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Molecular Aspects (molecular + aspect)
Selected AbstractsNeuroendocrinological and Molecular Aspects of Insect ReproductionJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2004G. Simonet Abstract This review summarizes recent advances and novel concepts in the area of insect reproductive neuroendocrinology. The role of ,classic' hormones, such as ecdysteroids and juvenoids, to control reproduction is well documented in a large variety of insect species. In adult gonads, ecdysteroids appear to induce a cascade of transcription factors, many of which also occur during the larval molting response. Recent molecular and functional data have created opportunities to study an additional level of regulation, that of neuropeptides, growth factors and their respective receptors. As a result, many homologs of factors playing a role in vertebrate reproductive physiology have been discovered in insects. This review highlights several neuropeptides controlling the biosynthesis and release of the ,classic' insect hormones, as well as various peptides and biogenic amines that regulate behavioural aspects of the reproduction process. In addition, hormone metabolizing enzymes and second messenger pathways are discussed with respect to their role in reproductive tissues. Finally, we speculate on future prospects for insect neuroendocrinological research as a consequence of the recent ,Genomics Revolution'. [source] Molecular aspects of diagnostic nucleolar and nuclear envelope changes in prostate cancerJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2004Andrew H. Fischer Abstract Prostate cancer is still diagnosed by pathologists based on subjective assessment of altered cell and tissue structure. The cellular-level structural changes diagnostic of some forms of cancer are known to be induced by cancer genes, but the relation between specific cellular-level structural features and cancer genes has not been explored in the prostate. Two important cell structural changes in prostate cancer,nucleolar enlargement and nuclear envelope (NE) irregularity,are discussed from the perspective that they should also relate to the function of the genes active in prostate cancer. Enlargement of the nucleolus is the key diagnostic feature of high-grade prostatic intraepithelial neoplasia (PIN), an early stage that appears to be the precursor to the majority of invasive prostate cancers. Nucleolar enlargement classically is associated with increased ribosome production, and production of new ribosomes appears essential for cell-cycle progression. Several cancer genes implicated in PIN are known (in other cell types) to augment ribosome production, including c-Myc, p27, retinoblastoma, p53, and growth factors that impact on ERK signaling. However, critical review of the available information suggests that increased ribosome production per se may be insufficient to explain nucleolar enlargement in PIN, and other newer functions of nucleoli may therefore need to be invoked. NE irregularity develops later in the clonal evolution of some prostate cancers, and it has adverse prognostic significance. Nuclear irregularity has recently been shown to develop dynamically during interphase following oncogene expression, without a requirement for post-mitotic NE reassembly. NE irregularity characteristic of some aggressive prostate cancers could reflect cytoskeletal forces exerted on the NE during active cell locomotion. NE irregularity could also promote chromosomal instability because it leads to chromosomal asymmetry in metaphase. Finally, NE irregularity could impact replication competence, transcriptional programming and nuclear pore function. © 2003 Wiley-Liss, Inc. [source] Molecular aspects of healing in stabilized and non-stabilized fracturesJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 1 2001A. X. Le Bone formation is a continuous process that is initiated during fetal development and persists in adults in the form of bone regeneration and remodeling. These latter two aspects of bone formation are clearly influenced by the mechanical environment. In this study we tested the hypothesis that alterations in the mechanical environment regulate the program of mesenchymal cell differentiation, and thus the formation of a cartilage or bony callus, at the site of injury. As a first step in testing this hypothesis we produced stabilized and non-stabilized tibial fractures in a mouse model, then used molecular and cellular methods to examine the stage of healing. Using the "molecular map" of the fracture callus, we divided our analyzes into three phases of fracture healing: the inflammatory or initial phase of healing, the soft callus or intermediate stage, and the hard callus stage. Our results show that indian hedgehog(ihh), which regulates aspects of chondrocyte maturation during fetal and early postnatal skeletogenesis, was expressed earlier in an non-stabilized fracture callus as compared to a stabilized callus, ihh persisted in the non-stabilized fracture whereas its expression was down-regulated in the stabilized bone. IHH exerts its effects on chondrocyte maturation through a feedback loop that