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1.
Cell death can be divided into the anti-inflammatory process of apoptosis and the
pro-inflammatory process of necrosis. Necrosis, as apoptosis, is a regulated form of cell
death, and Poly-(ADP-Ribose) Polymerase-1 (PARP-1) and Receptor-Interacting Protein (RIP)
1/3 are major mediators. We previously showed that absence or inhibition of PARP-1
protects mice from nephritis, however only the male mice. We therefore hypothesized that
there is an inherent difference in the cell death program between the sexes. We show here
that in an immune-mediated nephritis model, female mice show increased apoptosis compared
to male mice. Treatment of the male mice with estrogens induced apoptosis to levels
similar to that in female mice and inhibited necrosis. Although PARP-1 was activated in
both male and female mice, PARP-1 inhibition reduced necrosis only in the male mice. We
also show that deletion of RIP-3 did not have a sex bias. We demonstrate here that male
and female mice are prone to different types of cell death. Our data also suggest that
estrogens and PARP-1 are two of the mediators of the sex-bias in cell death. We therefore
propose that targeting cell death based on sex will lead to tailored and better treatments
for each gender. 相似文献
2.
3.
4.
Orwah Saleh Bertolt Gust Bj?rn Boll Hans-Peter Fiedler Lutz Heide 《The Journal of biological chemistry》2009,284(21):14439-14447
The bacterium Streptomyces anulatus 9663, isolated from the
intestine of different arthropods, produces prenylated derivatives of
phenazine 1-carboxylic acid. From this organism, we have identified the
prenyltransferase gene ppzP. ppzP resides in a gene cluster
containing orthologs of all genes known to be involved in phenazine
1-carboxylic acid biosynthesis in Pseudomonas strains as well as
genes for the six enzymes required to generate dimethylallyl diphosphate via
the mevalonate pathway. This is the first complete gene cluster of a phenazine
natural compound from streptomycetes. Heterologous expression of this cluster
in Streptomyces coelicolor M512 resulted in the formation of
prenylated derivatives of phenazine 1-carboxylic acid. After inactivation of
ppzP, only nonprenylated phenazine 1-carboxylic acid was formed.
Cloning, overexpression, and purification of PpzP resulted in a 37-kDa soluble
protein, which was identified as a 5,10-dihydrophenazine 1-carboxylate
dimethylallyltransferase, forming a C–C bond between C-1 of the
isoprenoid substrate and C-9 of the aromatic substrate. In contrast to many
other prenyltransferases, the reaction of PpzP is independent of the presence
of magnesium or other divalent cations. The Km value for
dimethylallyl diphosphate was determined as 116 μm. For
dihydro-PCA, half-maximal velocity was observed at 35 μm.
Kcat was calculated as 0.435 s-1. PpzP shows
obvious sequence similarity to a recently discovered family of
prenyltransferases with aromatic substrates, the ABBA prenyltransferases. The
present finding extends the substrate range of this family, previously limited
to phenolic compounds, to include also phenazine derivatives.The transfer of isoprenyl moieties to aromatic acceptor molecules gives
rise to an astounding diversity of secondary metabolites in bacteria, fungi,
and plants, including many compounds that are important in pharmacotherapy.
However, surprisingly little biochemical and genetic data are available on the
enzymes catalyzing the C-prenylation of aromatic substrates. Recently, a new
family of aromatic prenyltransferases was discovered in streptomycetes
(1), Gram-positive soil
bacteria that are prolific producers of antibiotics and other biologically
active compounds (2). The
members of this enzyme family show a new type of protein fold with a unique
α-β-β-α architecture
(3) and were therefore termed
ABBA prenyltransferases (1).
Only 13 members of this family can be identified by sequence similarity
searches in the data base at present, and only four of them have been
investigated biochemically
(3–6).
