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1.
In the giant-celled marine algae Valonia utricularis the turgor-sensing mechanism of the plasmalemma and the role of the tonoplast in turgor regulation is unknown because of
the lack of solid data about the individual electrical properties of the plasmalemma and the vacuolar membrane. For this reason,
a vacuolar perfusion technique was developed that allowed controlled manipulation of the vacuolar sap under turgescent conditions
(up to about 0.3 MPa). Charge-pulse relaxation studies on vacuolarly perfused cells at different turgor pressure values showed
that the area-specific resistance of the total membrane barrier (tonoplast and plasmalemma) exhibited a similar dependence
on turgor pressure as reported in the literature for nonperfused cells: the resistance assumed a minimum value at the physiological
turgor pressure of about 0.1 MPa. The agreement of the data suggested that the perfusion process did not alter the transport
properties of the membrane barrier.
Addition of 16 μm of the H+-carrier FCCP (carbonylcyanide p-trifluoromethoxyphenyhydrazone) to the perfusion solution resulted in a drop of the total membrane potential from +4 mV to
−22 mV and in an increase of the area-specific membrane resistance from 6.8 × 10−2 to 40.6 × 10−2Ωm2. The time constants of the two exponentials of the charge pulse relaxation spectrum increased significantly. These results
are inconsistent with the assumption of a high-conductance state of the tonoplast (R. Lainson and C.P. Field, J. Membrane Biol.
29:81–94, 1976).
Depending on the site of addition, the pore-forming antibiotics nystatin and amphotericin B affected either the time constant
of the fast or of the slow relaxation (provided that the composition of the perfusion solution and the artificial sea water
were replaced by a cytoplasma-analogous medium). When 50 μm of the antibiotics were added externally, the fast relaxation process disappeared. Contrastingly, the slow relaxation process
disappeared upon vacuolar addition. The antibiotics cannot penetrate biomembranes rapidly, and therefore, the findings suggested
that the fast and slow relaxations originated exclusively from the electrical properties of the plasmalemma and the tonoplast
respectively. This interpretation implies that the area-specific resistance of the tonoplast is significantly larger than
that of the plasmalemma (consistent with the FCCP data) and that the area-specific capacitance of the tonoplast is unusually
high (6.21 × 10−2 Fm−2 compared to 0.77 × 10−2 Fm−2 of the plasmalemma). Thus, we have to assume that the vacuolar membrane of V. utricularis is highly folded (by a factor of about 9 in relation to the geometric area) and/or contains a fairly high concentration of
mobile charges of an unknown electrogenic ion carrier system.
Received: 22 October 1996/Revised: 16 January 1997 相似文献
2.
Seedling roots of corn were treated with different concentrations of mannitol-containing solution for 1 to 1.5 hr, and net
fluxes of Ca2+ and H+ were measured in the elongation region. H+ fluxes were much more sensitive to osmotic pressure than were Ca2+ fluxes. Oscillations of 7-min period in H+ flux, normally observed in the control, were almost fully suppressed at high osmotic concentrations. Net H+ flux was shifted from average efflux of 25 ± 3 nmol m−2 sec−1 to average influx of 10 ± 5 nmol m−2 sec−1 after the incubation in 100 mm mannitol. The larger the osmotic concentration, the larger was the H+ influx. This flux caused the unbuffered solution of pH 4.85 to change to pH 5.3 after mannitol application. It appears that
the osmoticum suppresses oscillatory H+ extrusion at the plasma membrane. Discrete Fourier Transforms of the H+ flux data showed that, apart from suppression of the 7-min oscillations in H+ flux, mannitol also promoted the appearance of faster 2-min oscillations. Ca2+ influx slightly increased after mannitol treatment. In addition the 7-min oscillatory component of Ca2+ flux remained apparent thereby showing independence of H+ flux.
Received: 25 April 1997/Revised: 11 August 1997 相似文献
3.
A Patch-Clamp Study of Ion Channels in Protoplasts Prepared from the Marine Alga Valonia utricularis
The giant marine alga Valonia utricularis is a classical model system for studying the electrophysiology and water relations of plant cells by using microelectrode
and pressure probe techniques. The recent finding that protoplasts can be prepared from the giant ``mother cells' (Wang,
J., Sukhorukov, V.L., Djuzenova, C.S., Zimmermann, U., Müller, T., Fuhr, G., 1997, Protoplasma
196:123–134) allowed the use of the patch-clamp technique to examine ion channel activity in the plasmalemma of this species.
