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1.
Rassokhin T. I. Golovin A. V. Petrova E. V. Spiridonova V. A. Karginova O. A. Rozhdestvenskii T. S. Brosius J. Kopylov A. M. 《Molecular Biology》2001,35(4):527-535
Both structural and thermodynamic studies are necessary to understand the ribosome assembly. An initial step was made in studying the interaction between a 16S rRNA fragment and S7, a key protein in assembling the prokaryotic ribosome small subunit. The apparent dissociation constant was obtained for complexes of recombinant Escherichia coliandThermus thermophilusS7 with a fragment of the 3" domain of the E. coli16S rRNA. Both proteins showed high rRNA-binding activity, which was not observed earlier. Since RNA and proteins are conformationally labile, their folding must be considered to correctly describe the RNA–protein interactions. 相似文献
2.
《Structure (London, England : 1993)》2014,22(6):923-930
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3.
Joanna Boros Nausica Arnoult Vincent Stroobant Jean-Fran?ois Collet Anabelle Decottignies 《Molecular and cellular biology》2014,34(19):3662-3674
Methylation of histone H3 on lysine 9 or 27 is crucial for heterochromatin formation. Previously considered hallmarks of, respectively, constitutive and facultative heterochromatin, recent evidence has accumulated in favor of coexistence of these two marks and their cooperation in gene silencing maintenance. H3K9me2/3 ensures anchorage at chromatin of heterochromatin protein 1α (HP1α), a main component of heterochromatin. HP1α chromoshadow domain, involved in dimerization and interaction with partners, has additional but still unclear roles in HP1α recruitment to chromatin. Because of previously suggested links between polycomb repressive complex 2 (PRC2), which catalyzes H3K27 methylation, and HP1α, we tested whether PRC2 may regulate HP1α abundance at chromatin. We found that the EZH2 and SUZ12 subunits of PRC2 are required for HP1α stability, as knockdown of either protein led to HP1α degradation. Similar results were obtained upon overexpression of H3K27me2/3 demethylases. We further showed that binding of HP1α/β/γ to H3K9me3 peptides is greatly increased in the presence of H3K27me3, and this is dependent on PRC2. These data fit with recent proteomic studies identifying PRC2 as an indirect H3K9me3 binder in mouse tissues and suggest the existence of a cooperative mechanism of HP1α anchorage at chromatin involving H3 methylation on both K9 and K27 residues. 相似文献
4.
Brain myosin V is a member of a widely distributed class of unconventional myosins that may be of
central importance to organelle trafficking in all eukaryotic cells. Molecular constituents that target this
molecular motor to organelles have not been previously identified. Using a combination of immunopurification, extraction, cross-linking, and coprecipitation assays, we demonstrate that the tail domain of brain
myosin V forms a stable complex with the synaptic vesicle membrane proteins, synaptobrevin II and synaptophysin. While myosin V was principally bound to synaptic vesicles during rest, this putative transport
complex was promptly disassembled upon the depolarization-induced entry of Ca2+ into intact nerve endings.
Coimmunoprecipitation assays further indicate that
Ca2+ disrupts the in vitro binding of synaptobrevin II to
synaptophysin in the presence but not in the absence of
Mg2+. We conclude that hydrophilic forces reversibly
couple the myosin V tail to a biochemically defined
class of organelles in brain nerve terminals.Synaptic vesicles are neuronal organelles that sequester, store, and release neurotransmitters. Functionally mature synaptic vesicles are assembled locally,
in the nerve terminal, from at least two different types of
precursor vesicles (Okada et al., 1995). Once the mature
synaptic vesicle becomes docked at the presynaptic membrane, it is prepared (“primed”) to rapidly discharge its
shipment of transmitter into the synaptic cleft upon the arrival of an action potential. This secretory response is triggered by the opening of voltage-regulated Ca2+ channels
and is the principle mechanism used by neurons to exchange information.A majority of the synaptic vesicles in a nerve terminal
are sequestered into clusters that are not immediately
available for exocytosis (Landis et al., 1988; Hirokawa et
al., 1989). Thus, the initial burst of Ca2+-triggered exocytosis is presently understood to result from the fusion of predocked vesicles that had matured to a fusion-competent
