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Conserved Mechanism (conserved + mechanism)
Selected AbstractsTonotopic gradients of Eph family proteins in the chick nucleus laminaris during synaptogenesisDEVELOPMENTAL NEUROBIOLOGY, Issue 1 2004Abigail L. Person Abstract Topographically precise projections are established early in neural development. One such topographically organized network is the auditory brainstem. In the chick, the auditory nerve transmits auditory information from the cochlea to nucleus magnocellularis (NM). NM in turn innervates nucleus laminaris (NL) bilaterally. These projections preserve the tonotopy established at the level of the cochlea. We have begun to examine the expression of Eph family proteins during the formation of these connections. Optical density measurements were used to describe gradients of Eph proteins along the tonotopic axis of NL in the neuropil, the somata, and the NM axons innervating NL at embryonic day 10, when synaptic connections from NM to NL are established. At E10,11, NL dorsal neuropil expresses EphA4 at a higher concentration in regions encoding high frequency sounds, decreasing in concentration monotonically toward the low frequency (caudolateral) end. In the somata, both EphA4 and ephrin-B2 are concentrated at the high frequency end of the nucleus. These tonotopic gradients disappear between E13 and E15, and expression of these molecules is completely downregulated by hatching. The E10,11 patterns run counter to an apparent gradient in dendrite density, as indicated by microtubule associated protein 2 (MAP2) immunolabeling. Finally, ephrin-B2 is also expressed in a gradient in tissue ventral to the NL neuropil. Our findings thus suggest a possible conserved mechanism for establishing topographic projections in diverse sensory systems. These results of this study provide a basis for the functional examination of the role of Eph proteins in the formation of tonotopic maps in the brainstem. © 2004 Wiley Periodicals, Inc. J Neurobiol 60: 28,39, 2004 [source] Natural transformation of Vibrio fischeri requires tfoX and tfoYENVIRONMENTAL MICROBIOLOGY, Issue 8 2010Amber Pollack-Berti Summary Recent evidence has indicated that natural genetic transformation occurs in Vibrio cholerae, and that it requires both induction by chitin oligosaccharides, like chitohexaose, and expression of a putative regulatory gene designated tfoX. Using sequence and phylogenetic analyses we have found two tfoX paralogues in all sequenced genomes of the genus Vibrio. Like V. cholerae, when grown in chitohexaose, cells of V. fischeri are able to take up and incorporate exogenous DNA. Chitohexaose-independent transformation by V. fischeri was observed when tfoX was present in multicopy. The second tfoX paralogue, designated tfoY, is also required for efficient transformation in V. fischeri, but is not functionally identical to tfoX. Natural transformation of V. fischeri facilitates rapid transfer of mutations across strains, and provides a highly useful tool for experimental genetic manipulation in this species. The presence of chitin-induced competence in several vibrios highlights the potential for a conserved mechanism of genetic exchange across this family of environmentally important marine bacteria. [source] An evolutionary transition of vasa regulation in echinodermsEVOLUTION AND DEVELOPMENT, Issue 5 2009Celina E. Juliano SUMMARY Vasa, a DEAD box helicase, is a germline marker that may also function in multipotent cells. In the embryo of the sea urchin Strongylocentrotus purpuratus, Vasa protein is posttranscriptionally enriched in the small micromere lineage, which results from two asymmetric cleavage divisions early in development. The cells of this lineage are subsequently set aside during embryogenesis for use in constructing the adult rudiment. Although this mode of indirect development is prevalent among echinoderms, early asymmetric cleavage divisions are a derived feature in this phylum. The goal of this study is to explore how vasa is regulated in key members of the phylum with respect to the evolution of the micromere and small micromere lineages. We find that although striking similarities exist between the vasa mRNA expression patterns of several sea urchins and sea stars, the time frame of enriched protein expression differs significantly. These results suggest that a conserved mechanism of vasa regulation was shifted earlier in sea urchin embryogenesis with the derivation of micromeres. These data also shed light on the phenotype of a sea urchin embryo upon removal of the Vasa-positive micromeres, which appears to revert to a basal mechanism used by extant sea stars and pencil urchins to regulate Vasa protein accumulation. Furthermore, in all echinoderms tested here, Vasa protein and/or message is enriched in the larval coelomic pouches, the site of adult rudiment formation, thus suggesting a conserved role for vasa in undifferentiated multipotent cells set aside during embryogenesis for use in juvenile development. [source] Calorie restriction reduces rDNA recombination independently of