may involve bone morphogenetic protein 6 [bmp6; (S. Pathi, J.B. Rutenberg, R.L. Johnson, A. Vortkamp, Developmental Biology 209 (1999) 239,253)] and the transcription factor gli3, bmp6 and gli3 were re-induced in domain adjacent to the ihh -positive cells during the soft and hard callus stages of healing. Thus, stabilizing the fracture, which circumvents or decreases the cartilaginous phase of bone repair, correlates with a decrease in ihh signaling in the fracture callus. Collectively, our results illustrate that the ihh signaling pathway participates in fracture repair, and that the mechanical environment affects the temporal induction of ihh, bmp6 and gli3. These data support the hypothesis that mechanical influences affect mesenchymal cell differentiation to bone. © 2001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Molecular aspects on the interaction of protoberberine, benzophenanthridine, and aristolochia group of alkaloids with nucleic acid structures and biological perspectivesMEDICINAL RESEARCH REVIEWS, Issue 5 2007Motilal Maiti Abstract Alkaloids occupy an important position in chemistry and pharmacology. Among the various alkaloids, berberine and coralyne of the protoberberine group, sanguinarine of the benzophenanthridine group, and aristololactam-,- d -glucoside of the aristolochia group have potential to form molecular complexes with nucleic acid structures and have attracted recent attention for their prospective clinical and pharmacological utility. This review highlights (i) the physicochemical properties of these alkaloids under various environmental conditions, (ii) the structure and functional aspects of various forms of deoxyribonucleic acid (DNA) (B-form, Z-form, HL -form, protonated form, and triple helical form) and ribonucleic acid (RNA) (A-form, protonated form, and triple helical form), and (iii) the interaction of these alkaloids with various polymorphic DNA and RNA structures reported by several research groups employing various analytical techniques like absorbance, fluorescence, circular dichroism, and NMR spectroscopy; electrospray ionization mass spectrometry, thermal melting, viscosity, and DNase footprinting as well as molecular modeling and thermodynamic studies to provide detailed binding mechanism at the molecular level for structure,activity relationship. Nucleic acids binding properties of these alkaloids are interpreted in relation to their biological activity. © 2006 Wiley Periodicals, Inc. Med Res Rev, 27, No. 5, 649,695, 2007 [source] Molecular Evolution of the S Locus Controlling Mating in the BrassicaceaePLANT BIOLOGY, Issue 2 2004I. Fobis-Loisy Abstract: Flowering plants possess self-incompatibility (SI) mechanisms that promote outbreeding and thereby increase their genetic diversity. In the self-incompatible Brassicaceae, recognition and rejection of self-pollen is based on a receptor-ligand interaction between male and female SI determinants. A transmembrane receptor kinase (S locus Receptor Kinase, SRK) determines the SI specificity in stigmatic cells, whereas a pollen coat-localized ligand (S locus Cysteine-Rich, SCR) determines the SI specificity in pollen. During recent years, major advances have been made in the understanding of the molecular basis of self-pollen recognition by stigmatic cells. In this review, we will focus on evolutionary aspects of the SI system in Brassicaceae. We will describe how the study of the molecular aspect of SI, not only in the historical Brassica model but also in Arabidopsis species, has contributed to highlight certain aspects of evolution of SI in the Brassicaceae. [source] Growth and differentiation of the developing limb bud from the perspective of chondrogenesisDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 6 2007Hirohito Shimizu Limb skeletal elements develop from a cartilage template, which is formed by the process termed chondrogenesis. This process is crucial in determining the shape and size of definitive bones in vertebrates. During chondrogenesis, aggregated mesenchymal cells undergo a highly organized process of proliferation and maturation along with secretion of extracellular matrix followed by programmed cell death and replacement by bone. The molecular mechanisms underlying this sophisticated process have been extensively studied. It has been demonstrated that several transcription factors such as Sox genes and Runx genes are indispensable for the major steps in chondrogenesis. Additionally, a number of signaling molecules including Bmps, Fgfs and Ihh/PTHrP are known to regulate chondrogenesis through highly coordinated interactions. This review is meant to provide an overview of the current knowledge of chondrogenesis with particular emphasis on the cellular and molecular aspects. [source] Comparative mechanisms of zearalenone and ochratoxin A toxicities on cultured HepG2 cells: Is oxidative stress a common process?ENVIRONMENTAL TOXICOLOGY, Issue 6 2009Emna El Golli Bennour Abstract Zearalenone (ZEN) and Ochratoxin A (OTA) are structurally diverse fungal metabolites that can contaminate feed and foodstuff and can cause serious health problems for animals as well as for humans. In this study, we get further insight