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At least 703 records · Page 39Linked to original sources
PubMed2001

Nitric oxide: an unconventional messenger in the nervous system of an orthopteroid insect.

Nitric oxide (NO) is a membrane-permeant messenger molecule generated from the amino acid L-arginine. NO can activate soluble guanylyl cyclase leading to the formation of cyclic GMP (cGMP) in target cells. In the nervous system, NO/cGMP signalling is thought to play essential roles in synaptic plasticity during development and also in the mature animal. This paper examines biochemical, cell biological, and physiological investigations of NO/cGMP signalling in the nervous system of the locust, a commonly used neurobiological preparation. Biochemical investigations suggest that an identical enzyme is responsible for both NO synthase (NOS) and NADPH-diaphorase activity after tissue fixation. Immunocytochemical staining of an olfactory center in the locust brain shows that NOS-immunoreactivity colocalizes with NADPH-diaphorase at the cellular level. The cytochemical staining of NO donor and target cells in adult animals suggests functions in olfaction, vision, and sensorimotor integration. During development, NO is implicated in axonal outgrowth and synaptogenesis. The cellular distribution of NO-responsive cells in neural circuits reflects potential functions of NO as a retrograde synaptic messenger, as an intracellular messenger, and as a lateral diffusible messenger independent of conventional synaptic connectivity.

Animals↗
PubMed2004

RAGE potentiates Abeta-induced perturbation of neuronal function in transgenic mice.

Receptor for Advanced Glycation Endproducts (RAGE), a multiligand receptor in the immunoglobulin superfamily, functions as a signal-transducing cell surface acceptor for amyloid-beta peptide (Abeta). In view of increased neuronal expression of RAGE in Alzheimer's disease, a murine model was developed to assess the impact of RAGE in an Abeta-rich environment, employing transgenics (Tgs) with targeted neuronal overexpression of RAGE and mutant amyloid precursor protein (APP). Double Tgs (mutant APP (mAPP)/RAGE) displayed early abnormalities in spatial learning/memory, accompanied by altered activation of markers of synaptic plasticity and exaggerated neuropathologic findings, before such changes were found in mAPP mice. In contrast, Tg mice bearing a dominant-negative RAGE construct targeted to neurons crossed with mAPP animals displayed preservation of spatial learning/memory and diminished neuropathologic changes. These data indicate that RAGE is a cofactor for Abeta-induced neuronal perturbation in a model of Alzheimer's-type pathology, and suggest its potential as a therapeutic target to ameliorate cellular dysfunction.

Alzheimer Disease↗
PubMed2000

The AMPAR subunit GluR2: still front and center-stage.

Abnormal influx of Ca(2+) through AMPA-type glutamate receptors (AMPARs) is thought to contribute to the neuronal death associated with a number of brain disorders. AMPARs exist as both Ca(2+)-impermeable and Ca(2+)-permeable channels. AMPARs are encoded by four genes designated GluR1 (GluR-A) through GluR4 (GluR-D). The presence of the GluR2 subunit renders heteromeric AMPA receptor assemblies Ca(2+)-impermeable. Molecular diversity of AMPARs under physiological and pathological conditions is generated by differential spatio-temporal patterns of GluR expression, by alternative RNA splicing and editing and by targeting and trafficking of receptor subunits at dendritic spines. The GluR2 gene is under transcriptional control by the RE1 element specific transcription factor, a gene silencing factor which renders it neuron-specific. GluR2 transcripts are edited by ADAR2 (double-stranded RNA-specific editase 1). AMPAR targeting and trafficking to spines are regulated by synaptic activity and are critical to synaptic plasticity. Recent studies involving animal models of transient forebrain ischemia and epilepsy show that GluR2 mRNA and GluR2 subunit expression are downregulated in vulnerable neurons prior to cell death. Ca(2+) imaging and electrical recording from individual pyramidal neurons in hippocampal slices reveal changes in AMPAR functional properties after ischemia. In slices from post-ischemia animals, CA1 neurons with robust action potentials exhibit greatly enhanced AMPA-elicited rises in intracellular Ca(2+). Excitatory postsynaptic currents in post-ischemic CA1 exhibit an enhanced Ca(2+)-dependent component that appears to be mediated by Ca(2+)-permeable AMPARs. These studies provide evidence for Ca(2+) influx through AMPARs in neurons destined to die. To examine whether acute GluR2 downregulation, even in the absence of a neurological insult, can induce neuronal death, we performed knockdown experiments in rats and gerbils with antisense oligonucleotides targeted to GluR2 mRNA. GluR2 antisense oligonucleotide induced neuronal cell death of pyramidal neurons and enhanced pathogenicity of brief ischemic episodes. These observations provide evidence for Ca(2+) influx through AMPARs in neurons destined to die and implicate Ca(2+)-permeable AMPARs in the pathogenesis of ischemia-induced neuronal death.