Up to now, only phenolic compounds have been identified as aromatic substrates
of ABBA prenyltransferases. We now report the discovery of a new member of the
ABBA prenyltransferase family, catalyzing the transfer of a dimethylallyl
moiety to C-9 of 5,10-dihydrophenazine 1-carboxylate
(dihydro-PCA).2
Streptomyces strains produce many of prenylated phenazines as natural
products. For the first time, the present paper reports the identification of
a prenyltransferase involved in their biosynthesis.Streptomyces anulatus 9663, isolated from the intestine of
different arthropods, produces several prenylated phenazines, among them
endophenazine A and B (Fig.
1A) (7).
We wanted to investigate which type of prenyltransferase might catalyze the
prenylation reaction in endophenazine biosynthesis. In streptomycetes and
other microorganisms, genes involved in the biosynthesis of a secondary
metabolite are nearly always clustered in a contiguous DNA region. Therefore,
the prenyltransferase of endophenazine biosynthesis was expected to be
localized in the vicinity of the genes for the biosynthesis of the phenazine
core (i.e. of PCA).Open in a separate windowFIGURE 1.A, prenylated phenazines from S. anulatus 9663.
B, biosynthetic gene cluster of endophenazine A.In Pseudomonas, an operon of seven genes named phzABCDEFG
is responsible for the biosynthesis of PCA
(8). The enzyme PhzC catalyzes
the condensation of phosphoenolpyruvate and erythrose-4-phosphate
(i.e. the first step of the shikimate pathway), and further enzymes
of this pathway lead to the intermediate chorismate. PhzD and PhzE catalyze
the conversion of chorismate to 2-amino-2-deoxyisochorismate and the
subsequent conversion to 2,3-dihydro-3-hydroxyanthranilic acid, respectively.
These reactions are well established biochemically. Fewer data are available
about the following steps (i.e. dimerization of
2,3-dihydro-3-hydroxyanthranilic acid, several oxidation reactions, and a
decarboxylation, ultimately leading to PCA via several instable
intermediates). From Pseudomonas, experimental data on the role of
PhzF and PhzA/B have been published
(8,
9), whereas the role of PhzG is
yet unclear. Surprisingly, the only gene cluster for phenazine biosynthesis
described so far from streptomycetes
(10) was found not to contain
a phzF orthologue, raising the question of whether there may be
differences in the biosynthesis of phenazines between Pseudomonas and
Streptomyces.Screening of a genomic library of the endophenazine producer strain S.
anulatus now allowed the identification of the first complete gene
cluster of a prenylated phenazine, including the structural gene of
dihydro-PCA dimethylallyltransferase. 相似文献
5.
6.
Roujian Lu Yong Li Youwen Zhang Yunjia Chen Angela D. Shields Danny G. Winder Timothy Angelotti Kai Jiao Lee E. Limbird Yi Zhou Qin Wang 《The Journal of biological chemistry》2009,284(19):13233-13243
Although ligand-selective regulation of G protein-coupled receptor-mediated
signaling and trafficking are well documented, little is known about whether
ligand-selective effects occur on endogenous receptors or whether such effects
modify the signaling response in physiologically relevant cells. Using a gene
targeting approach, we generated a knock-in mouse line, in which N-terminal
hemagglutinin epitope-tagged α2A-adrenergic receptor (AR)
expression was driven by the endogenous mouse α2AAR gene
locus. Exploiting this mouse line, we evaluated α2AAR
trafficking and α2AAR-mediated inhibition of Ca2+
currents in native sympathetic neurons in response to clonidine and
guanfacine, two drugs used for treatment of hypertension, attention deficit
and hyperactivity disorder, and enhancement of analgesia through actions on
the α2AAR subtype. We discovered a more rapid desensitization
of Ca2+ current suppression by clonidine than guanfacine, which
paralleled a more marked receptor phosphorylation and endocytosis of
α2AAR evoked by clonidine than by guanfacine.
