bluuebunny/crossref_metadata_2025_split huggingface dataset:
The genetic control of lignin deposition during plant growth and development
Authors: Rogers Louisa A. , Campbell Malcolm M. 
Published: September 2004

SummaryLignins are complex, three‐dimensional polymers embedded in the cell walls of specialised plant cells, where they play important roles in plant growth and development. Plants must possess mechanisms to coordinate lignin deposition so that its synthesis occurs at the appropriate time and place, in response to endogenous and exogenous cues. Here we consider the genetic basis of the control of lignin deposition. We focus on the transcriptional regulation of lignification, considering how the genes encoding the lignin biosynthetic pathway might be co‐ordinately controlled, and the transcription factors that are likely to be involved. We also discuss the mechanisms regulating lignification that have been revealed by mutants with altered lignin deposition. We conclude that, while transcriptional regulation is a common feature in the control of lignification, there are many different regulators that may bring about this common mode of regulation.

Contents

Summary
17

I.
Introduction
17

II.
Transcriptional regulation of genes encoding lignin biosynthetic enzymes
19

III.
Co‐ordinate regulation of genes encoding lignin biosynthetic enzymes
21

IV.
Mutants with altered spatial and temporal control of lignification
23

V.
Conclusion
28

Acknowledgements
28

References
28
Cryopreservation in Populus functional genomics
Authors: Tsai Chung‐Jui , Hubscher Sandra L. 
Published: September 2004

SummaryThe release of the first tree genome sequence for Populus tricocarpa, along with continuing rapid development of Populus EST, microarray and metabolomic technologies, promises to advance forest tree genomics. High throughput transformation by knockout or other gene manipulation strategies to generate large numbers of transgenic Populus for functional elucidation of the estimated 36 000 genes will soon follow. The efficacy of large‐scale transformation approaches for advancing Populus genomics will ultimately depend on the availability of properly maintained transgenic germ lines for distribution. The Arabidopsis community has already demonstrated the value of shared genetic resources, especially mutant and transgenic seed stocks, in functional genomics research. Seed bank will not work for the Populus research community. Instead, a stock distribution center for transgenic Populus research will have to be based on long‐term preservation of clonal germplasm. This review presents recent progress in applying cryogenic techniques for clonal preservation of long‐lived trees and discusses the challenges facing Populus molecular geneticists in germplasm preservation.
Ustilago maydis: how its biology relates to pathogenic development
Authors: Kahmann Regine , Kämper Jörg 
Published: September 2004

SummaryThe smut fungus Ustilago maydis is a ubiquitous pathogen of corn. Although of minor economical importance, U. maydis has become the most attractive model among the plant pathogenic basidiomycetes under study. This fungus undergoes a number of morphological transitions throughout its life‐cycle, the most prominent being the dimorphic switch from budding to filamentous growth that is prerequisite for entry into the biotrophic phase. The morphological transition is controlled by the tetrapolar mating system. Understanding the mating system has allowed connections to signalling cascades operating during pathogenic development. Here, we will review the status and recent insights into understanding pathogenic development of U. maydis and emphasize areas and directions of future research.

Contents

Summary
31

I.
Introduction
31

II.
Important tools for exprimentation with Ustilago myadis
32

III.
Cell fusion requres a complex signalling network
33

IV.
Development of the dikaryon: the bE/bW complex at work
34

V.
A connection between cell cycle, morphogenesis and virulence
36

VI.
The early infection stages
38

VII.
Proliferation and differentiaton in the plant host
38

VIII.
The Ustilago maydis genome
39

IX.
Conclusions
40

Acknowledgements
40

References
40
Revisiting tree maturation and floral initiation in the poplar functional genomics era
Authors: Brunner Amy M. , Nilsson Ove 
Published: September 2004