Animals↗
PubMed1986

Plasticity in the olfactory cortex: age-dependent effects of deafferentation.

In order to assess the role of input-target interactions in the development of olfactory cortex, the primary afferent fibers from the olfactory bulb to the superficial part of layer I of the cortex (layer Ia) were removed in developing and mature rats. After survival periods that vary from a few days to 2-6 months, changes were assessed in (1) the radial thickness of layer I, (2) the laminar distribution of intracortical associational fibers, which normally terminate in a deep part of layer I (layer Ib), and (3) the distribution of glia in layer I. The findings indicate that the lamination of fibers within layer I is not intrinsically prespecified, but gradually becomes "set" during the first month after birth. If the fibers from the olfactory bulb are removed, the dendrites of cortical cells are capable of accepting inputs from other fiber systems, depending on the maturational state of the dendrites and the ingrowing axons. Development of the abnormal inputs is associated with relatively normal dendritic growth, whereas lack of adequate input results in dendritic atrophy. Thus, after neonatal bulb ablation, the intracortical fibers occupy both superficial and deep parts of layer I, and a normal synaptic density is established throughout the layer. Layer I also develops to nearly its normal adult thickness, although the high density of glia that normally characterizes layer Ia is not apparent. With bulb ablation at progressively older ages (from postnatal day (P-) 3 to 21), the cortical associational fibers show progressively less extension into the denervated layer Ia. Layer I continues to grow, but not to the same extent as after P-1 ablations. In these experiments the glia distribution resembles the pattern present at the time of denervation. After adult olfactory bulb ablation, the long intracortical fibers extend very little into layer Ia, which undergoes pronounced shrinkage and becomes filled with a high concentration of glia. However, partial reinnervation of layer Ia is accomplished by the proliferation of a normally sparse native fiber system, which has been identified only with the Timm method. These results are interpreted as evidence that the normal development of lamination of afferent fibers to the olfactory cortex depends on axodendritic interaction during development.

Age Factors↗
PubMed2004

Postsynaptic density scaffolding proteins at excitatory synapse and disorders of synaptic plasticity: implications for human behavior pathologies.

Excitatory synapses are characterized by an electron-dense thickening at the cytoplasmic surface of the postsynaptic membrane, called the postsynaptic density (PSD). The PSD is a fibrous specialization of the submembrane cytoskeleton approximately 30-40 nm thick and about 100 nm wide. Hundreds of molecules have been identified in the PSD: ion-gated and G-protein-coupled receptors, association, adaptors, and scaffolding proteins, key enzymes involved in phosphorylation-dephosphorylation mechanisms, and cytoskeletal proteins. Each of these proteins may have a pivotal function in setting the molecular scenario for the development of synaptic plasticity. Scaffolding proteins are major players in the organization of the postsynaptic signal transduction machinery,they regulate receptor trafficking and clustering, modulate axon pathfinding,and drive the correct targeting of neuronal proteins to their appropriate cytoplasmic compartment. Emerging findings suggest a relevant involvement of PSD scaffolding/adaptor proteins in behavior modulation in animal models of synaptic plasticity disorders and pharmacological isomorphisms.

Adaptor Proteins, Signal Transducing↗
PubMed1997

High dose IL-2-activated murine natural killer (A-NK) cells accumulate glycogen and granules, lose cytotoxicity, and alter target cell interaction in vitro.

Activated natural killer (A-NK) cells, defined by immunophenotype and selected by adherence to the plastic, were cultured from murine splenocytes for up to 10 days with the addition of 1000 U/ml of recombinant human IL-2 at 48 h intervals. During culture days 2-4 with high DNA synthesis the initially non-granulated small cells established large granular lymphocyte (LGL) morphology and then differentiated further into giant hypergranulated cells with huge accumulations of glycogen. Timed EM observations indicated that specific dual-compartment (lytic) granules arose by a sequence of events starting with neo-synthesis of small progenitors with a dense core and a few membranous lamellae at one pole. Core and vesicular regions probably expanded independently to give the mature organization of the granule. Eventually, the vesicular region of granules contained large amounts of multi-lamellar material and probable debris, and the dense core could be multiplied. Intracellular proteoglycans, visualized with Cupromeronic Blue cytochemistry, were organized in a three-dimensional network within the dense cores. In contrast with earlier reports, and in spite of several-fold increased granularity, the in vitro cytotoxicity of the A-NK cells against YAC-1 and B16 cells decreased after the third day of culture. A-NK cells with glycogen accumulations caused focal clearing in melanoma monolayers whereas younger effectors adhered to the targets. It is concluded that high dose IL-2 stimulation causes more far-going progressive morphological and functional differentiations of the A-NK cells than has previously been observed with bearing for the use of these cells in experimental adoptive immunotherapy.