state before the action potential arrived (Südhof, 1995;
Rosenmund and Stevens, 1996). The current working
model further interprets the existence of vesicle clusters as
a potential reserve pool of synaptic vesicles that may be
mobilized in a use-dependent manner to replenish the
pool of readily releasable vesicles. Several independent
lines of experimental evidence support this scheme. Electrophysiological measurements of membrane fusion report that hippocampal synapses recover from complete
synaptic fatigue with a time constant of ∼10 s (Stevens and
Tsujimoto, 1995; Rosenmund and Stevens, 1996), suggesting that mechanisms exist for actively replenishing the
readily releasable pool of synaptic vesicles. The kinetics of
synaptic vesicle recycling indicate that recently retrieved
vesicle membranes do not completely fulfill the demand
for releasable vesicles during periods of intense secretory
activity (Ryan et al., 1993; Ryan and Smith, 1995). This
analysis implies that a supply of fresh synaptic vesicles
must somehow move from a reserve pool to the presynaptic membrane. In fact, movements of synaptic vesicles have
now been observed in a variety of different synaptic preparations (Llinas et al., 1989; Koenig et al., 1993; Henkel et
al., 1996). These movements are inconsistent with simple
diffusion, since they are reported to be both ATP-dependent and vectorial in nature. Integral synaptic vesicle proteins are transported to the terminal by a microtubule-based superfamily of motor proteins, the kinesins (Okada
et al., 1995). However, microtubules do not extend into
the cortical cytoskeletal matrix of terminals (Landis et al.,
1988; Hirokawa et al., 1989), and the kinesins are rapidly
degraded upon their arrival in the terminal (Okada et al.,
1995). Moreover, recent imaging studies have shown that
intracellular particles move along actin bundles in nerve
growth cones, rather than microtubules (Evans and Bridgman, 1995). For these reasons, it seems unlikely that the
kinesins move synaptic vesicles between their putative
storage sites (the vesicle clusters) and the sites of their release (the active zones). Despite intensive study of the molecular events that govern synaptic vesicle recycling, relatively little is known about the mechanisms that control
synaptic vesicle movements within the nerve terminal.Brain myosins V (p190, dilute, myr 6) are presently the
leading candidates for a synaptic vesicle motor protein
(Langford, 1995). In the nervous system, the mouse dilute
(Mercer et al., 1991) and chicken myosin V (p190; Espreafico et al., 1992) proteins are localized within neurons and
are more abundant than myr 6, which is concentrated in
the dentate gyrus and choroid plexus (Zhao et al., 1996).
The myosin superfamily includes at least 11 different molecular motors that possess a conserved motor domain attached to a variety of neck and tail domains with distinguishing structural and biochemical characteristics
(Cheney et al., 1993b
; Mooseker and Cheney, 1995). Both
the conventional myosins II and unconventional myosins V
have been localized within presynaptic terminals (Espreafico et al., 1992; Mochida et al., 1994; see also Miller et al.,
1992); form a two-headed structure that is capable of generating mechanochemical force and moving actin filaments; and possess actin-activated Mg2+-ATPase activity.
In addition, both forms of myosins have neck domains that
contain variable numbers of putative regulatory calmodulin light chain binding cassettes, and a flexible coiled-coil
stalk that is followed by a tail domain which ends as a large
(∼400 amino acids) COOH-terminal globular structure
(Espreafico et al., 1992; Cheney et al., 1993a
). Diversification of the intracellular localization and functions of the
myosins seems to depend on the COOH-terminal tail
which is variable in sequence and length (Cheney et al.,
1993b
). Myosins II and V appear to regulate complementary presynaptic functions: actin dynamics and the transport of membrane-bound organelles, respectively. The
heavy chains of myosins IIA and IIB bind to acidic phospholipids and self-assemble into contractile filaments on the
subplasmallemal surface (Murakami et al., 1995; Verkhovsky
et al., 1995), which may play an important role in growth
cone motility (Miller et al., 1992), the cycling of cortical actin assembly (Bernstein and Bamburg, 1989), and the regulation of neurotransmitter release (Mochida et al., 1994).