SummaryThe recent release of the Populus trichocarpa genome sequence will dramatically enhance the efficiency of functional and comparative genomics research in trees. This provides researchers studying various developmental processes related to the perennial and tree life strategies with a completely new set of tools. Intimately associated with the life strategy of trees are their abilities to maintain juvenile or nonflowering phases for years to decades, and once reproductively competent, to alternate between the production of vegetative and reproductive shoots. Most of what we know about the regulation of the floral transition comes from research on Arabidopsis thaliana, a small, herbaceous, rapid‐cycling, annual plant. In this review, we discuss the similarities and differences between Arabidopsis and tree flowering, and how recent findings in Arabidopsis, coupled to comparative and functional genomics in poplars, will help answer the question of how tree maturation and floral initiation is regulated.
Tension wood as a model for functional genomics of wood formation
Authors: Pilate Gilles , Déjardin Annabelle , Laurans Françoise , Leplé Jean‐Charles 
Published: September 2004

SummaryWood is a complex and highly variable tissue, the formation of which is developmentally and environmentally regulated. In reaction to gravitropic stimuli, angiosperm trees differentiate tension wood, a wood with specific anatomical, chemical and mechanical features. In poplar the most significant of these features is an additional layer that forms in the secondary wall of tension wood fibres. This layer is mainly constituted of cellulose microfibrils oriented nearly parallel to the fibre axis. Tension wood formation can be induced easily and strongly by bending the stem of a tree. Located at the upper side of the bent stem, tension wood can be compared with the wood located on its lower side. Therefore tension wood represents an excellent model for studying the formation of xylem cell walls. This review summarizes results recently obtained in the field of genomics on tension wood. In addition, we present an example of how the application of functional genomics to tension wood can help decipher the molecular mechanisms responsible for cell wall characteristics such as the orientation of cellulose microfibrils.
Effects of psychotomimetic and antipsychotic agents on neocortical and striatal concentrations of various amino acids in the rat
Authors: Sakurai Shin‐ichiro , Ishii Sumikazu , Umino Asami , Shimazu Dai , Yamamoto Naoki , Nishikawa Toru 
Published: September 2004

AbstractA subcutaneous injection of small and moderate doses (1.6, 3.2, 4.0 and 4.8 mg/kg) of the schizophrenomimetic methamphetamine caused a dose‐related increase in the tissue content (the net content) of l‐Arg and l‐Asn in the neocortex and striatum at 60 min, but not at 360 min, after injection. The methamphetamine‐induced (4.8 mg/kg) increases in levels of these amino acids were significantly attenuated by pretreatment with an antipsychotic drug, haloperidol (1 mg/kg) or clozapine (10 mg/kg). In the neocortex, a clozapine‐reversible increase in the level of l‐Thr was also observed 60 min after methamphetamine administration. Striatal concentrations of l‐Glu, l‐Ser, l‐Thr, Gly and l‐Ala were augmented by the same regimen in a haloperidol‐ and clozapine‐sensitive fashion. A moderate dose of another schizophrenomimetic phencyclidine (7.5 mg/kg) given subcutaneously induced robust abnormal behavior, a diminution in the neocortical and striatal levels of l‐Asp and an increase in the striatal l‐Ala content without significant effects on the other amino acids studied. These results suggest that neocortical and striatal l‐Arg, l‐Asn, l‐Thr, Gly, l‐Ala or l‐Ser may be implicated in the psychotomimetic effects of methamphetamine and might display mutual interaction with cerebral dopaminergic transmission. The differential effects of methamphetamine and phencyclidine on the net neocortical and striatal concentrations of various amino acids might, at least in part, underlie the distinct features of psychoses induced by these two drugs.
Intermediate‐conductance calcium‐activated potassium channels in enteric neurones of the mouse: pharmacological, molecular and immunochemical evidence for their role in mediating the slow afterhyperpolarization
Authors: Neylon Craig B. , Nurgali Kulmira , Hunne Billie , Robbins Heather L. , Moore Stephen , Chen Mao Xiang , Furness John B. 
Published: September 2004