Clonidine-induced α2AAR desensitization, but not receptor
phosphorylation, was attenuated by blockade of endocytosis with concanavalin
A, indicating a critical role for internalization of α2AAR in
desensitization to this ligand. Our data on endogenous receptor-mediated
signaling and trafficking in native cells reveal not only differential
regulation of G protein-coupled receptor endocytosis by different ligands, but
also a differential contribution of receptor endocytosis to signaling
desensitization. Taken together, our data suggest that these
HA-α2AAR knock-in mice will serve as an important model in
developing ligands to favor endocytosis or nonendocytosis of receptors,
depending on the target cell and pathophysiology being addressed.G protein-coupled receptors
(GPCRs)4 represent the
largest family of cell surface receptors mediating responses to hormones,
cytokines, neurotransmitters, and therapeutic agents
(1). In addition to regulating
downstream signaling, ligand binding to a receptor can initiate
phosphorylation of the active conformation of the receptor by G protein
receptor kinases (GRKs) and subsequent binding of arrestins, thus restricting
the magnitude and duration of the ligand-evoked signaling responses
(2,
3). Binding of arrestins to
GPCRs also leads to GPCR internalization
(4,
5), a process that has been
proposed as a means to desensitize receptor signaling at the cell surface,
resensitize receptors, and/or initiate intracellular signaling
(6,
7).Different ligands are able to induce distinct signaling and internalization
profiles of the same receptor
(8-14).
However, the lack of available tools to study trafficking of endogenous GPCRs
in native target cells has limited our understanding of ligand-selective
endocytosis profiles and the relative contribution of receptor endocytosis to
desensitization in native biological settings.To specifically test hypotheses regarding ligand-selective effects on GPCR
internalization, and functional consequences of this trafficking on signaling,
we utilized a homologous recombination gene targeting strategy to introduce a
hemagglutinin (HA) epitope-tagged wild type α2A-adrenergic
receptor (AR) into the mouse ADRA2A gene locus
(“knock-in”). The α2AAR is a prototypical GPCR
that couples to the Gi/o subfamily of G proteins
(15). Studies on genetically
engineered mice made null or mutant for the α2AAR have
revealed that this subtype mediates the therapeutic effects of
α2-adrenergic agents on blood pressure, pain perception,
volatile anesthetic sparing, analgesia, and working memory enhancement
(16-18).
Two classic α2-ligands, clonidine and guanfacine, have been
widely used to treat hypertension
(19), attention deficit and
hyperactivity disorder (20),
and to elicit analgesia (19,
21) mediated via the
α2AAR. Clinically guanfacine has a much longer duration of
action than clonidine
(22-24);
this longer duration of action cannot be accounted for by the pharmacokinetic
profile of these agents in human beings, as both drugs have a half-life of
12-14 h (25,
26). Because ligand-induced
desensitization and trafficking of GPCRs have been implicated as critical
mechanisms for modulating response duration in vivo
(3), one hypothesis underlying
the difference in duration between clonidine and guanfacine is that clonidine
provokes accelerated desensitization of the α2AAR via one or
several mechanisms, whereas guanfacine does not. Signaling desensitization in
response to these two agonists has not been compared under the same
experimental settings. To specifically test this hypothesis, we have exploited
our HA-α2AAR knock-in mice so that we could examine these
properties of guanfacine and clonidine in native target cells.We compared internalization of the α2AAR and inhibition of
Ca2+ currents induced by clonidine and guanfacine in primary
superior cervical ganglia (SCG) neurons, where the α2AAR is
the major adrenergic receptor subtype controlling norepinephrine release and
sympathetic tone (17,
27). Our data revealed a
differential regulation of α2AAR trafficking and signaling
duration by clonidine versus guanfacine, i.e. clonidine
induced a more dramatic desensitization of the α2AAR than
guanfacine, and this desensitization was largely because of
α2AAR internalization. These studies reveal the powerful tool
that the HA-α2AAR knock-in mice provide for identifying
endocytosis-dependent and -independent physiological phenomena for this
receptor subtype as a first step in defining novel loci for therapeutic
intervention in the α2AAR signaling/trafficking cascade. 相似文献
7.
