty acids as specific reporters. Using this method, we observed that in nonphotosynthesizing Arabidopsis (Arabidopsis thaliana) tissues, nonenzymatic LPO was almost exclusively catalyzed by free radicals both under normal and oxidative stress conditions. However, in leaf tissues under optimal growth conditions, 1O2 was responsible for more than 80% of the nonenzymatic LPO. In Arabidopsis mutants favoring 1O2 production, photooxidative stress led to a dramatic increase of 1O2 (type II) LPO that preceded cell death. Furthermore, under all conditions and in mutants that favor the production of superoxide and hydrogen peroxide (two sources for type I LPO reactions), plant cell death was nevertheless always preceded by an increase in 1O2-dependent (type II) LPO. Thus, besides triggering a genetic cell death program, as demonstrated previously with the Arabidopsis fluorescent mutant, 1O2 plays a major destructive role during the execution of reactive oxygen species-induced cell death in leaf tissues.
Functional Diversification of CLAVATA3-Related CLE Proteins in Meristem Maintenance in Rice
Authors: Suzaki Takuya , Yoshida Akiko , Hirano Hiro-Yuki 
Published: August 2008

AbstractPostembryonic development in plants depends on the activity of the shoot apical meristem (SAM) and root apical meristem (RAM). In Arabidopsis thaliana, CLAVATA signaling negatively regulates the size of the stem cell population in the SAM by repressing WUSCHEL. In other plants, however, studies of factors involved in stem cell maintenance are insufficient. Here, we report that two proteins closely related to CLAVATA3, FLORAL ORGAN NUMBER2 (FON2) and FON2-LIKE CLE PROTEIN1 (FCP1/Os CLE402), have functionally diversified to regulate the different types of meristem in rice (Oryza sativa). Unlike FON2, which regulates the maintenance of flower and inflorescence meristems, FCP1 appears to regulate the maintenance of the vegetative SAM and RAM. Constitutive expression of FCP1 results in consumption of the SAM in the vegetative phase, and application of an FCP1 CLE peptide in vitro disturbs root development by misspecification of cell fates in the RAM. FON1, a putative receptor of FON2, is likely to be unnecessary for these FCP1 functions. Furthermore, we identify a key amino acid residue that discriminates between the actions of FCP1 and FON2. Our results suggest that, although the basic framework of meristem maintenance is conserved in the angiosperms, the functions of the individual factors have diversified during evolution.
ArabidopsisProtein Disulfide Isomerase-5 Inhibits Cysteine Proteases during Trafficking to Vacuoles before Programmed Cell Death of the Endothelium in Developing Seeds
Authors: Andème Ondzighi Christine , Christopher David A. , Cho Eun Ju , Chang Shu-Choeng , Staehelin L. Andrew 
Published: August 2008

AbstractProtein disulfide isomerase (PDI) oxidizes, reduces, and isomerizes disulfide bonds, modulates redox responses, and chaperones proteins. The Arabidopsis thaliana genome contains 12 PDI genes, but little is known about their subcellular locations and functions. We demonstrate that PDI5 is expressed in endothelial cells about to undergo programmed cell death (PCD) in developing seeds. PDI5 interacts with three different Cys proteases in yeast two-hybrid screens. One of these traffics together with PDI5 from the endoplasmic reticulum through the Golgi to vacuoles, and its recombinant form is functionally inhibited by recombinant PDI5 in vitro. Peak PDI5 expression in endothelial cells precedes PCD, whereas decreasing PDI5 levels coincide with the onset of PCD-related cellular changes, such as enlargement and subsequent collapse of protein storage vacuoles, lytic vacuole shrinkage and degradation, and nuclear condensation and fragmentation. Loss of PDI5 function leads to premature initiation of PCD during embryogenesis and to fewer, often nonviable, seeds. We propose that PDI5 is required for proper seed development and regulates the timing of PCD by chaperoning and inhibiting Cys proteases during their trafficking to vacuoles before PCD of the endothelial cells. During this transitional phase of endothelial cell development, the protein storage vacuoles become the de facto lytic vacuoles that mediate PCD.
A Bayesian approach to inverse modelling of stratigraphy, part 1: method
Authors: Charvin Karl , Gallagher Kerry , Hampson Gary L. , Labourdette Richard 
Published: August 2008