of the molecular aspects of ZEN and OTA toxicities in cultured human HepG2 hepatocytes. In this context, we have monitored the effects of ZEN and OTA on (i) cell viability, (ii) heat shock protein (Hsp) 70 and Hsp 27 gene expressions as a parameter of protective and adaptive response, (iii) oxidative damage, and (iv) cell death pathways. Our results clearly showed that both ZEN and OTA inhibit cell proliferation. For ZEN, a significant induction of Hsp 70 and Hsp 27 was observed. In the same conditions, ZEN generated an important amount of reactive oxygen species (ROS). Antioxidant supplements restored the major part of cell mortality induced by ZEN. However, OTA treatment downregulated Hsp 70 and Hsp 27 protein and mRNA levels and did not induce ROS generation. Antioxidant supplements did not have a significant effect on OTA-induced cell mortality. Using another cell system (Vero monkey kidney cells), we demonstrated that OTA downregulates three members of HSP 70 family: Hsp 70, Hsp 75, and Hsp 78. Our findings showed that oxidative damage seemed to be the predominant toxic effect for ZEN, while OTA toxicity seemed to be rather because of the absence of Hsps protective response. Furthermore, the two mycotoxins induced an apoptotic cell death. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2009. [source] Genetic and molecular aspects of Alzheimer's disease shed light on new mechanisms of transcriptional regulationGENES, BRAIN AND BEHAVIOR, Issue 3 2005P. Marambaud Rapid advances made in biological research aimed at understanding the molecular basis of the pathogenesis of Alzheimer's disease have led to the characterization of a novel catalytic activity termed ,-secretase. First described for its ,-amyloid-producing function, ,-secretase is now actively studied for its role in a novel signal transduction paradigm, which implicates cell-surface receptor proteolysis and direct surface-to-nucleus signal transduction. ,-Secretase targets numerous type I protein receptors involved in diverse functions ranging from normal development to neurodegeneration. In this Review we discuss how the study of the genetic and molecular aspects of Alzheimer's disease has revealed a dual role of ,-secretase in transcriptional regulation and in the pathogenesis of familial Alzheimer's disease. [source] Access to immunology through the Gene OntologyIMMUNOLOGY, Issue 2 2008Ruth C. Lovering Summary The Gene Ontology (GO) is widely recognized as the premier tool for the organization and functional annotation of molecular aspects of cellular systems. However, for many immunologists the use of GO is a very foreign concept. Indeed, as a controlled vocabulary, GO can almost be considered a new language, and it can be difficult to appreciate the use and value of this approach for understanding the immune system. This review reflects on the application of GO to the field of immunology and explains the process of GO annotation. Finally, this review hopes to inspire immunologists to invest time and energy in improving both the content of the GO and the quality of GO annotations associated with genes of immunological interest. [source] Multiple strategies for O2 transport: from simplicity to complexityIUBMB LIFE, Issue 8-9 2007Paolo Ascenzi Abstract O2carriers (extracellular and intracellular as well as monomeric and multimeric) have evolved over the last billion of years, displaying iron and copper reactive centers; very different O2carriers may co-exist in the same organism. Circulating O2carriers, faced to the external environment, are responsible for maintaining an adequate delivery of O2to tissues and organs almost independently of the environmental O2partial pressure. Then, intracellular globins facilitate O2transfer to mitochondria sustaining cellular respiration. Here, molecular aspects of multiple strategies evolved for O2transport and delivery are examined, from the simplest myoglobin to the most complex giant O2carriers and the red blood cell, mostly focusing on the aspects which have been mainly addressed by the so called 'Rome Group'. [source] Oncogenic KRAS provides a uniquely powerful and variable oncogenic contribution among RAS family members in the colonic epitheliumJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2007Jeffrey W. Keller Activating mutations of the RAS family of small GTPases are among the most common genetic events in human tumorigenesis. Constitutive activation of the three canonical family members, KRAS, NRAS, and HRAS segregate strongly by tissue type. Of these, KRAS mutations predominate in human tumors, including those arising from the colon and lung. We sought to compare the oncogenic contributions of different RAS isoforms in a comparable genetic setting and to explore downstream molecular changes that may explain the apparent differential oncogenic effects of the various RAS family members. We utilized colorectal cancer cell lines characterized by oncogenic KRAS in parallel with isogenically derived lines in which the mutant allele has been disrupted. We additionally attempted to reconstitute the isogenic derivatives with oncogenic forms of other RAS family members and analyze them in parallel. Pairwise analysis