In contrast, myosins V are not filament-forming, and they
colocalize with intracellular membranes (Cheney et al.,
1993a
). The class V myosins may have a role in regulating
the extension of growth cone filapodia during neuronal
development (Wang et al., 1996), as well as the movement
of axoplasmic organelles (Kuznetsov et al., 1992; Bearer et
al., 1993; Langford, 1995). A potential role for brain myosin
V in organelle trafficking and transport is indirectly supported by the finding that this motor protein is capable of
moving relatively large (800 nm) artificial beads in motility
assays (Wolenski et al., 1995). Moreover, functional null
mutations have established that the class V myosins are required in yeast for the intracellular transport of post-Golgi
secretory vesicles (Johnston et al., 1991; Lillie and Brown,
1992; Govindan et al., 1995).Myosin motors bound directly to synaptic vesicles may
have an important role in regulating the availability of synaptic vesicles for exocytosis. The present study demonstrates that 2,3-butanedione-2-monoxime (BDM),1 a pharmacological inhibitor of endogenous myosin Mg2+-ATPase
activity, significantly decreases the Ca2+-dependent release of glutamate from isolated nerve endings (synaptosomes). In addition, our data reveal that a major portion
of the myosin V in nerve terminals was bound to synaptic
vesicles and that this interaction was regulated by Ca2+
concentrations that are of physiological relevance. Cross-linking experiments indicated that myosin V specifically
complexes with the synaptic vesicle proteins synaptobrevin and synaptophysin. Interactions between these two integral membrane proteins may impose an important additional constraint on the regulated pathway of secretion
(Calakos and Scheller, 1994; Edelmann et al., 1995). We
now present evidence that the cytoplasmic domain of the
synaptobrevin–synaptophysin complex may also function
as a binding partner for myosin V, forming a multimeric
complex that shall be referred to as the “myosin V transport complex.” 相似文献
5.
6.
Sohani Das Sharma Jelena J. Kraft W. Allen Miller Dixie J. Goss 《The Journal of biological chemistry》2015,290(18):11268-11281
Barley yellow dwarf virus mRNA, which lacks both cap and poly(A) tail, has a translation element (3′-BTE) in its 3′-UTR essential for efficient translation initiation at the 5′-proximal AUG. This mechanism requires eukaryotic initiation factor 4G (eIF4G), subunit of heterodimer eIF4F (plant eIF4F lacks eIF4A), and 3′-BTE-5′-UTR interaction. Using fluorescence anisotropy, SHAPE (selective 2′-hydroxyl acylation analyzed by primer extension) analysis, and toeprinting, we found that (i) 40S subunits bind to BTE (Kd = 350 ± 30 nm), (ii) the helicase complex eIF4F-eIF4A-eIF4B-ATP increases 40S subunit binding (Kd = 120 ± 10 nm) to the conserved stem-loop I of the 3′-BTE by exposing more unpaired bases, and (iii) long distance base pairing transfers this complex to the 5′-end of the mRNA, where translation initiates. Although 3′-5′ interactions have been recognized as important in mRNA translation, barley yellow dwarf virus employs a novel mechanism utilizing the 3′-UTR as the primary site of ribosome recruitment. 相似文献
7.
8.
Andrew Kodani Vinh Tonthat Beibei Wu Christine Sütterlin 《Molecular biology of the cell》2010,21(19):3376-3385
The centrosome contains proteins that control the organization of the microtubule cytoskeleton in interphase and mitosis. Its protein composition is tightly regulated through selective and cell cycle–dependent recruitment, retention, and removal of components. However, the mechanisms underlying protein delivery to the centrosome are not completely understood. We describe a novel function for the polarity protein Par6α in protein transport to the centrosome. We detected Par6α at the centrosome and centriolar satellites where it interacted with the centriolar satellite protein PCM-1 and the dynactin subunit p150Glued. Depletion of Par6α caused the mislocalization of p150Glued and centrosomal components that are critical for microtubule anchoring at the centrosome. As a consequence, there were severe alterations in the organization of the microtubule cytoskeleton in the absence of Par6α and cell division was blocked. We propose a model in which Par6α controls centrosome organization through its association with the dynactin subunit p150Glued. 相似文献
9.