ABSTRACTThe inference of ancient environmental conditions from their preserved response in the sedimentary record still remains an outstanding issue in stratigraphy. Since the 1970s, conceptual stratigraphic models (e.g. sequence stratigraphy) based on the underlying assumption that accommodation space is the critical control on stratigraphic architecture have been widely used. Although these methods considered more recently other possible parameters such as sediment supply and transport efficiency, they still lack in taking into account the full range of possible parameters, processes, and their complex interactions that control stratigraphic architecture. In this contribution, we present a new quantitative method for the inference of key environmental parameters (specifically sediment supply and relative sea level) that control stratigraphy. The approach combines a fully non‐linear inversion scheme with a ‘process–response’ forward model of stratigraphy. We formulate the inverse problem using a Bayesian framework in order to sample the full range of possible solutions and explicitly build in prior geological knowledge. Our methodology combines Reversible Jump Markov chain Monte Carlo and Simulated Tempering algorithms which are able to deal with variable‐dimensional inverse problems and multi‐modal posterior probability distributions, respectively. The inverse scheme has been linked to a forward stratigraphic model, BARSIM (developed by Joep Storms, University of Delft), which simulates shallow‐marine wave/storm‐dominated systems over geological timescales. This link requires the construction of a likelihood function to quantify the agreement between simulated and observed data of different types (e.g. sediment age and thickness, grain size distributions). The technique has been tested and validated with synthetic data, in which all the parameters are specified to produce a ‘perfect’ simulation, although we add noise to these synthetic data for subsequent testing of the inverse modelling approach. These tests addressed convergence and computational‐overhead issues, and highlight the robustness of the inverse scheme, which is able to assess the full range of uncertainties on the inferred environmental parameters and facies distributions.
Siglec‐F antibody administration to mice selectively reduces blood and tissue eosinophils
Authors: Zimmermann N. , McBride M. L. , Yamada Y. , Hudson S. A. , Jones C. , Cromie K. D. , Crocker P. R. , Rothenberg M. E. , Bochner B. S. 
Published: August 2008

Background:  Sialic acid‐binding immunoglobulin‐like lectins (Siglecs) are a family of receptors that bind sialic acid and mostly contain immunoreceptor tyrosine‐based inhibitory motifs, suggesting that these molecules possess inhibitory functions. We have recently identified Siglec‐8 as an eosinophil‐prominent Siglec, and cross‐linking of Siglec‐8 on human eosinophils induces apoptosis. In this article, we address the in vivo consequences of Siglec engagement. We and others have identified mouse Siglec‐F as the closest functional paralog of human Siglec‐8, based on shared ligand‐binding and expression pattern. We therefore hypothesized that Siglec‐F engagement would affect levels and viability of eosinophils in vivo.Methods:  Wild type and hypereosinophilic mice were administered Siglec‐F antibody and levels of eosinophils in peripheral blood and tissue were measured. Eosinophil apoptosis (in vivo and in vitro) was determined by binding of Annexin‐V.Results:  Studies in IL‐5 transgenic mice, displaying hypereosinophilia, show that administration of a single dose of Siglec‐F antibody results in rapid reductions in quantum of eosinophils in the blood. This decrease was accompanied by reductions in tissue eosinophils. Quantum of eosinophils in blood was decreased using two separate antibodies, as well as in other mouse models (wild type mice and in a mouse model of chronic eosinophilic leukemia). Mechanistic studies demonstrated that Siglec‐F antibody administration induced apoptosis of eosinophils in vivo and in vitro.Conclusion:  These data demonstrate that activation of innate immune receptors, like Siglec‐F, can significantly reduce mouse eosinophil viability. As such, targeting Siglec‐8/F may be a therapeutic approach for eosinophilic disorders.
Ultrasonographic Examination of the Scrotal Content in the Rabbit
Authors: Aksoy M , Erdem H , Hatipoğlu F , Lehimcioğlu NC , Akman O , Özkan K 
Published: August 2008

ContentsThis study was performed to describe a practical technique for ultrasound examination of the scrotal content of the rabbit. The scrotal content of normal rabbits and those with induced lesions (i.e. needle biopsy of the testis and epididymal ligation) were viewed using a portable scanner connected to a 5 or 7.5 MHz real time, B‐mode linear array transducer. The effect of frequency (5 and 7.5 MHz), pad material placed under the testicle (rubber, plastic and carton) and the presence of a water sack between the probe and organ were examined to optimize the technique. The best image quality was obtained using a 5‐MHz probe when the testicle was fixed on a rubber pad and covered by a water sack. Testicular parenchyma was imaged as homogeneous and moderately echoic. Caput and cauda epididymis were identified as homogeneous and less echoic compared with the testis parenchyma. Variations in the testicular echotexture that occur secondarily to epididymal ligation and testis biopsy could be screened readily. In conclusion, real‐time ultrasonography, performed as described in this study, may provide a valuable tool to screen scrotal contents and to identify certain pathological conditions that affect fertility in the rabbit.
Human adenosine deaminase as an allosteric modulator of human A1adenosine receptor: abolishment of negative cooperativity for [3H](R)‐pia binding to the caudate nucleus
Authors: Gracia Eduard , Cortés Antoni , Meana J. Javier , García‐Sevilla Jesus , Herhsfield Michael S. , Canela Enric I. , Mallol Josefa , Lluís Carmen , Franco Rafael , Casadó Vicent 
Published: August 2008