of HCT 116 and DLD-1 cell lines as well as their isogenic derivatives reveals distinct K-RASG13D signatures despite the genetic similarities of these cell lines. In DLD-1, for example, oncogenic K-RAS enhances the motility of these cells by downregulation of Rap1 activity, yet is not associated with increased ERK1/2 phosphorylation. In HCT 116, however, ERK1/2 phosphorylation is elevated relative to the isogenic derivative, but Rap1 activity is unchanged. K-RAS is uniquely oncogenic in the colonic epithelium, though the molecular aspects of its oncogenic contribution are not necessarily conserved across cell lines. We therefore conclude that the oncogenic contribution of K-RAS is a function of its multifaceted functionality and is highly context-dependent. J. Cell. Physiol. 210: 740,749, 2007. © 2006 Wiley-Liss, Inc. [source] WHO/EORTC classification of cutaneous lymphomas 2005: histological and molecular aspectsJOURNAL OF CUTANEOUS PATHOLOGY, Issue 10 2005Günter Burg It reflects the unique features of lymphoproliferative diseases of the skin, and at the same time it is as compatible as possible with the concepts underlying the WHO classification for nodal lymphomas and the EORTC classification of cutaneous lymphomas. This article reviews the histological, phenotypical, and molecular genetic features of the various nosological entities included in this new classification. These findings always have to be interpreted in the context of the clinical features and biologic behavior. Aim:, To review the histological, phenotypical and molecular genetic features of the various nosological entities of the new WHO/EORTC classification for cutaneous lymphomas. Methods:, Extensive review of the literature cited in Medline and own data of the authors. Results:, The WHO/EORTC classification of cutaneous lymphomas comprises mature T-cell and NK-cell neoplasms, mature B-cell neoplasms and immature hematopoietic malignancies. It reflects the unique features of primary cutaneous lymphoproliferative diseases. Conclusion:, This classification is as much as possible compatible with the concept of the WHO classification for nodal lymphomas and the EORTC classification of cutaneous lymphomas. The histological, phenotypical and molecular genetic features always have to be interpreted in the context of the clinical features and biologic behavior. [source] Novel alternatively spliced endoplasmic reticulum retention signal in the cytoplasmic loop of Proteolipid Protein-1JOURNAL OF NEUROSCIENCE RESEARCH, Issue 3 2007Cherie Southwood Abstract Increased awareness about the importance of protein folding and trafficking to the etiology of gain-of-function diseases has driven extensive efforts to understand the cell and molecular biology underlying the life cycle of normal secretory pathway proteins and the detrimental effects of abnormal proteins. In this regard, the quality-control machinery in the endoplasmic reticulum (ER) has emerged as a major mechanism by which cells ensure that secreted and transmembrane proteins either adopt stable secondary, tertiary, and quaternary structures or are retained in the ER and degraded. Here we examine cellular and molecular aspects of ER retention in transfected fibroblasts expressing missense mutations in the Proteolipid Protein-1 (PLP1) gene that cause mild or severe forms of neurodegenerative disease in humans. Mild mutations cause protein retention in the ER that is partially dependent on the presence of a cytoplasmically exposed heptapeptide, KGRGSRG. In contrast, retention associated with severe mutations occurs independently of this peptide. Accordingly, the function of this novel heptapeptide has a significant impact on pathogenesis and provides new insight into the functions of the two splice isoforms encoded by the PLP1 gene, PLP1 and DM-20. © 2006 Wiley-Liss, Inc. [source] Nuclear receptors and drug disposition gene regulationJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 6 2005Rommel G. Tirona Abstract In this minireview, the role of various nuclear receptors and transcription factors in the expression of drug disposition genes is summarized. Specifically, the molecular aspects and functional impact of the aryl hydrocarbon receptor (AhR), nuclear factor-E2 p45-related factor 2 (Nrf2), hepatocyte nuclear factor 1, (HNF1,), constitutive androstane receptor (LAR), pregnane X receptor (PXR), farnesoid X receptor (FXR), peroxisome proliferator-activated receptor , (PPAR,), hepatocyte nuclear factor 4, (HNF4,), vitamin D receptor (VDR), liver receptor homolog 1 (LRH1), liver X receptor (LXR,), small heterodimer partner-1 (SHP-1), and glucocorticoid receptor (GR) on gene expression are detailed. Finally, we discuss some current topics and themes in nuclear receptor-mediated regulation of drug metabolizing enzymes and drug transporters. © 2005 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 94:1169,1186, 2005 [source] Combined BubR1 protein down-regulation and RASSF1A hypermethylation in Wilms tumors with diverse cytogenetic changesMOLECULAR CARCINOGENESIS, Issue 9 2008Masayuki Haruta Abstract BUB1B and RASSF1A genes play specific roles in the mitotic checkpoint, and their defects may cause chromosome