Mammalian defensins are cationic antimicrobial peptides that play a central
role in host innate immunity and as regulators of acquired immunity. In
animals, three structural defensin subfamilies, designated as α, β,
and θ, have been characterized, each possessing a distinctive
tridisulfide motif. Mature α- and β-defensins are produced by
simple proteolytic processing of their prepropeptide precursors. In contrast,
the macrocyclic θ-defensins are formed by the head-to-tail splicing of
nonapeptides excised from a pair of prepropeptide precursors. Thus,
elucidation of the θ-defensin biosynthetic pathway provides an
opportunity to identify novel factors involved in this unique process. We
incorporated the θ-defensin precursor, proRTD1a, into a bait construct
for a yeast two-hybrid screen that identified rhesus macaque stromal
cell-derived factor 2-like protein 1 (SDF2L1), as an interactor. SDF2L1 is a
component of the endoplasmic reticulum (ER) chaperone complex, which we found
to also interact with α- and β-defensins. However, analysis of the
SDF2L1 domain requirements for binding of representative α-, β-,
and θ-defensins revealed that α- and β-defensins bind SDF2L1
similarly, but differently from the interactions that mediate binding of
SDF2L1 to pro-θ-defensins. Thus, SDF2L1 is a factor involved in
processing and/or sorting of all three defensin subfamilies.Mammalian defensins are tridisulfide-containing antimicrobial peptides that
contribute to innate immunity in all species studied to date. Defensins are
comprised of three structural subfamilies: the α-, β-, and
θ-defensins (1). α-
and β-Defensins are peptides of about 29–45-amino acid residues
with similar three-dimensional structures. Despite their similar tertiary
conformations, the disulfide motifs of α- and β-defensins differ.
Expression of human α-defensins is tissue-specific. Four myeloid
α-defensins (HNP1–4) are expressed predominantly by neutrophils
and monocytes wherein they are packaged in granules, while two enteric
α-defensins (HD-5 and HD-6) are expressed at high levels in Paneth cells
of the small intestine. Myeloid α-defensins constitute about 5% of the
protein mass of human neutrophils. HNPs are discharged into the phagosome
during phagocytic ingestion of microbial particles. HD-5 and HD-6 are produced
and stored as propeptides in Paneth cell granules and are processed
extracellularly by intestinal trypsin
(2). β-Defensins are
produced primarily by various epithelia (e.g. skin, urogenital tract,
airway) and are secreted by the producing cells in their mature forms. In
contrast to pro-α-defensins, which contain a conserved prosegment of
∼40 amino acids, the prosegments in β-defensins vary in length and
sequence. θ-Defensins are found only in Old World monkeys and orangutans
and are the only known circular peptides in animals. These 18-residue
macrocyclic peptides are formed by ligation of two nonamer sequences excised
from two precursor polypeptides, which are truncated versions of ancestral
α-defensins. Like myeloid α-defensins, θ-defensins are
stored primarily in neutrophil and monocyte granules
(3).Numerous laboratories have demonstrated that the antimicrobial properties
of defensins derive from their ability to bind and disrupt target cell
membranes (4), and studies have
shown defensins to be active against Gram-positive and -negative bacteria
(5), viruses
(6–9),
fungi (10,
11), and parasites such as
Giardia lamblia (12).
Defensins also play a regulatory role in acquired immunity as they are known
to chemoattract T lymphocytes, monocytes, and immature dendritic cells
(13,
14), act as adjuvants,
stimulate B cell responses, and up-regulate proliferation and cytokine
production by spleen cells and T helper cells
(15,
16).Defensins are produced as pre-propeptides and undergo post-translational
processing to form the mature peptides. While much has been learned about
regulation of defensin expression, little is known about the factors involved
in their biosynthesis. Valore and Ganz
(17) investigated the
processing of defensins in cultured cells and demonstrated that maturation of
HNPs occurs through two proteolytic steps that lead to formation of mature
α-defensins, but the proteases involved have yet to be identified.
Moreover, there are virtually no published data regarding endoplasmic
reticulum (ER)2
factors that are responsible for the folding, processing, and sorting steps
necessary for defensin maturation and secretion or trafficking to the proper
subcellular compartment. It is likely that several chaperones, proteases, and
protein-disulfide isomerase (PDI) family proteins are involved. Consistent
with this possibility, Gruber et al.
(18) recently demonstrated the
role of a PDI in biosynthesis of cyclotides, small ∼30-residue macrocyclic
peptides produced by plants.The primary structures of α- and θ-defensin precursors are
closely related. We therefore undertook studies to identify proteins that
interact with representative propeptides of each defensin subfamily with the
goal of determining common and unique processes that regulate biosynthesis of
α- and θ-defensins. We used two-hybrid analysis to first identify
interactors of the θ-defensin precursor, proRTD1a. As described, we
identified SDF2L1, a component of the ER-chaperone complex as an interactor,
and showed that it also specifically interacts with α- and
β-defensins. This suggests that SDF2L1 is involved in the
maturation/trafficking of defensins at a step common to all three subfamilies
of mammalian defensins. 相似文献
10.