Animals↗
PubMed1977

Natural cell-mediated immunity to lymphoma cells. I. Characteristics of effector cells in a cytostasis assay in vitro.

Spleen cells from normal, nonimmune, CBA or (CBA X AKR)F1 mice markedly and rapidly inhibited the incorporation of [3H]thymidine by two different T-cell lymphomas in an in vitro cytostasis assay. These were the I-529 lymphoma of spontaneous AKR origin and the Moloney murine leukemia virus-induced YAC lymphoma of A mouse origin. Spleen cells were the most efficient inhibitors for both types of target cells, whereas lymph node cells were much less active and thymus cells showed little or no activity. Granulocytes, as well as conventional T- and B-lymphocytes, were excluded as important contributors to the cytostatic cell population. Spleen cells were separated on nylon wool, Sephadex G-10 columns, or plastic petri dishes and tested for activity in the cytostasis assay or for cytotoxicity against 51Cr-labeled lymphoma target cells. Adherent cells carried almost all cytostatic activity against the AKR lymphoma but also showed significant cytotoxic activity against these target cells. In addition, the cytostatic activity against the YAC lymphoma was mainly due to adherent spleen cells, but nonadherent cells were relatively more active against this target than against I-529 cells. Such nonadherent spleen cells further showed increased cytotoxic activity, compared to the whole spleen cell population.

Animals↗
PubMed2005

Aesthetic septorhinoplasty in the burned nose.

Patients who have survived thermal injuries to the face suffer severe disfigurement from the devastating deformities of full-thickness facial burns. The nose is the prominent central organ of the face, which has crucial effect on Aesthetic appearance. The plastic surgeon's role to deal with such cases is to undertake procedures to produce a more pleasant look although the target organ could be the non-burned areas of the face. It is a common belief that surgical intervention under the scarred or grafted nose is risky and may result in skin or covering graft necrosis. For this reason, plastic surgeons are cautious and hesitate to perform Aesthetic surgery on burn scarred tissue. We present 13 cases, 10 women and three men with complete or subtotal nasal burn. Classic Aesthetic Rhinoplasty operations were performed to create a better appearance and correct any internal or external deviations. These procedures are carried out under severely burned skins, or previously grafted and reconstructed noses. Cases were followed for about a one-year period. There was no necrosis in any part of skin after surgery. We believe that Aesthetic rhinoplasty can be done safely in these victims with pleasing outcome. The problems that we encountered in these cases were irregularities of burned alar margins, multiple operations and intractable nasal deviation in severe cases.

Adolescent↗
PubMed1997

Plasticity: implications for opioid and other pharmacological interventions in specific pain states.

The spinal mechanisms of action of opioids under normal conditions are reasonably well understood. The spinal effects of opioids can be enhanced or reduced depending on pathology and activity in other segmental and nonsegmental pathways. This plasticity will be considered in relation to the control of different pain states using opioids. The complex and contradictory findings on the supraspinal actions of opioids are explicable in terms of heterogeneous descending pathways to different spinal targets using multiple transmitters and receptors--therefore opioids can both increase and decrease activity in descending pathways. These pathways could exhibit considerable plasticity. There is increasing evidence that delta opioid receptor agonists have the potential to replace morphine as major analgesics with reduced side-effect profiles. The concept of preemptive analgesia, based on preventing the induction of some of the negative plastic influences on opioid controls and the detrimental effects of pain, is sound, but experimental verification in the clinical setting is difficult. For example, a delayed compensatory upregulation of inhibitory systems, particularly in inflammation, may counter persistent painful inputs. Combination therapy with opioids may be beneficial in many pain states where either negative influences are blocked or inhibitory controls are enhanced. Finally, developmental aspects of these systems are discussed in connection with the treatment of pain in young children, where inhibitory systems in the spinal cord are immature.