instability or aneuploidy in mouse fibroblasts and human cancer cell lines; however, few studies have reported a correlation between defects in these genes and chromosome changes in human tumor samples. We examined chromosome abnormalities in 25 Wilms tumors by metaphase comparative genomic hybridization, and classified them into 14 hyperdiploid (50,,,chromosomes), 2 near-or-pseudodiploid, and 9 diploid tumors. We also examined various molecular aspects of BUB1B and RASSF1A, and evaluated the relationship between chromosome changes and the status of both genes. No tumors showed BUB1B mutation. BubR1 protein (BUB1B gene product) expression was undetectable or decreased in five of six hyperdiploid or near-or-pseudodiploid tumors and increased in four of five diploid tumors, whereas all seven tumors examined showed BUB1B mRNA expression irrespective of their chromosome pattern. Furthermore, while complete promoter methylation of RASSF1A was found in 13 of 16 hyperdiploid or near-or-pseudodiploid tumors, unmethylated RASSF1A was found in 5 of 9 diploid tumors. Partial RASSF1A methylation was found in three hyperdiploid or near-or-pseudodiploid tumors and in four diploid tumors. Thus, BubR1 protein expression decreased, and the promoter region of RASSF1A was completely methylated in the great majority of hyperdiploid or near-or-pseudodiploid tumors, BubR1 protein expression increased and RASSF1A was unmethylated in the majority of diploid tumors. These findings suggest that the combined BubR1 protein down-regulation and RASSF1A hypermethylation might be implicated in the formation of chromosomal changes found in Wilms tumors. © 2008 Wiley-Liss, Inc. [source] Tobacco blue mould disease caused by Peronospora hyoscyami f. sp. tabacinaMOLECULAR PLANT PATHOLOGY, Issue 1 2010ORLANDO BORRÁS-HIDALGO SUMMARY Blue mould [Peronospora hyoscyami f. sp. tabacina (Adam) Skalicky 1964] is one of the most important foliar diseases of tobacco that causes significant losses in the Americas, south-eastern Europe and the Middle East. This review summarizes the current knowledge of the mechanisms employed by this oomycete pathogen to colonize its host, with emphasis on molecular aspects of pathogenicity. In addition, key biochemical and molecular mechanisms involved in tobacco resistance to blue mould are discussed. Taxonomy: Kingdom: Chromista (Straminipila); Phylum: Heterokontophyta; Class: Oomycete; Order: Peronosporales; Family: Peronosporaceae; Genus: Peronospora; Species: Peronospora hyoscyami f. sp. tabacina. Disease symptoms: The pathogen typically causes localized lesions on tobacco leaves that appear as single, or groups of, yellow spots that often coalesce to form light-brown necrotic areas. Some of the leaves exhibit grey to bluish downy mould on their lower surfaces. Diseased leaves can become twisted, such that the lower surfaces turn upwards. In such cases, the bluish colour of the diseased plants becomes quite conspicuous, especially under moist conditions when sporulation is abundant. Hence the name of the disease: tobacco blue mould. Infection process: The pathogen develops haustoria within plant cells that are thought to establish the transfer of nutrients from the host cell, and may also act in the delivery of effector proteins during infection. Resistance: Several defence responses have been reported to occur in the Nicotiana tabacum,P. hyoscyami f. sp. tabacina interaction. These include the induction of pathogenesis-related genes, and a correlated increase in the activities of typical pathogenesis-related proteins, such as peroxidases, chitinases, ,-1,3-glucanases and lipoxygenases. Systemic acquired resistance is one of the best characterized tobacco defence responses activated on pathogen infection. [source] Physiology and molecular aspects of Verticillium wilt diseases caused by V. dahliae and V. albo-atrumMOLECULAR PLANT PATHOLOGY, Issue 2 2006EMILIE F. FRADIN SUMMARY Introduction:,Verticillium spp. are soil-borne plant pathogens responsible for Verticillium wilt diseases in temperate and subtropical regions; collectively they affect over 200 hosts, including many economically important crops. There are currently no fungicides available to cure plants once they are infected. Taxonomy:, Kingdom: Fungi, phylum: Ascomycota, subphylum, Pezizomycotina, class: Sordariomycetes, order: Phyllachorales, genus: Verticillium. Host range and disease symptoms:, Over 200 mainly dicotyledonous species including herbaceous annuals, perennials and woody species are host to Verticillium diseases. As Verticillium symptoms can vary between hosts, there are no unique symptoms that belong to all plants infected by this fungus. Disease symptoms may comprise wilting, chlorosis, stunting, necrosis and vein clearing. Brown vascular discoloration may be observed in stem tissue cross-sections. Pathogenicity:,Verticillium spp. have been reported to produce cell-wall-degrading enzymes and phytotoxins that all have been implicated in symptom development. Nevertheless, evidence for a crucial role of toxins in pathogenicity is inconsistent and therefore not generally accepted. Microsclerotia and melanized mycelium play an important role in the disease cycle