AbstractIt has been shown that adenosine deaminase (ADA; EC 3.5.4.4) behaves as an ecto‐enzyme anchored to membrane proteins, among them A1adenosine receptors (A1Rs). Bovine ADA interacts with A1Rs from many species and regulates agonists binding to receptors in an activity‐independent form. However, it was not known whether human ADA exerted any effect on the agonist binding to human A1Rs, because of both technical difficulties in obtaining pure human ADA and tissues containing human A1Rs. In this study, human ADA was purified to homogeneity. Taking in consideration that A1Rs form homodimers and taking advantage of a new procedure to fit binding data to receptors dimers, which allows to calculate ligand dissociation constants and the degree of cooperativity between the two subunits in the dimer, here it is demonstrated that human ADA markedly enhances the agonist and antagonist affinity and abolishes the negative cooperativity on agonist binding to human striatal A1Rs. ADA also increases the ability of the agonist to decrease the forskolin‐induced cAMP levels. The results show that human ADA, apart from reducing the adenosine concentration and thus preventing A1R desensitization, binds to A1R behaving as an allosteric effector that markedly enhances agonist affinity and increases receptor functionality. The physiological role of the interaction is to make receptors more sensitive to adenosine. This powerful regulation has important implications for the physiology and pharmacology of neuronal A1Rs.
Lipid peroxidation up‐regulates BACE1 expression in vivo: a possible early event of amyloidogenesis in Alzheimer’s disease
Authors: Chen Liuji , Na Ren , Gu Mingjun , Richardson Arlan , Ran Qitao 
Published: August 2008

AbstractIncreased lipid peroxidation is shown to be an early event of Alzheimer’s disease (AD). However, it is not clear whether and how increased lipid peroxidation might lead to amyloidogenesis, a hallmark of AD. Glutathione peroxidase 4 (Gpx4) is an essential antioxidant defense enzyme that protects an organism against lipid peroxidation. Gpx4+/− mice show increased lipid peroxidation in brain, as evidenced by their elevated levels of 4‐hydroxy‐2‐nonenal. To understand the role of lipid peroxidation in amyloidogenesis, we studied secretase activities in Gpx4+/− mice as a function of age. Both young (6 months) and middle‐aged (17–20 months) Gpx4+/− mice had higher levels of β‐secretase activity than their age‐matched wildtype controls, and the increased β‐secretase activity in Gpx4+/− mice was a result of up‐regulation of β‐site amyloid precursor protein cleavage enzyme 1 (BACE1) expression at the protein level. The high level of BACE1 protein led to increased endogenous β‐amyloid (Aβ)1–40 in middle‐aged Gpx4+/− mice. We further studied amyloidogenesis in APPGpx4+/− mice. Our data indicate that APPGpx4+/− mice had significantly increased amyloid plaque burdens and increased Aβ1–40 and Aβ1–42 levels compared with APPGpx4+/+ mice. Therefore, our results indicate that increased lipid peroxidation leads to increased amyloidogenesis through up‐regulation of BACE1 expression in vivo, a mechanism that may be important in pathogenesis of AD at early stages.
Mitochondrial alterations in Parkinson’s disease: new clues
Authors: Vila Miquel , Ramonet David , Perier Celine 
Published: August 2008

AbstractMitochondrial dysfunction has long been associated with Parkinson’s disease (PD). In particular, complex I impairment and subsequent oxidative stress have been widely demonstrated in experimental models of PD and in post‐mortem PD samples. A recent wave of new studies is providing novel clues to the potential involvement of mitochondria in PD. In particular, (i) mitochondria‐dependent programmed cell death pathways have been shown to be critical to PD‐related dopaminergic neurodegeneration, (ii) many disease‐causing proteins associated with familial forms of PD have been demonstrated to interact either directly or indirectly with mitochondria, (iii) aging‐related mitochondrial changes, such as alterations in mitochondrial DNA, are increasingly being associated with PD, and (iv) anomalies in mitochondrial dynamics and intra‐neuronal distribution are emerging as critical participants in the pathogenesis of PD. These new findings are revitalizing the field and reinforcing the potential role of mitochondria in the pathogenesis of PD. Whether a primary or secondary event, or part of a multi‐factorial pathogenic process, mitochondrial dysfunction remains at the forefront of PD research and holds the promise as a potential molecular target for the development of new therapeutic strategies for this devastating, currently incurable, disease.