rDNA silencingAGING CELL, Issue 6 2009Michèle Riesen Summary Calorie restriction (CR) extends lifespan in yeast, worms, flies and mammals, suggesting that it acts via a conserved mechanism. In yeast, activation of the NAD-dependent histone deacetylase, Sir2, by CR is thought to increase silencing at the ribosomal DNA, thereby reducing the recombination-induced generation of extrachromosomal rDNA circles, hence increasing replicative lifespan. Although accumulation of extrachromosomal rDNA circles is specific to yeast aging, it is thought that Sirtuin activation represents a conserved longevity mechanism through which the beneficial effects of CR are mediated in various species. We show here that growing yeast on 0.05 or 0.5% glucose (severe and moderate CR, respectively) does not increase silencing at either sub-telomeric or rDNA loci compared with standard (2% glucose) media. Furthermore, rDNA silencing was unaffected in the hxk2,, sch9, and tor1, genetic mimics of CR, but inhibited by FOB1 deletion. All these interventions extend lifespan in multiple yeast backgrounds, revealing a poor correlation between rDNA silencing and longevity. In contrast, CR and deletion of the FOB1, HXK2, SCH9 and TOR1 genes, all significantly reduced rDNA recombination. This silencing-independent mechanism for suppressing rDNA recombination may therefore contribute to CR-mediated lifespan extension. [source] Methionine sulfoxide reductase A expression is regulated by the DAF-16/FOXO pathway in Caenorhabditis elegansAGING CELL, Issue 6 2009Alicia N. Minniti Summary The methionine sulfoxide reductase system has been implicated in aging and protection against oxidative stress. This conserved system reverses the oxidation of methionine residues within proteins. We analyzed one of the components of this system, the methionine sulfoxide reductase A gene, in Caenorhabditis elegans. We found that the msra-1 gene is expressed in most tissues, particularly in the intestine and the nervous system. Worms carrying a deletion of the msra-1 gene are more sensitive to oxidative stress, show chemotaxis and locomotory defects, and a 30% decrease in median survival. We established that msra-1 expression decreases during aging and is regulated by the DAF-16/FOXO3a transcription factor. The absence of this enzyme decreases median survival and affects oxidative stress resistance of long lived daf-2 worms. A similar effect of MSRA-1 absence in wild-type and daf-2 (where most antioxidant enzymes are activated) backgrounds, suggests that the lack of this member of the methionine repair system cannot be compensated by the general antioxidant response. Moreover, FOXO3a directly activates the human MsrA promoter in a cell culture system, implying that this could be a conserved mechanism of MsrA regulation. Our results suggest that repair of oxidative damage in proteins influences the rate at which tissues age. This repair mechanism, rather than the general decreased of radical oxygen species levels, could be one of the main determinants of organisms' lifespan. [source] JNK signaling in insulin-producing cells is required for adaptive responses to stress in DrosophilaAGING CELL, Issue 3 2009Jason Karpac Summary Adaptation to environmental challenges is critical for the survival of an organism. Repression of Insulin/IGF Signaling (IIS) by stress-responsive Jun-N-terminal Kinase (JNK) signaling is emerging as a conserved mechanism that allows reallocating resources from anabolic to repair processes under stress conditions. JNK activation in Insulin-producing cells (IPCs) is sufficient to repress Insulin and Insulin-like peptide (ILP) expression in rats and flies, but the significance of this interaction for adaptive responses to stress is unclear. In this study, it is shown that JNK activity in IPCs of flies is required for oxidative stress-induced repression of the Drosophila ILP2. It is found that this repression is required for growth adaptation to heat stress as well as adult oxidative stress tolerance, and that induction of stress response genes in the periphery is in part dependent on IPC-specific JNK activity. Endocrine control of IIS by JNK in IPCs is thus critical for systemic adaptation to stress. [source] Vibrio cholerae cytolysin is composed of an ,-hemolysin-like corePROTEIN SCIENCE, Issue 2 2003Rich Olson VCC, Vibrio cholerae cytolysin; ,HL, ,-hemolysin; LukF, leukocidin F component Abstract The enteric pathogen Vibrio cholerae secretes a water-soluble 80-kD cytolysin, Vibrio cholerae cytolysin (VCC) that assembles into pentameric channels following proteolytic activation by exogenous proteases. Until now, VCC has been placed in a unique class of pore-forming toxins, distinct from paradigms such as Staphyloccal ,-hemolysin. However, as reported here, amino acid sequence analysis and three-dimensional structure modeling indicate that the core component of the VCC toxin is related in sequence and structure to a family of hemolysins from Staphylococcus aureus that include leukocidin F and ,-hemolysin. Furthermore, our analysis has identified the channel-forming region of VCC and a