Victoria L Alonso Carla Ritagliati Pamela Cribb Esteban C Serra 《Memórias do Instituto Oswaldo Cruz》2014,109(8):1081-1085
We present here three expression plasmids for Trypanosoma cruzi
adapted to the Gateway® recombination cloning system. Two of
these plasmids were designed to express trypanosomal proteins fused to a double tag
for tandem affinity purification (TAPtag). The TAPtag and Gateway®
cassette were introduced into an episomal (pTEX) and an integrative (pTREX) plasmid.
Both plasmids were assayed by introducing green fluorescent protein (GFP) by
recombination and the integrity of the double-tagged protein was determined by
western blotting and immunofluorescence microscopy. The third Gateway adapted vector
assayed was the inducible pTcINDEX. When tested with GFP,
pTcINDEX-GW showed a good response to tetracycline, being less
leaky than its precursor (pTcINDEX). 相似文献
8.
Haihong Zong Claire C. Bastie Jun Xu Reinhard Fassler Kevin P. Campbell Irwin J. Kurland Jeffrey E. Pessin 《The Journal of biological chemistry》2009,284(7):4679-4688
Integrin receptor plays key roles in mediating both inside-out and
outside-in signaling between cells and the extracellular matrix. We have
observed that the tissue-specific loss of the integrin β1 subunit in
striated muscle results in a near complete loss of integrin β1 subunit
protein expression concomitant with a loss of talin and to a lesser extent, a
reduction in F-actin content. Muscle-specific integrin β1-deficient mice
had no significant difference in food intake, weight gain, fasting glucose,
and insulin levels with their littermate controls. However, dynamic analysis
of glucose homeostasis using euglycemichyperinsulinemic clamps demonstrated a
44 and 48% reduction of insulin-stimulated glucose infusion rate and glucose
clearance, respectively. The whole body insulin resistance resulted from a
specific inhibition of skeletal muscle glucose uptake and glycogen synthesis
without any significant effect on the insulin suppression of hepatic glucose
output or insulin-stimulated glucose uptake in adipose tissue. The reduction
in skeletal muscle insulin responsiveness occurred without any change in GLUT4
protein expression levels but was associated with an impairment of the
insulin-stimulated protein kinase B/Akt serine 473 phosphorylation but not
threonine 308. The inhibition of insulin-stimulated serine 473 phosphorylation
occurred concomitantly with a decrease in integrin-linked kinase expression
but with no change in the mTOR·Rictor·LST8 complex (mTORC2).
These data demonstrate an in vivo crucial role of integrin β1
signaling events in mediating cross-talk to that of insulin action.Integrin receptors are a large family of integral membrane proteins
composed of a single α and β subunit assembled into a heterodimeric
complex. There are 19 α and 8 β mammalian subunit isoforms that
combine to form 25 distinct α,β heterodimeric receptors
(1-5).
These receptors play multiple critical roles in conveying extracellular
signals to intracellular responses (outside-in signaling) as well as altering
extracellular matrix interactions based upon intracellular changes (inside-out
signaling). Despite the large overall number of integrin receptor complexes,
skeletal muscle integrin receptors are limited to seven α subunit
subtypes (α1, α3, α4, α5, α6, α7, and
αν subunits), all associated with the β1 integrin subunit
(6,
7).Several studies have suggested an important cross-talk between
extracellular matrix and insulin signaling. For example, engagement of β1
subunit containing integrin receptors was observed to increase
insulin-stimulated insulin receptor substrate
(IRS)2
phosphorylation, IRS-associated phosphatidylinositol 3-kinase, and activation
of protein kinase B/Akt
(8-11).
Integrin receptor regulation of focal adhesion kinase was reported to modulate
insulin stimulation of glycogen synthesis, glucose transport, and cytoskeleton
organization in cultured hepatocytes and myoblasts
(12,
13). Similarly, the
integrin-linked kinase (ILK) was suggested to function as one of several
potential upstream kinases that phosphorylate and activate Akt
(14-18).