Humans↗
PubMed2003

Musings on the wanderer: what's new in our understanding of vago-vagal reflexes? III. Activity-dependent plasticity in vago-vagal reflexes controlling the stomach.

Vago-vagal reflex circuits modulate digestive functions from the oral cavity to the transverse colon. Previous articles in this series have described events at the level of the sensory receptors encoding the peripheral stimuli, the transmission of information in the afferent vagus, and the conversion of this data within the dorsal vagal complex (DVC) to impulses in the preganglionic efferents. The control by vagal efferents of the postganglionic neurons impinging on the glands and smooth muscles of the target organs has also been illustrated. Here we focus on some of the mechanisms by which these apparently static reflex circuits can be made quite plastic as a consequence of the action of modulatory inputs from other central nervous system sources. A large body of evidence has shown that the neuronal elements that constitute these brain stem circuits have nonuniform properties and function differently according to status of their target organs and the level of activity in critical modulatory inputs. We propose that DVC circuits undergo a certain amount of short-term plasticity that allows the brain stem neuronal elements to act in harmony with neural systems that control behavioral and physiological homeostasis.

Animals↗
PubMed2004

Applications of manganese-enhanced magnetic resonance imaging (MEMRI) to image brain plasticity in song birds.

The song control system of song birds is an excellent model for studying brain plasticity and has thus far been extensively analyzed by histological and electrophysiological methods. However, these approaches do not provide a global view of the brain and/or do not allow repeated measures, which are necessary to establish correlations between alterations in neural substrate and behavior. Application of in vivo manganese-enhanced MRI enabled us for the first time to visualize the song control system repeatedly in the same bird, making it possible to quantify dynamically the volume changes in this circuit as a function of seasonal and hormonal influences. In this review, we introduce and explore the song control system of song birds as a natural model for brain plasticity to validate a new cutting edge technique, which we called 'repeated dynamic manganese enhanced MRI' or D-MEMRI. This technique is based on the use of implanted permanent cannulae--for accurate repeated manganese injections in a defined target area--and the subsequent MRI acquisition of the dynamics of the accumulation of manganese in projection brain targets. A compilation of the D-MEMRI data obtained thus far in this system demonstrates the usefulness of this new method for studying brain plasticity. In particular it is shown to be a perfect tool for long-term studies of morphological and functional responses of specific brain circuits to changes in endocrine conditions. The method was also successfully applied to obtain quantitative measures of changes in activity as a function of auditory stimuli in different neuronal populations of a same nucleus that project to different targets. D-MEMRI, combined with other MRI techniques, clearly harbors potential for unraveling seasonal, hormonal, pharmacological or even genetically driven changes in a neuronal circuit, by simultaneously measuring changes in morphology, activity and connectivity.

Adaptation, Physiological↗
PubMed2006

Presynaptic modulation of parallel fibre signalling to Bergmann glia.

Transmission at the parallel fibre-Purkinje neurone synapse of the cerebellum can be depressed by a number of presynaptic receptors: endocannabinoid (CB1), metabotropic glutamate (mGluR4), adenosine (A1) and GABA (GABA(B)), which have been implicated in both short- and long-term synaptic plasticity. Stimulation of parallel fibres also activates glutamate receptors and transporters on the Bergmann glial cell that forms a sheath around the synapse. The resulting glial extrasynaptic currents (ESC) exhibit short- and long-term plasticity, which differs from the plasticity of adjacent synapses. This functional independence could arise from differential modulation of presynaptic release sites targeted to synapses or glia, but the sensitivity of glial ESC to these inhibitory pathways is unknown. Here I show that all four presynaptic receptors depress parallel fibre-Bergmann glial cell signalling with similar potency to synaptic transmission. Depression of glial ESC is accompanied by a decrease in paired pulse ratio. However, application of receptor antagonists had no effect on ESC amplitude, indicating that tonic activation of these pathways does not occur, and antagonists failed to block the activity-dependent depression of glial ESC observed during tetanic or low frequency stimulation. These data suggest that modulation of presynaptic glutamate release does not underlie glial plasticity.

Animals↗
PubMed1994

Neuropeptides in the sympathetic system: presence, plasticity, modulation, and implications.