AbstractCalcium‐activated potassium channels are critically important in modulating neuronal cell excitability. One member of the family, the intermediate‐conductance potassium (IK) channel, is not thought to play a role in neurones because of its predominant expression in non‐excitable cells such as erythrocytes and lymphocytes, in smooth muscle tissues, and its lack of apparent expression in brain. In the present study, we demonstrate that IK channels are localized on specific neurones in the mouse enteric nervous system where they mediate the slow afterhyperpolarization following an action potential. IK channels were localized by immunohistochemistry on intrinsic primary afferent neurones, identified by their characteristic Dogiel type II morphology. The slow afterhyperpolarization recorded from these cells was abolished by the IK channel blocker clotrimazole. RT–PCR and western analysis of extracts from the colon revealed an IK channel transcript and protein identical to the IK channel expressed in other cell types. These results indicate that IK channels are expressed in neurones where they play an important role in modulating firing properties.
Differential gene expression induced by chronic levodopa treatment in the striatum of rats with lesions of the nigrostriatal system
Authors: Ferrario Juan E. , Taravini Irene R. E. , Mourlevat Sophie , Stefano Andrea , Delfino Marina A. , Raisman‐Vozari Rita , Murer M. Gustavo , Ruberg Merle , Gershanik Oscar 
Published: September 2004

AbstractLevodopa, the major treatment for patients with Parkinson's disease, has been shown to induce a variety of compensatory effects, including facilitation of sprouting by dopaminergic neurons, in experimental animals with lesions leading to denervation of the striatum. To better understand the cellular and molecular environment where most of these compensatory changes take place, in particular elements that might contribute to the recovery of dopaminergic innervation, we have constructed a differential expression library enriched in transcripts from the striata of rats with lesions of the medial forebrain bundle treated with levodopa for 6 months. We have used this library to screen an expression array of rat genes representing the major cell functions, and have identified several that are involved in neurotrophic mechanisms and plasticity. We have confirmed the differential expression of selected transcripts by non‐radioactive in situ hybridization, and report that the growth factor pleiotrophin, myelin basic protein and calmodulin are overexpressed in the denervated striatum of levodopa‐treated rats.
Conserved residues within the putative active site of γ‐secretase differentially influence enzyme activity and inhibitor binding
Authors: Wrigley Jonathan D. J. , Nunn Emma J. , Nyabi Omar , Clarke Earl E. , Hunt Peter , Nadin Alan , De Strooper Bart , Shearman Mark S. , Beher Dirk 
Published: September 2004

Abstractγ‐Secretase performs the final processing step in the generation of amyloid‐β (Aβ) peptides, which are believed to be causative for Alzheimer's disease. Presenilins (PS) are required for γ‐secretase activity and the presence of two essential intramembranous aspartates (D257 and D385) has implicated this region as the putative catalytic centre of an aspartyl protease. The presence of several key hydrogen‐bonding residues around the active site of classical aspartyl proteases led us to investigate the role of both the critical aspartates and two nearby conserved hydrogen bond donors in PS1. Generation of cell lines stably overexpressing the D257E, D385E, Y256F and Y389F engineered mutations has enabled us to determine their role in enzyme catalysis and binding of a transition state analogue γ‐secretase inhibitor. Here we report that replacement of either tyrosine residue alters γ‐secretase cleavage specificity, resulting in an increase in the production of the more pathogenic Aβ(42) peptide in both cells and membranous enzyme preparations, without affecting inhibitor binding. In contrast, replacement of either of the aspartate residues precludes inhibitor binding in addition to inactivation of the enzyme. Together, these data further incriminate the region around the intramembranous aspartates as the active site of the enzyme, targeted by transition state analogue inhibitors, and highlight the roles of individual residues.
Cerebral creatine kinase deficiency influences metabolite levels and morphology in the mouse brain: a quantitative in vivo1H and 31P magnetic resonance study
Authors: In‘t Zandt H. J. A. , Renema W. K. J. , Streijger F. , Jost C. , Klomp D. W. J. , Oerlemans F. , Van der Zee C. E. E. M. , Wieringa B. , Heerschap A. 
Published: September 2004