In this regard small interfering RNA gene silencing of ILK in fibroblasts and
conditional ILK gene knockouts in macrophages resulted in a near complete
inhibition of insulin-stimulated Akt serine 473 (Ser-473) phosphorylation
concomitant with an inhibition of Akt activity and phosphorylation of Akt
downstream targets (19).
However, a complex composed of mTOR·Rictor·LST8 (termed mTORC2)
has been identified in several other studies as the Akt Ser-473 kinase
(20,
21). In addition to Ser-473,
Akt protein kinase activation also requires phosphorylation on threonine 308
Thr-30 by phosphoinositide-dependent protein kinase, PDK1
(22-24).In vivo, skeletal muscle is the primary tissue responsible for
postprandial (insulin-stimulated) glucose disposal that results from the
activation of signaling pathways leading to the translocation of the
insulin-responsive glucose transporter, GLUT4, from intracellular sites to the
cell surface membranes (25,
26). Dysregulation of any step
of this process in skeletal muscle results in a state of insulin resistance,
thereby predisposing an individual for the development of diabetes
(27-33).
Although studies described above have utilized a variety of tissue culture
cell systems to address the potential involvement of integrin receptor
signaling in insulin action, to date there has not been any investigation of
integrin function on insulin action or glucose homeostasis in vivo.
To address this issue, we have taken advantage of Cre-LoxP technology to
inactivate the β1 integrin receptor subunit gene in striated muscle. We
have observed that muscle creatine kinase-specific integrin β1 knock-out
(MCKItgβ1 KO) mice display a reduction of insulin-stimulated glucose
infusion rate and glucose clearance. The impairment of insulin-stimulated
skeletal muscle glucose uptake and glycogen synthesis resulted from a decrease
in Akt Ser-473 phosphorylation concomitant with a marked reduction in ILK
expression. Together, these data demonstrate an important cross-talk between
integrin receptor function and insulin action and suggests that ILK may
function as an Akt Ser-473 kinase in skeletal muscle. 相似文献
9.
10.
11.
12.
13.
Zhang L Kinkelaar D Huang Y Li Y Li X Wang HH 《Applied and environmental microbiology》2011,77(20):7134-7141
The rapid emergence of antibiotic resistance (AR) is a major public health concern. Recent findings on the prevalence of food-borne antibiotic-resistant (ART) commensal bacteria in ready-to-consume food products suggested that daily food consumption likely serves as a major avenue for dissemination of ART bacteria from the food chain to human hosts. To properly assess the impact of various factors, including the food chain, on AR development in hosts, it is important to determine the baseline of ART bacteria in the human gastrointestinal (GI) tract. We thus examined the gut microbiota of 16 infant subjects, from the newborn stage to 1 year of age, who fed on breast milk and/or infant formula during the early stages of development and had no prior exposure to antibiotics. Predominant bacterial populations resistant to several antibiotics and multiple resistance genes were found in the infant GI tracts within the first week of age. Several ART population transitions were also observed in the absence of antibiotic exposure and dietary changes. Representative AR gene pools including tet(M), ermB, sul2, and bla(TEM) were detected in infant subjects. Enterococcus spp., Staphylococcus spp., Klebsiella spp., Streptococcus spp., and Escherichia coli/Shigella spp. were among the identified AR gene carriers. ART bacteria were not detected in the infant formula and infant foods examined, but small numbers of skin-associated ART bacteria were found in certain breast milk samples. The data suggest that the early development of AR in the human gut microbiota is independent of infants' exposure to antibiotics but is likely impacted by exposure to maternal and environmental microbes during and after delivery and that the ART population is significantly amplified within the host even in the absence of antibiotic selective pressure. 相似文献
14.
15.
16.
17.