Neuropeptides are ubiquitous in the sympathetic system and modulate transmission at the levels of the intermediolateral cell column, sympathetic ganglia, and neuroeffector junctions. Several neuropeptide-containing pathways from the hypothalamus and medulla modulate excitability of preganglionic neurons. Neuropeptides coexist with norepinephrine or acetylcholine in subpopulations of chemically coded, target-specific sympathetic ganglion neurons. Neuropeptide Y is colocalized in adrenergic vasoconstrictor neurons, whereas vasoactive intestinal polypeptide is colocalized in cholinergic sudomotor neurons. Neuropeptide expression is plastic; during development, neurons that switch from a noradrenergic to a cholinergic phenotype increase expression of vasoactive intestinal polypeptide, somatostatin, and substance P. Preganglionic inputs increase neuropeptide Y and inhibit substance P expression. Sympathetic denervation produces sprouting of sensory fibers containing substance P and calcitonin gene-related peptide in target tissues. Neuropeptides from preganglionic fibers (e.g., enkephalin) and primary afferents (e.g., substance P, vasoactive intestinal polypeptide) modulate transmission in sympathetic ganglia. Neuropeptide Y produces vasoconstriction, prejunctional inhibition of norepinephrine release, and postjunctional potentiation of norepinephrine effects. Plasma neuropeptide Y increases during intense sympathoexcitation, hypertension, and pheochromocytoma. Dystrophic neurites containing neuropeptide Y occur in human sympathetic ganglia during aging, diabetes, and dysautonomia. Sympathetic neuropeptides may thus have important clinical implications.

Aging↗
PubMed2006

Glutamate receptors and endoplasmic reticulum quality control: looking beneath the surface.

Glutamate is the principal excitatory neurotransmitter in the mammalian central nervous system. The cellular regulation of glutamate receptor (GluR) ion channel function and expression is important for maintaining or adjusting target cell excitability to meet ever-changing demands, for example, in relation to developmental or use-dependent synaptic plasticity. Dysregulation of GluR function or expression may be a contributing factor in certain forms of epilepsy, stroke/ischemia, head trauma, cognitive impairments, and neurodegenerative disease. Recent years have seen substantial progress in understanding how GluRs operate in terms of their structural and functional properties, their synaptic targeting and membrane anchoring by PDZ-domain proteins, and their activity-dependent cycling at the plasma membrane. Yet precious little is known about the earliest events in GluR biogenesis or the mechanisms in place to ensure the GluRs that reach the cell surface are processed, folded, and oligomerized in an appropriate manner. Indeed, only a minor fraction of the GluR content of cells is expressed at any given time on the cell surface, whereas most of the remaining receptors exist in the endoplasmic reticulum (ER). The functional competence and significance of the ER fraction of receptors are presently unknown, but they are generally thought to represent immature, unassembled, or improperly assembled subunits. Some are ultimately destined for insertion in the plasma membrane. Others may be targeted for proteosomal degradation. Still others might provide a latent pool of fully functional receptors that can be recruited to enhance cell excitability in response to specific signals or under pathological conditions. This review will explore the structural and functional elements that regulate GluR assembly and export from the ER.

Animals↗
PubMed1986

Morphological alterations in subcortical vibrissal relays following vibrissal follicle destruction at birth in the mouse.

Morphological modifications of two subcortical vibrissal relays were analyzed, following destruction of vibrissal follicles in newborn mice. The volume of the nucleus interpolaris (NI) of the trigeminal nuclear complex in the brainstem decreased by 33%, while the number of its neuronal perikarya decreased only moderately. Vibrissal deafferentation caused no shrinkage of the ventrobasal complex (VB). In the damaged medial vibrissal part of VB (VBm), however, neuronal density was higher than normal, indicating the prevention or retardation of physiologically programmed cell death in the afferentation deprived thalamic somatosensory relay station. It is suggested that the difference in neuron density produced by deafferentation is related to the states of maturation at birth of the two subcortical vibrissal relays. Following vibrissal deafferentation the basic organization of the synaptic neuropil appeared to be similar to the control. Quantitative electron microscopic (EM) analysis revealed, however, an increased number of axon terminals with ovoid synaptic vesicles in both deafferented relay stations. The increased density of gamma-aminobutyric acid (GABA)-immunostained boutons observed in the VBm following vibrissal deprivation suggested a compensatory increase most probably of the inhibitory axon endings. Quantitative EM analysis also provided evidence that many or most of the specific afferent terminals in the damaged VBm were not identical with but were substitutes for the original "vibrissal" specific afferents. Forty percent of all "specific" afferents were shown to be modified corticothalamic terminals. The modification and the resemblence of some cortical endings to specific afferents demonstrated the morphogenetic plasticity of synaptogenesis in these terminals during development as well as the importance and inductive potential of the postsynaptic target in the differentiation of presynaptic axon terminals.