We have determined the chromosomal localization of the gene for the regulatory subunit RIIα of cAMP-dependent protein kinase (locus PRKAR2A) to human chromosome 3 using polymerase chain reaction (PCR) and Southern blot analysis of two different somatic cell hybrid mapping panels. Furthermore, PCR analysis of a chromosome 3 mapping panel revealed the presence of a human RIIα-specific amplification product only in cell lines containing the region 3p21.3–p21.2. The localization of PRKAR2A was confirmed by PCR mapping using the Stanford G3 Radiation Hybrid Panel as template. The results from this analysis demonstrated that PRKAR2A is most closely linked to D3S3334 (lod score 12.5) and flanked by D3S1322E and D3S1581. 相似文献
11.
12.
Giovanni Esposito Maria R Amoroso Carmela Bergamasco Elia Di Schiavi Paolo Bazzicalupo 《BMC biology》2010,8(1):138
Background
Polymodal, nociceptive sensory neurons are key cellular elements of the way animals sense aversive and painful stimuli. In Caenorhabditis elegans, the polymodal nociceptive ASH sensory neurons detect aversive stimuli and release glutamate to generate avoidance responses. They are thus useful models for the nociceptive neurons of mammals. While several molecules affecting signal generation and transduction in ASH have been identified, less is known about transmission of the signal from ASH to downstream neurons and about the molecules involved in its modulation. 相似文献13.
Zamaratski E Trifonova A Acharya P Isaksson J Maltseva T Chattopadhayaya J 《Nucleosides, nucleotides & nucleic acids》2001,20(4-7):1219-1223
In a wide range of salt concentrations, 10-30 mM phosphate buffer containing up to 0.5 M Li2SO4 and 300 mM NaCl, 7.5 mM Mg2+, pH 5.5-7.5, a mixture of the 16 mer and the 25 mer RNA strands does not form a hammerhead in any amount detectable by NMR at 600 MHz. The imino-, amino-, aromatic- and anomeric protons in the NMR spectra of both the 16 mer and the 25 mer RNA have been assigned separately. Both the 16 mer and the 25 mer RNA both take up very stable hairpin structures, and when mixed together there is no major change of conformation in neither oligo-RNA. 相似文献
14.
Pedro José Pinés Corrales María P. López Garrido Silvia Aznar Rodríguez Lynda Louhibi Rubio Luz M. López Jiménez Cristina Lamas Oliveira Jose J. Alfaro Martínez Jose J. Lozano García Antonio Hernández López Ramón Requejo Castillo Julio Escribano Martínez Francisco Botella Romero 《Endocrinología y nutrición》2010,57(1):4-8
ObjectiveThe aim of our study was to describe and evaluate the clinical and metabolic characteristics of patients with MODY-3, MODY-2 or type 2 diabetes who presented I27L polymorphism in the HNF1α gene.MethodsThe study included 31 previously diagnosed subjects under follow-up for MODY-3 (10 subjects from 5 families), MODY-2 (15 subjects from 9 families), or type 2 diabetes (6 subjects) with I27L polymorphism in the HNF1α gene. The demographic, clinical, metabolic, and genetic characteristics of all patients were analyzed.ResultsNo differences were observed in distribution according to sex, age of onset, or form of diagnosis. All patients with MODY-2 or MODY-3 had a family history of diabetes. In contrast, 33.3% of patients with type 2 diabetes mellitus and I27L polymorphism in the HNF1α gene had no family history of diabetes (p < 0.05). No differences were observed in body mass index, prevalence of hypertension, or microvascular or macrovascular complications. Drug therapy was required by 100% of MODY-3 patients, but not required by 100% of MODY-2 patients or 16.7% of patients with type 2 diabetes mellitus and I27L polymorphism in the HNF1α gene (p < 0.05).ConclusionsOccasional difficulties may be encountered when classifying patients with MODY-2, MODY-3 or type 2 diabetes of atypical characteristics, in this case patients who present I27L polymorphism in the HNF1α gene. 相似文献
15.
Background
The transition from growth to development in Dictyostelium is initiated by amino acid starvation of growing amobae. In other eukaryotes, a key sensor of amino acid starvation and mediator of the resulting physiological responses is the GCN2 protein, an eIF2α kinase. GCN2 downregulates the initiation of translation of bulk mRNA and enhances translation of specific mRNAs by phosphorylating the translation initiation factor eIF2α. Two eIF2α kinases were identified in Dictyostelium and studied herein. 相似文献16.
17.