AbstractCreatine kinase (CK)‐catalysed ATP–phosphocreatine (PCr) exchange is considered to play a key role in energy homeostasis of the brain. This study assessed the metabolic and anatomical consequences of partial or complete depletion of this system in transgenic mice without cytosolic B‐CK (B‐CK–/–), mitochondrial ubiquitous CK (UbCKmit–/–), or both isoenzymes (CK –/–), using non‐invasive quantitative magnetic resonance (MR) imaging and spectroscopy. MR imaging revealed an increase in ventricle size in a subset of B‐CK–/– mice, but not in animals with UbCKmit or compound CK mutations. Mice lacking single CK isoenzymes had normal levels of high‐energy metabolites and tissue pH. In the brains of CK double knockouts pH and ATP and Pi levels were also normal, even though PCr had become completely undetectable. Moreover, a 20–30% decrease was observed in the level of total creatine and a similar increase in the level of neuronal N‐acetyl‐aspartate compounds. Although CKs themselves are not evenly distributed throughout the CNS, these alterations were uniform and concordant across different brain regions. Changes in myo‐inositol and glutamate peaks did appear to be mutation type and brain area specific. Our results challenge current models for the biological significance of the PCr–CK energy system and suggest a multifaceted role for creatine in the brain.
Cloning and expression of the mouse histamine H3 receptor: evidence for multiple isoforms
Authors: Rouleau Agnès , Héron Anne , Cochois Véronique , Pillot Catherine , Schwartz Jean‐Charles , Arrang Jean‐Michel 
Published: September 2004

AbstractThe existence of mouse H3‐receptor isoforms was investigated by PCR analysis and cDNA cloning. Splicing mechanisms previously reported in various species are conserved in the mouse. The retention/deletion of a fragment in the third intracellular loop of the mouse receptor leads to the existence of three isoforms designated mH3(445), mH3(413) and mH3(397) according to the length of their deduced amino acid sequence. PCR analysis showed that mouse H3‐receptor isoforms display different expression patterns in the brain. Following expression in Cos‐1 cells, [125I]iodoproxyfan binding indicated similar pharmacological profiles of the mH3(445), mH3(413) and mH3(397) isoforms. The pharmacological profile of the mouse H3 receptor is more similar to the rat receptor than to the human receptor, although some differences were also observed between the mouse and rat receptors. For example, the potency of thioperamide and ciproxifan is slightly higher at the mouse receptor than at the rat receptor but 40–100‐fold higher than at the human receptor. In situ hybridization histochemistry showed that the distribution of H3‐receptor mRNAs in the mouse brain is rather similar to that previously reported in the rat brain. However, the autoradiographic and cellular expression patterns observed in several brain areas such as the thalamus or hippocampus reveal important differences between the two species.
Mechanism of promoter activity of the β‐amyloid precursor protein gene in different cell lines: identification of a specific 30 bp fragment in the proximal promoter region
Authors: Ge Yuan‐Wen , Ghosh Chandramallika , Song Weihong , Maloney Bryan , Lahiri Debomoy K. 
Published: September 2004

AbstractThe amyloid β‐protein (Aβ) deposited in brains of Alzheimer's disease (AD) patients is proteolytically derived from a large Aβ precursor protein (APP). APP gene expression patterns in the AD brain region indicate that abnormalities of gene regulation may be important in AD pathology. To understand the contribution of different cell types to APP gene expression, we studied it at four levels: promoter activity (by reporter gene assay of transfected cells), DNA–nuclear protein interaction (by electrophoretic mobility shift assay), RNA message and protein (by northern and western blotting, respectively). APP mRNA and protein expression levels were greater in neuroblastoma and PC12 cells than in glial or cervix epithelial cells. Relative activity among 12 different promoter regions and within single regions varied according to cell type/cell line. An upstream regulatory region containing a GATA‐1 site is necessary for activity in PC12 and glial cells but not in neuroblastoma cells. DNA–protein interactions were examined in three distal and one proximal promoter elements in nuclear extracts belonging to neuronal and non‐neuronal cells. The proximal promoter region is important for cell line‐specific APP gene expression. Characterization of the APP regulatory region's interaction with cell type‐specific nuclear factor(s) is important to understand tissue‐specific expression of APP seen in AD subjects.
Developmental expression of receptor for advanced glycation end products (RAGE), amphoterin and sulfoglucuronyl (HNK‐1) carbohydrate in mouse cerebellum and their role in neurite outgrowth and cell migration
Authors: Chou Denise K. H. , Zhang Jinghua , Smith Frances I. , McCaffery Peter , Jungalwala Firoze B. 
Published: September 2004