Irmgard Paris Carolina Perez-Pastene Eduardo Couve Pablo Caviedes Susan LeDoux Juan Segura-Aguilar 《The Journal of biological chemistry》2009,284(20):13306-13315
Parkinsonism is one of the major neurological symptoms in Wilson disease,
and young workers who worked in the copper smelting industry also developed
Parkinsonism. We have reported the specific neurotoxic action of
copper·dopamine complex in neurons with dopamine uptake.
Copper·dopamine complex (100 μm) induces cell death in
RCSN-3 cells by disrupting the cellular redox state, as demonstrated by a
1.9-fold increase in oxidized glutathione levels and a 56% cell death
inhibition in the presence of 500 μm ascorbic acid; disruption
of mitochondrial membrane potential with a spherical shape and well preserved
morphology determined by transmission electron microscopy; inhibition (72%,
p < 0.001) of phosphatidylserine externalization with 5
μm cyclosporine A; lack of caspase-3 activation; formation of
autophagic vacuoles containing mitochondria after 2 h; transfection of cells
with green fluorescent protein-light chain 3 plasmid showing that 68% of cells
presented autophagosome vacuoles; colocalization of positive staining for
green fluorescent protein-light chain 3 and Rhod-2AM, a selective indicator of
mitochondrial calcium; and DNA laddering after 12-h incubation. These results
suggest that the copper·dopamine complex induces mitochondrial
autophagy followed by caspase-3-independent apoptotic cell death. However, a
different cell death mechanism was observed when 100 μm
copper·dopamine complex was incubated in the presence of 100
μm dicoumarol, an inhibitor of NAD(P)H quinone:oxidoreductase
(EC 1.6.99.2, also known as DT-diaphorase and NQ01), because a more extensive
and rapid cell death was observed. In addition, cyclosporine A had no effect
on phosphatidylserine externalization, significant portions of compact
chromatin were observed within a vacuolated nuclear membrane, DNA laddering
was less pronounced, the mitochondria morphology was more affected, and the
number of cells with autophagic vacuoles was a near 4-fold less.A possible role of copper in the neurodegeneration of dopaminergic neurons
is supported by the fact that patients with neurological Wilson disease, a
copper deposition disorder, display a number of extrapyramidal motor symptoms,
including Parkinsonism. The cerebral manifestations in neurological Wilson
disease are expressed as bradykinesia, rigidity, tremor, dyskinesia, and
dysarthria (1). It has been
proposed that neurological Wilson disease can be assigned to the group of
secondary Parkinsonian syndromes
(2). Interestingly, young
workers who worked in the copper smelting industry also developed Parkinsonism
(3).Studies performed in rats showed copper (Cu2+)-induced
degeneration of dopaminergic neurons in the nigrostriatal system. Likewise, it
was described that copper neurotoxicity in rat substantia nigra and striatum
is dependent on NAD(P)H dehydrogenase inhibition
(4,
5). All of these results
support a possible role for copper in the neurodegeneration of dopaminergic
neurons.The general mechanism of toxicity, induced by the reduced form of copper
(Cu+) catalyzing the formation of hydroxyl radicals in the presence
of hydrogen peroxide through the Fenton reaction, cannot explain the specific
degeneration of dopaminergic neurons in Parkinsonism induced in neurological
Wilson disease, or in miners working in the copper smelting industry. The
selective action of copper can be explained by the ability of copper to form a
complex with dopamine, allowing this metal to be transported by cells that
have the ability to take up dopamine
(6). This specific neurotoxic
action of copper in neurons with dopamine uptake is dependent on (i) the
ability of copper to form a complex with dopamine
(Cu·DA)2
(6,
7), (ii) uptake of Cu·DA
complex by dopamine transporters, (iii) oxidation of dopamine to aminochrome,
and (iv) one-electron reduction of aminochrome by inhibiting NAD(P)H
dehydrogenase (6). These
findings may explain the selective neurotoxic action of copper in the brain,
but they do not explain the cell death mechanism.Currently, cell death is divided into three categories: apoptosis,
autophagy, and necrosis. At the current time, only apoptosis and autophagic
cell death are generally accepted as being legitimate forms of programmed cell
death. Alternative models of cell death have therefore been proposed,
including para-apoptosis, mitotic catastrophe, oncosis, and pyroptosis
(8–12).