Lumsden JM Schwenk RJ Rein LE Moris P Janssens M Ofori-Anyinam O Cohen J Kester KE Heppner DG Krzych U 《PloS one》2011,6(7):e20775
A phase 2a RTS,S/AS malaria vaccine trial, conducted previously at the Walter Reed Army Institute of Research, conferred sterile immunity against a primary challenge with infectious sporozoites in 40% of the 80 subjects enrolled in the study. The frequency of Plasmodium falciparum circumsporozoite protein (CSP)-specific CD4(+) T cells was significantly higher in protected subjects as compared to non-protected subjects. Intrigued by these unique vaccine-related correlates of protection, in the present study we asked whether RTS,S also induced effector/effector memory (T(E/EM)) and/or central memory (T(CM)) CD4(+) T cells and whether one or both of these sub-populations is the primary source of cytokine production. We showed for the first time that PBMC from malaria-non-exposed RTS,S-immunized subjects contain both T(E/EM) and T(CM) cells that generate strong IL-2 responses following re-stimulation in vitro with CSP peptides. Moreover, both the frequencies and the total numbers of IL-2-producing CD4(+) T(E/EM) cells and of CD4(+) T(CM) cells from protected subjects were significantly higher than those from non-protected subjects. We also demonstrated for the first time that there is a strong association between the frequency of CSP peptide-reactive CD4(+) T cells producing IL-2 and the titers of CSP-specific antibodies in the same individual, suggesting that IL-2 may be acting as a growth factor for follicular Th cells and/or B cells. The frequencies of CSP peptide-reactive, TNF-α-producing CD4(+) T(E/EM) cells and of CD4(+) T(E/EM) cells secreting both IL-2 and TNF-α were also shown to be higher in protected vs. non-protected individuals. We have, therefore, demonstrated that in addition to TNF-α, IL-2 is also a significant contributing factor to RTS,S/AS vaccine induced immunity and that both T(E/EM) and T(CM) cells are major producers of IL-2. 相似文献
18.
19.
Miroslava Hancarova Sarka Vejvalkova Marie Trkova Jana Drabova Alzbeta Dleskova Marketa Vlckova Zdenek Sedlacek 《Gene》2013
Microdeletions spanning 2p14–p15 have recently been described in two patients with developmental and speech delay and intellectual disability but no congenital malformations or severe facial dysmorphism. We report a 4-year-old boy with a de novo 3.7 Mb long deletion encompassing the region deleted in the previous cases. The patient had clinical features partly consistent with the published cases including intellectual disability, absent speech, microcephaly, long face, bulbous nasal tip and thin upper lip, but his overall clinical picture was more severe compared to the published patients. The identification of this additional patient and a detailed analysis of deletions identified in various patient cohorts and in normal individuals support the existence of a new rare microdeletion syndrome in 2p14–p15. Its critical region is in the vicinity of but clearly separate from the minimal region deleted in the well established 2p15–p16.1 microdeletion syndrome. A thorough comparison of the deletions and phenotypes indicates that multiple genes located in this region may be involved in intellectual functioning, and that some patients may show composite and more complex phenotypes due to deletions spanning both critical regions. 相似文献
20.
Takehisa?Matsumoto Masatomo?Kawakubo Mayumi?Shiohara Toshiko?Kumagai Eiko?Hidaka Kazuyoshi?Yamauchi Kozue?Oana Kenji?Matsuzawa Hiroyoshi?Ota Yoshiyuki?Kawakami
“Helicobacter heilmannii” is an uncultivable spiral-shaped bacterium inhabiting the human gastric mucosa. It is larger and more tightly-coiled than
H. pylori. We encountered a patient with chronic gastritis infected a “H. heilmannii”-like organism (HHLO), designated as SH6. Gastric mucosa derived from the patient was orally ingested by specific pathogen
free mice. Colonization of the mice by SH6 was confirmed by electron microscopy of gastric tissue specimens. In an attempt
to characterize SH6, 16S rRNA and urease genes were sequenced. The 16S rRNA gene sequence was most similar (99.4%; 1,437/1,445
bp) to HHLO C4E from a cheetah. However, the urease gene sequence displayed low similarity (81.7%; 1,240/1,516 bp) with HHLO
C4E. Taxonomic analysis disclosed that SH6 represents a novel strain and should constitute a novel taxon in the phylogenetic
trees, being discriminated from any other taxon, with the ability of infecting human gastric mucosa. 相似文献