potential lipid head-group binding site, and suggests a conserved mechanism of assembly and lysis. An additional domain in the VCC toxin is related to plant lectins, conferring additional target cell specificity to the toxin. [source] A conserved mechanism of autoinhibition for the AMPK kinase domain: ATP-binding site and catalytic loop refolding as a means of regulationACTA CRYSTALLOGRAPHICA SECTION F (ELECTRONIC), Issue 2 2010Dene R. Littler The AMP-activated protein kinase (AMPK) is a highly conserved trimeric protein complex that is responsible for energy homeostasis in eukaryotic cells. Here, a 1.9,Å resolution crystal structure of the isolated kinase domain from the ,2 subunit of human AMPK, the first from a multicellular organism, is presented. This human form adopts a catalytically inactive state with distorted ATP-binding and substrate-binding sites. The ATP site is affected by changes in the base of the activation loop, which has moved into an inhibited DFG-out conformation. The substrate-binding site is disturbed by changes within the AMPK,2 catalytic loop that further distort the enzyme from a catalytically active form. Similar structural rearrangements have been observed in a yeast AMPK homologue in response to the binding of its auto-inhibitory domain; restructuring of the kinase catalytic loop is therefore a conserved feature of the AMPK protein family and is likely to represent an inhibitory mechanism that is utilized during function. [source] Leukotrienes and other mast cell mediators cause asthmatic airway obstructionCLINICAL & EXPERIMENTAL ALLERGY REVIEWS, Issue 2004S.-E. Dahlén Summary From an evolutionary perspective, bronchoconstriction is a highly conserved mechanism for defence against stimuli that are noxious for the lung and airways. The presence of mast cells in all layers of the airways makes them ideally situated to function as sensors of environmental changes that require such a host defence reaction. In addition to being activated by high affinity IgE receptors, many other trigger factors are known to activate signal transduction pathways leading to mast cell degranulation. This includes changes in the physical and chemical composition of the environment, exposure to endotoxin and other microbial factors acting on Toll-like receptors [1], intake of certain drugs and in particular virtually all nonsteroidal anti-inflammatory drugs (NSAIDs) in subjects with the peculiar syndrome aspirin-intolerant asthma (AIA) [2]. Irrespective of the trigger, the consequence of mast cell activation is release of biologically active smooth muscle stimulating mediators as well as the secretion of cytokines, chemotactic factors and enzymes that are believed to trigger further cascades contributing to long-term tissue remodelling and chronic airway inflammation. [source] The role of NAAG and NAALADase in axon-to-glia signallingJOURNAL OF NEUROCHEMISTRY, Issue 2002R. M. Grossfeld Recent investigations from our laboratories have identified N-acetylaspartylglutamate (NAAG) as the probable primary axon-to-glia signalling agent and source of signalling glutamate (GLU) at nonsynaptic regions of crayfish nerve fibers. NAAG is released from giant axons and mimics the action of the natural signalling agent in hyperpolarizing the glia. GLU formed extracellularly during inactivation of NAAG by NAALADase has a similar, but smaller, effect on the glia. A consequence of these actions of NAAG and GLU appears to be an activation of a signal transduction cascade leading to modulation of water and K+ homeostasis of the neuronal microenvironment. GLU or a related substance also appears to be a neuron-glia signalling agent at nonsynaptic and synaptic regions of vertebrate nervous system. Therefore, conserved mechanisms of neuron-glia signalling, mediated at least in part by NAAG and/or GLU, may regulate signal transmission and processing at axons and synapses under physiological and pathological conditions in invertebrates and vertebrates. Acknowledgements: ,Supported by NIH grant NS34799 and Guilford Pharmaceuticals (Baltimore, MD). [source] Evolution at the host,retrovirus interfaceBIOESSAYS, Issue 12 2006Robert J. Gifford Retroviruses are unusual amongst animal viruses in their capacity to integrate into host genomes and be transmitted vertically to host progeny. Vertebrate genomes contain numerous and diverse retrovirus-derived sequences reflecting a long co-evolutionary history during which genome invasion has occurred repeatedly, with wide-ranging evolutionary consequences. Over the past 10 years, a detailed picture of retroviral diversity throughout vertebrate genomes has emerged, revealing striking and informative patterns that differ markedly across species. The power of these data to deliver far-reaching insights into the biology and evolution of retroviruses has been significantly advanced by recent studies identifying ongoing genome invasion in wild populations,(1) and by the characterisation of conserved mechanisms of innate antiretroviral defence.(2,3) BioEssays 28: 1153,1156, 2006. © 2006 Wiley Periodicals, Inc. [source] | |||||||||||||