as they are a major inoculum source and are the primary long-term survival structures. Resistance:, Different defence responses in the prevascular and the vascular stage of Verticillium wilt diseases determine resistance. Although resistance physiology is well established, the molecular processes underlying this physiology remain largely unknown. Resistance against Verticillium largely depends on the isolation of the fungus in contained parts of the xylem tissues followed by subsequent elimination of the fungus. Although genetic resistance has been described in several plant species, only one resistance locus against Verticillium has been cloned to date. Useful website:,http://cbr-rbc.nrc-cnrc.gc.ca/services/cogeme/ [source] Claviceps purpurea: molecular aspects of a unique pathogenic lifestyleMOLECULAR PLANT PATHOLOGY, Issue 5 2004PAUL TUDZYNSKI SUMMARY Claviceps purpurea is a ubiquitous pathogen of cereals and grasses, causing Ergot disease, which results in substitution of grains by sclerotia. These overwintering structures contain ergot-alkaloids, which can cause severe intoxication in mammals. C. purpurea is an interesting model system for the study of host,pathogen interaction. It displays strict organ specificity, attacking exclusively young grass ovaries. It is optimally adapted to this special niche of infection, probably by mimicry of pollen tubes: there are no resistance genes known, and no effective resistance reactions can be detected in the early steps of infection. In this early phase of host tissue colonization the fungus shows directed, almost unbranched growth towards the base of the ovary. Thus, C. purpurea represents one of the few systems in which directed growth in filamentous fungi can be studied. Finally, the fungus behaves as a true biotroph in planta, although it can be easily grown in axenic culture. We describe here the tools available to study this interesting pathogen, report on recent molecular investigations concerning the role of cell-wall-degrading enzymes and of reactive oxygen species in this specialized interaction, and present an update of the signalling cascades involved in early events of pathogenesis. [source] Bipolaris sorokiniana, a cereal pathogen of global concern: cytological and molecular approaches towards better control,MOLECULAR PLANT PATHOLOGY, Issue 4 2002Jagdish Kumar Summary Bipolaris sorokiniana (teleomorph Cochliobolus sativus ) is the causal agent of common root rot, leaf spot disease, seedling blight, head blight, and black point of wheat and barley. The fungus is one of the most serious foliar disease constraints for both crops in warmer growing areas and causes significant yield losses. High temperature and high relative humidity favour the outbreak of the disease, in particular in South Asia's intensive ,irrigated wheat,rice' production systems. In this article, we review the taxonomy and worldwide distribution, as well as strategies to counteract the disease as an emerging threat to cereal production systems. We also review the current understanding of the cytological and molecular aspects of the interaction of the fungus with its cereal hosts, which makes B. sorokiniana a model organism for studying plant defence responses to hemibiotrophic pathogens. The contrasting roles of cell death and H 2O2 generation in plant defence during biotrophic and necrotrophic fungal growth phases are discussed. [source] Clinical and genetic aspects of distal myopathiesMUSCLE AND NERVE, Issue 11 2001David S. Saperstein MD Abstract Although most muscle disorders produce proximal weakness, some myopathies may manifest predominantly or exclusively distal weakness. Although several congenital, inflammatory, or metabolic myopathies may produce mainly distal weakness, there are several distinct entities, typically referred to as distal myopathies. Most of these are inherited conditions. The distal myopathies are rare, but characteristic clinical and histological features aid in their identification. Advances in molecular genetics have led to the identification of the gene lesions responsible for several of these entities and have also expanded our understanding of the genetic relationships of distal myopathies to other inherited disorders of muscle. This review summarizes current knowledge of the clinical and molecular aspects of the distal myopathies. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 1440,1450, 2001 [source] Cerebral amyloid angiopathy: An overviewNEUROPATHOLOGY, Issue 1 2000Masahito Yamada Cerebral amyloid angiopathy (CAA) is characterized by amyloid deposition in cortical and leptomeningeal vessels. Several cerebrovascular amyloid proteins (amyloid ,-protein (A,), cystatin C (ACys), prion protein (AScr), transthyretin (ATTR), gelsolin (AGel), and ABri (or A-WD)) have been identified, leading to the classification of several types of CAA. Sporadic CAA of A, type is commonly found in elderly individuals and patients with Alzheimer's disease. Cerebral amyloid angiopathy is an important cause of cerebrovascular disorders including lobar cerebral hemorrhage, leukoencephalopathy, and small cortical hemorrhage and infarction. We review the clinicopathological and molecular