Animals↗
PubMed2000

Human retrovirus 5 sequences in peripheral blood cells of patients with B-cell non-Hodgkin's lymphoma.

A recently described sequence from a probable 5th human exogenous retrovirus, HRV-5, is related to type A, B and D retroviruses. It was initially detected in a salivary gland biopsy from a patient with Sjögren's syndrome, but it is not consistently associated with this disease. We searched for the HRV-5 sequence in DNA extracted from whole blood of 300 blood donors, 81 patients with hematological malignancy and 21 patients with neurological disease using PCR. While samples from none of the blood donors and the neurological patients became positive, 3 of the 81 patients with hematological malignancy were HRV-5 DNA positive. All 3 had B-cell non-Hodgkin's lymphoma of low grade. The difference in frequency between NHL and controls is statistically significant. HRV-5 DNA was found in DNA from whole blood and in plastic-adherent cells but not in tumor cell DNA. Thus, monocytes/macrophages may be preferred targets for HRV-5. Our result, together with a previous finding of HRV-5 DNA in 2 NHL cases, is compatible with an association between HRV-5 and NHL, whether causal or not.

Base Sequence↗
PubMed1989

Abrogated NK-cell lysis of human papillomavirus (HPV)-16-bearing keratinocytes in patients with pre-cancerous and cancerous HPV-induced anogenital lesions.

Natural-cell-mediated cytotoxicity against K-562 erythroleukemic cells and human papillomavirus (HPV)-16 harboring Sk-v keratinocytes was tested in 38 age- and sex-matched healthy volunteers and in patients with HPV-induced benign and malignant anogenital lesions: 9 persons with HPV-16-induced bowenoid papulosis (BP), 8 with anogenital carcinomas (5 with HPV-16- or 33-associated squamous-cell carcinomas of Bowen's type and 3 with HPV-6-associated Buschke-Loewenstein verrucous carcinomas) and 12 with HPV-6-induced condylomata acuminata. Both K-562 and Sk-v cells were killed by a non-adherent CD16+ subset of PBMC as revealed by cell fractionation on the basis of their adherence to plastic and by treatment with Leu-IIb monoclonal antibody (MAb) and complement. "Cold" target competitive assays demonstrated that both cell types inhibited lysis of labelled Sk-v cells. In patients with BP and anogenital carcinomas induced by HPV-16 or 33, there was a significant (at least at p less than 0.01) decrease of Sk-v cell lysis as compared with the healthy control group. Anti-K-562 activity was not affected. In patients with anogenital carcinomas the degree of Sk-v lysis was decreased in proportion to the duration of lesions (correlation coefficient-r = -0.79). Neither anti-K-562 nor anti-Sk-v cytotoxicities were significantly affected in patients with condylomata and with HPV-6 associated verrucous carcinomas. Short-term (3 hr) pre-incubation of normal PBMC with sera from patients with BP and HPV-16-associated anogenital carcinomas resulted in significant inhibition of their ability to lyse Sk-v cells. Lysis of K-562 cells remained unaffected. In patients with carcinomas, the suppressive effect of sera was associated with a lowering of the ability of their PBMC to lyse Sk-v cells (r = -0.79). In patients with longer tumor persistence, the suppressive effect of serum was proportionally higher (r = 0.86).

Adult↗
PubMed1993

Plasmid pHH1 of Halobacterium salinarium: characterization of the replicon region, the gas vesicle gene cluster and insertion elements.

The DNA sequence of the 5.7 kb plasmid pHH9 containing the replicon region of the 150 kb plasmid pHH1 from Halobacterium salinarium was determined. The minimal region necessary for stable plasmid maintenance lies within a 2.9 kb fragment, as defined by transformation experiments. The DNA sequence contained two open reading frames arranged in opposite orientations, separated by an unusually high AT-rich (60-70% A+T) sequence of 350 bp. All H. salinarium strains (H. halobium, H. cutirubrum) investigated harbour endogenous plasmids containing the pHH1 replicon; however, these pHH1-type plasmids differ by insertions and deletions. Adjacent to the replicon, and separated by a copy of each of the insertion elements ISH27 and ISH26, is the 9 kb p-vac region required for gas vesicle synthesis. Analysis of these and other ISH element copies in pHH1 revealed that most of them lack the target DNA duplication usually found with recently transposed ISH elements. These results underline the plasticity of plasmid pHH1.

Base Sequence↗