Necrosis is characterized mostly by the absence of caspase activation,
cytochrome c release, and DNA oligonucleosomal fragmentation.
Apoptotic cells are characterized by the formation of blebs, chromatin
condensation, DNA oligonucleosomal fragmentation, and exposure of
phosphatidylserine on the external membrane. This mode of cell death can be
dependent or independent of activation of caspases
(13). On the other hand,
autophagy can be distinguished from apoptosis by sequestration of bulk
cytoplasm and organelles in double or multimembrane autophagic vacuoles that
then fuse with the lysosomal system. Some of these described mechanisms are
related to neurological diseases such as Parkinson disease
(14,
15). Cells can use different
methods to activate their own destruction, and more than one death program may
be activated at the same time
(16,
17).The purpose of this study was to examine the Cu·DA complex-induced
cell death mechanism in RCSN-3 cells, a cell line that expresses dopamine,
norepinephrine, and serotonin transporters
(18,
19). 相似文献
18.
To the memory of William Ronald Sendall
Sternaspid polychaetes are common and often abundant in soft bottoms in the world oceans. Some authors suggest that only one species should be recognized, whereas others regard a few species as widely distributed in many seas and variable depths from the low intertidal to about 4400 m. There are some problems with species delineation and the distinctive ventro-caudal shield has been disregarded or barely used for identifying species. In order to clarify these issues, the ventral shield is evaluated in specimens from the same locality and its diagnostic potential is confirmed. On this basis, a revision of Sternaspis Otto, 1821 (Polychaeta: Sternaspidae) is presented based upon type materials, or material collected from type localities. The sternaspid body, introvert hooks and shield show three distinct patterns, two genera have seven abdominal segments and tapered introvert hooks, and one genus has eight abdominal segments and spatulate introvert hooks. The ventro-caudal shield has three different patterns: stiff with ribs, and sometimes concentric lines, stiff with feebly-defined ribs but no concentric lines, and soft with firmly adhered sediment particles. Sternaspis is restricted to include species with seven abdominal segments, falcate introvert hooks, and stiff shields, often exhibiting radial ribs, concentric lines or both. Sternaspis includes, besides the type species, Sternaspis thalassemoides Otto, 1821 from the Mediterranean Sea, Sternaspis affinis Stimpson, 1864 from the Northeastern Pacific, Sternaspis africana Augener, 1918, stat. n. from Western Africa, Sternaspis andamanensis
sp. n. from the Andaman Sea, Sternaspis costata von Marenzeller, 1879 from Japan, Sternaspis fossor Stimpson, 1853 from the Northwestern Atlantic, Sternaspis islandica Malmgren, 1867 from Iceland, Sternaspis maior Chamberlin, 1919 from the Gulf of California, Sternaspis princeps Selenka, 1885 from New Zealand, Sternaspis rietschi Caullery, 1944 from abyssal depths around Indonesia, Sternaspis scutata (Ranzani, 1817) from the Mediterranean Sea, Sternaspis spinosa Sluiter, 1882 from Indonesia, and Sternaspis thorsoni
sp. n. from the Iranian Gulf. Two genera are newly proposed to incorporate the remaining species: Caulleryaspis and Petersenaspis. Caulleryaspis
gen. n. is defined by the presence of falcate introvert hooks, seven abdominal segments, and soft shields with sediment particles firmly adhered on them; it includes two species: Caulleryaspis gudmundssoni
sp. n. from Iceland and Caulleryaspis laevis (Caullery, 1944) comb. n. from Indonesia. Petersenaspis
gen. n. is defined by the presence of spatulate introvert hooks, eight abdominal segments, and stiff shields with poorly defined ribs but no concentric line; it includes Petersenaspis capillata (Nonato, 1966) from Brazil and Petersenaspis palpallatoci
sp. n. from the Philippines. Neotypes are proposed for eight species: Sternaspis thalassemoides, Sternaspis affinis, Sternaspis africana, Sternaspis costata, Sternaspis fossor, Sternaspis maior, Sternaspis scutata and Sternaspis spinosa, to stabilize these species-group names, and a lectotype is designated for Sternaspis laevis which is transferred to Caulleryaspis
gen. n. The geographic range of most species appears to be much smaller than previously indicated, and for some species additional material in good condition is needed to clarify their distributions. Keys to genera and to all species are also included. 相似文献
19.