aspects of CAA and discuss the pathogenesis of CAA with future perspectives. [source] Enhanced expression of genes for ACC synthase, ACC oxidase, and NAC protein during high-temperature-induced necrosis of young inflorescences of CymbidiumPHYSIOLOGIA PLANTARUM, Issue 3 2006Satoru Mita Growing Cymbidium under high-temperature conditions (25,30°C) results in the necrosis of young inflorescences. An increase in the evolution of ethylene was correlated with the necrosis. To study the molecular aspects of high-temperature-induced necrosis of Cymbidium floral buds, we isolated complementary DNA (cDNA) clones for proteins that are likely to be involved in the biosynthesis of ethylene during high-temperature-induced necrosis of young inflorescences, namely, 1-aminocyclopropane-1-carboxylic acid (ACC) synthase (CyACS1) and ACC oxidase (CyACO1). In addition, a cDNA (CyNAC1) encoding an NAC protein whose expression is modulated during high-temperature treatment was isolated by differential display. High levels of expression of CyACS1, CyACO1 and CyNAC1 were observed in the necrotic inflorescences of wild-type Cymbidium at high temperatures. Bud necrosis was not observed in the mericlone mutant (nhn, non,high-temperature-induced necrosis) of Cymbidium. Ethylene evolution was lower in nhn than in wild-type, but application of exogenous ACC or ethephon to the young inflorescences of nhn restored the high-temperature necrosis response. Expression of CyACS1, CyACO1 and CyNAC1 did not increase with high-temperature treatment in the nhn mutant. Expression levels of CyACS1, CyACO1 and CyNAC1 in necrotic inflorescences of nhn treated with 5.0 mM ACC were much lower than in necrotic inflorescences of wild-type at high temperatures, but CyACS1 and CyNAC1 were stimulated by ACC treatment. These results suggest that ethylene is involved in high-temperature necrosis of young inflorescences of Cymbidium and that an NAC protein may be involved in the regulatory mechanisms of genes that are regulated during necrosis. [source] Insights into the cellular mechanisms of desiccation tolerance among angiosperm resurrection plant speciesPLANT CELL & ENVIRONMENT, Issue 11 2004M. VICRÉ ABSTRACT Water is a major limiting factor in growth and reproduction in plants. The ability of tissues to survive desiccation is commonly found in seeds or pollen but rarely present in vegetative tissues. Resurrection plants are remarkable as they can tolerate almost complete water loss from their vegetative tissues such as leaves and roots. Metabolism is shut down as they dehydrate and the plants become apparently lifeless. Upon rehydration these plants recover full metabolic competence and ,resurrect'. In order to cope with desiccation, resurrection plants have to overcome a number of stresses as water is lost from the cells, among them oxidative stress, destabilization or loss of membrane integrity and mechanical stress. This review will mainly focus on the effect of dehydration in angiosperm resurrection plants and some of the strategies developed by these plants to tolerate desiccation. Resurrection plants are important experimental models and understanding the physiological and molecular aspects of their desiccation tolerance is of great interest for developing drought-tolerant crop species adapted to semi-arid areas. [source] Imprinted genes and human disease,AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 3 2010Rosanna Weksberg Abstract This issue of Seminars of Medical Genetics features a series of articles on human disorders caused by the dysregulation of imprinted genes. At the outset, there is a review of the general mechanisms by which genomic imprinting is normally regulated followed by an exploration of the clinical and molecular aspects of human imprinting disorders. As we enter an era of bioinformatics and genome-wide analyses with increasing access to high density microarrays and next generation sequencing, it is becoming apparent that the concept of a single mutation or epimutation leading to a disease is outdated. The role of the clinician will become increasingly important, in concert with these molecular advances, in terms of evaluating phenotypic variation to further our understanding of imprinting disorders. Such investigations will benefit children and families as we become better able to define recurrence risk, predict phenotype, and tailor medical management. © 2010 Wiley-Liss, Inc. [source] Carotenoids and retinoids as suppressors on adipocyte differentiation via nuclear receptorsBIOFACTORS, Issue 1-4 2000Teruo Kawada Abstract The adipocyte differentiation program is regulated by the sequential expression of transcriptional activators, mainly peroxisome proliferator activated receptor (PPAR) families. In the present study, we have decided to systematically examine the effects of vitamin A and its precursors, carotenoids and retinoids, on terminal differentiation from preadipocytes to adipocytes on the cellular and molecular aspects. The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators. RAR,, RAR,, RXR,, and RXR, mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. The autoregulated amplification of RAR, mRNA was observed by these own