AbstractReceptor for advanced glycation end products (RAGE) has been proposed as a signal transduction receptor to promote neurite outgrowth and cell migration, by its interaction with a neurite outgrowth promoting protein, Amphoterin. Amphoterin has been shown to interact with sulfoglucuronyl carbohydrate (SGC). The developmental expression of RAGE, Amphoterin and SGC was studied in pre‐natal and post‐natal mouse cerebellum to establish their cellular and subcellular localization and function. The amount of RAGE in the cerebellum increased with age. RAGE was expressed pre‐natally in the external germinal layer and post‐natally in the plasma membranes of the granule neurons of the external and internal granule cell layers and in Purkinje cells. Immunocytochemical analysis by high magnification confocal microscopy showed that RAGE was co‐expressed with Amphoterin and SGC in the cell surfaces of granule neurons. This co‐localization of RAGE, Amphoterin, and SGC was confirmed in isolated and cultured granule neurons and in migrating granule neurons in explant cultures. Anti‐RAGE antibodies inhibited neurite outgrowth and cell migration in explant and slice cultures, similar to anti‐Amphoterin and anti‐SGC antibodies shown previously. The results suggest that RAGE could act as a signaling molecule for neurite outgrowth and cell migration by its interaction with Amphoterin and that of Amphoterin with SGC.
Molecular aging of tau: disulfide‐independent aggregation and non‐enzymatic degradation in vitro and in vivo
Authors: Watanabe Atsushi , Hong Won‐Kyoung , Dohmae Naoshi , Takio Koji , Morishima‐Kawashima Maho , Ihara Yasuo 
Published: September 2004

AbstractSmearing from high‐molecular‐mass regions to low‐molecular‐mass regions on western blot is the most striking observation of the tau making up paired helical filaments in brain tissues affected by Alzheimer's disease. Because our previous study showed site‐specific deamidation/isomerization in the smeared tau in vivo, a feature of protein aging, recombinant tau was subjected to prolonged (up to 90 days) in vitro incubation. Carboxymethylated tau at ∼50 kDa gradually disappeared and was converted to dimers and to high‐ and low‐molecular‐mass smearing. In addition, the same site‐specific deamidation/isomerization as previously identified in the smeared tau in vivo emerged. Most importantly, tau was spontaneously degraded, generating fragments that start from bulky residues next to asparaginyl residues. This spontaneous degradation of tau probably represents non‐enzymatic cleavage through the formation of succinimide intermediates. Similar degradation products starting from the bulky residues next to asparaginyl residues were found in the smeared tau in vivo partially purified from the homogenates from Alzheimer's disease brains.
Apoptotic cell death influences the signaling activity of the amyloid precursor protein through ShcA and Grb2 adaptor proteins in neuroblastoma SH‐SY5Y cells
Authors: Venezia Valentina , Russo Claudio , Repetto Emanuela , Salis Serena , Dolcini Virginia , Genova Francesca , Nizzari Mario , Mueller Ulrike , Schettini Gennaro 
Published: September 2004

AbstractThe amyloid precursor protein (APP) is an ubiquitous receptor‐like molecule involved in the pathogenesis of Alzheimer's disease (AD). APP and some of its C‐terminal proteolytic fragments (CTFs) have been shown to be phosphorylated and to interact with cytosolic phosphotyrosine binding (PTB) domain containing proteins involved in cell signaling and vesicular transport. Among others, the interaction between tyrosine‐phosphorylated CTFs and ShcA‐Grb2 adaptors is highly enhanced in AD brain. Here we have identified in SH‐SY5Y neuroblastoma cells an interaction between APP holoprotein and the adaptor Grb2. Upon activation of apoptotic cell death this interaction is rapidly degraded, APP is partially cleaved and the complex APP/Grb2 is replaced by a new complex between CTFs and ShcA that still involves Grb2. The formation of these complexes is regulated by beta‐site APP‐cleaving enzyme 1 and influences the phosphorylation of mitogen‐activated protein kinase p44/42 extracellular signal‐regulated kinase as well as the level of apoptotic death of the cells. These data suggest a dual role in cell signaling for APP and its CTFs in neuroblastoma cells, in a manner similar to that previously reported for other tyrosine kinase receptor, through a tightly regulated coupling with alternative intracellular adaptors to control the signaling of the cell.