Vladimir I. Razinkov Grigory B. Melikyan Richard M. Epand Raquel F. Epand Fredric S. Cohen 《The Journal of general physiology》1998,112(4):409-422
Cells expressing the hemagglutinin protein of influenza virus were fused to planar bilayer membranes containing the fluorescent lipid probes octadecylrhodamine (R18) or indocarbocyanine (DiI) to investigate whether spontaneous curvature of each monolayer of a target membrane affects the growth of fusion pores.
R18 and DiI lowered the transition temperatures for formation of an inverted hexagonal phase, indicating that
these probes facilitate the formation of negative curvature structures. The probes are known to translocate from
one monolayer of a bilayer membrane to the other in a voltage-dependent manner. The spontaneous curvature of
the cis monolayer (facing the cells) or the trans monolayer could therefore be made more negative through control of the polarity of voltage across the planar membrane. Electrical admittance measurements showed that the
open times of flickering fusion pores were shorter when probes were in trans monolayers and longer when in cis
monolayers compared with times when probe was symmetrically distributed. Open times were the same for probe
symmetrically distributed as when probes were not present. Thus, open times were a function of the asymmetry of
the spontaneous curvature between the trans and cis monolayers. Enriching the cis monolayer with a negative curvature probe reduced the probability that a small pore would fully enlarge, whereas enriching the trans monolayer
promoted enlargement. Lysophosphatidylcholine has positive spontaneous curvature and does not translocate.
When lysophosphatidylcholine was placed in trans leaflets of planar membranes, closing of fusion pores was rare.
The effects of the negative and positive spontaneous curvature probes do not support the hypothesis that a flickering pore closes from an open state within a hemifusion diaphragm (essentially a “flat” structure). Rather, such effects support the hypothesis that the membrane surrounding the open pore forms a three-dimensional hourglass
shape from which the pore flickers shut. 相似文献
20.
Uridine 5′-diphosphate-glucose (UDP-Glc) is transported into the lumen of the Golgi cisternae, where is used for polysaccharide biosynthesis. When Golgi vesicles were incubated with UDP-[3H]Glc, [3H]Glc was rapidly transferred to endogenous acceptors and UDP-Glc was undetectable in Golgi vesicles. This result indicated that a uridine-containing nucleotide was rapidly formed in the Golgi vesicles. Since little is known about the fate of the nucleotide derived from UDP-Glc, we analyzed the metabolism of the nucleotide moiety of UDP-Glc by incubating Golgi vesicles with [α-32P]UDP-Glc, [β-32P]UDP-Glc, and [3H]UDP-Glc and identifying the resulting products. After incubation of Golgi vesicles with these radiolabeled substrates we could detect only uridine 5′-monophosphate (UMP) and inorganic phosphate (Pi). UDP could not be detected, suggesting a rapid hydrolysis of UDP by the Golgi UDPase. The by-products of UDP hydrolysis, UMP and Pi, did not accumulate in the lumen, indicating that they were able to exit the Golgi lumen. The exit of UMP was stimulated by UDP-Glc, suggesting the presence of a putative UDP-Glc/UMP antiporter in the Golgi membrane. However, the exit of Pi was not stimulated by UDP-Glc, suggesting that the exit of Pi occurs via an independent membrane transporter. 相似文献