ligands in 3T3-L1 cells. And, RA inhibited PPAR,2 expression more effectively and caused concomitantly a greater inhibition of adipocyte differentiation. These results suggest that the inhibitory action of adipocyte differentiation by carotenoids and retinoids are exhibited through the RAR up-regulation and the suppression of PPAR,2. The nature of the cross talk of vitamin A actions between the RARs, RXRs and PPARs via co-activator in adipose tissue will likely prove to be important for understanding the process of adipogenesis. [source] Regulation of cell death during infection by the severe acute respiratory syndrome coronavirus and other coronavirusesCELLULAR MICROBIOLOGY, Issue 11 2007Yee-Joo Tan Summary Both apoptosis and necrosis have been observed in cells infected by various coronaviruses, suggesting that the regulation of cell death is important for viral replication and/or pathogenesis. Expeditious research on the severe acute respiratory syndrome (SARS) coronavirus, one of the latest discovered coronaviruses that infect humans, has provided valuable insights into the molecular aspects of cell-death regulation during infection. Apoptosis was observed in vitro, while both apoptosis and necrosis were observed in tissues obtained from SARS patients. Viral proteins that can regulate apoptosis have been identified, and many of these also have the abilities to interfere with cellular functions. Occurrence of cell death in host cells during infection by other coronaviruses, such as the mouse hepatitis virus and transmissible porcine gastroenteritis virus, has also being extensively studied. The diverse cellular responses to infection revealed the complex manner by which coronaviruses affect cellular homeostasis and modulate cell death. As a result of the complex interplay between virus and host, infection of different cell types by the same virus does not necessarily activate the same cell-death pathway. Continuing research will lead to a better understanding of the regulation of cell death during viral infection and the identification of novel antiviral targets. [source] 2215: Animal models of herpetic retinitisACTA OPHTHALMOLOGICA, Issue 2010M LABETOULLE The Herpes simplex virus (HSV) is characterized its ability to replicate in the nervous system, before inducing a latent infection with potential reactivation. Most frequent ocular complications of recurrent HSV infection are keratitis and conjunctivitis. Less frequently, the iris and the ciliary body may also be involved (anterior uveitis). The most severe HSV ocular infection is retinitis, a rare but potentially blinding disease, due to frequent bilateral involvement. Studies on human post-mortem tissues showed that HSV is widely distributed in the population, with a preferential location within the trigeminal ganglions (innervating the cornea), but also in the superior cervical ganglions (innervating the iris) or in brain/medullar tissues (innervating the retina). Animal models have been developed to understand the pathogenic processes that lead to this rare but devastating retinal disease. Since human is the only natural host of HSV, it is difficult to obtain a perfect animal model that perfectly mimics the disease. Several animal models, based on different inoculation procedures, are thus necessary to circumscribe the anatomical, cellular and molecular aspects that lead to retinal infection. Finally, HSV retinitis appears as a clinical condition that is highly constrained by the relationships between the strain of the virus and the immune response of the host. [source] Clinical and molecular aspects of aniridiaCLINICAL GENETICS, Issue 5 2010H Kokotas Kokotas H, Petersen MB. Clinical and molecular aspects of aniridia. Aniridia is a severe, congenital ocular malformation inherited in an autosomal-dominant fashion with high penetrance and variable expression. Eye morphogenesis in humans involves a molecular genetic cascade in which a number of developmental genes interact in a highly organized process during the embryonic period to produce functional ocular structures. Among these genes, paired box gene 6 (PAX6) has an essential role as it encodes a phylogenetically conserved transcription factor almost universally employed for eye formation in animals with bilateral symmetry, despite widely different embryological origins. To direct eye development, PAX6 regulates the tissue-specific expression of diverse molecules, hormones, and structural proteins. In humans, PAX6 is located in chromosome 11p13, and its mutations lead to a variety of hereditary ocular malformations of the anterior and posterior segment, among which aniridia and most probably foveal hypoplasia are the major signs. Aniridia occurs due to decreased dosage of the PAX6 gene and exists in both sporadic and familial forms. The mutations are scattered throughout the gene and the vast majority of those reported so far are nonsense mutations, frameshift mutations, or splicing errors that are predicted to cause pre-mature truncation of the PAX6 protein, causing haploinsufficiency. Here we review the data regarding the mechanisms and the mutations that relate to aniridia. [source] | |||||||||||||||||||||||||||||||