Outside-out and cell-attached experiments displayed three different types of voltage-gated Cl− channels (VAC1, VAC2, VAC3, Valonia Anion Channel 1,2,3), one voltage-gated K+ channel (VKC1, Valonia K
+
Channel 1) as well as stretch-activated channels. In symmetrical 150 mm Cl− media, VAC1 was most frequently observed and had a single channel conductance of 36 ± 7 pS (n= 4) in the outside-out and 33 ± 5 pS (n= 10) in the cell-attached configuration. The reversal potential of the corresponding current-voltage curves was within 0
± 4 mV (n= 4, outside-out) and 9 ± 7 mV (n= 10, cell-attached) close to the Nernst potential of Cl− and shifted towards more negative values when cell-attached experiments were performed in asymmetrical 50:150 mm Cl− media (bath/pipette; E
Cl−
−20 ± 7 mV (n= 4); Nernst potential −28 mV). Consistent with a selectivity for Cl−, VAC1 was inhibited by 100 μM DIDS (4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid). VAC1 was activated by a hyperpolarization of the patch. Boltzmann
fits of the channel activity under symmetrical 150 mm Cl− conditions yielded a midpoint potential of −12 ± 5 mV (n= 4, outside-out) and −3 ± 6 mV (n= 9, cell-attached) and corresponding apparent minimum gating charges of 15 ± 3 (n= 4) and 18 ± 5 (n= 9). The midpoint potential shifted to more negative values in the presence of a Cl− gradient.
VAC2 was activated by voltages more negative than E
Cl−
and was always observed together with VAC1, but less frequently. It showed a ``flickering' gating. The single channel conductance
was 99 ± 10 pS (n= 6). VAC3 was activated by membrane depolarization and frequently exhibited several subconductance states. The single channel
conductance of the main conductance state was 36 ± 5 pS (n= 5). VKC1 was also activated by positive clamped voltages. Up to three conductance states occurred whereby the main conductance
state had a single channel conductance of 124 ± 27 pS (n= 6).
In the light of the above results it seems to be likely that VAC1 contributes mainly to the Cl− conductance of the plasmalemma of the turgescent ``mother cells' and that this channel (as well as VAC2) can operate in
the physiological membrane potential range. The physiological significance of VAC3 and VKC1 is unknown, but may be related
(as the stretch-activated channels) to processes involved in turgor regulation.
Received: 24 June 1999/Revised: 2 September 1999 相似文献
4.
5.
Stimulation with leukotriene D4 (LTD4) (3–100 nm) induces a transient increase in the free intracellular Ca2+ concentration ([Ca2+]
i
) in Ehrlich ascites tumor cells. The LTD4-induced increase in [Ca2+]
i
is, however, significantly reduced in Ca2+-free medium (2 mm EGTA), and under these conditions stimulation with a low LTD4 concentration (3 nm) does not result in any detectable increase in [Ca2+]
i
. Addition of LTD4 (3–100 nm) moreover accelerates the KCl loss seen during Regulatory Volume Decrease (RVD) in cells suspended in a hypotonic medium.
The LTD4-induced (100 nm) acceleration of the RVD response is also seen in Ca2+-free medium and also at 3 nm LTD4, indicating that LTD4 can open K+- and Cl−-channels without any detectable increase in [Ca2+]
i
. Buffering cellular Ca2+ with BAPTA almost completely blocks the LTD4-induced (100 nm) acceleration of the RVD response. Thus, the reduced [Ca2+]
i
level after BAPTA-loading or buffering of [Ca2+]
i
seems to inhibit the LTD4-induced stimulation of the RVD response even though the LTD4-induced cell shrinkage is not necessarily preceded by any detectable increase in [Ca2+]
i
. The LTD4 receptor antagonist L649,923 (1 μm) completely blocks the LTD4-induced increase in [Ca2+]
i
and inhibits the RVD response as well as the LTD4-induced acceleration of the RVD response. When the LTD4 receptor is desensitized by preincubation with 100 nm LTD4, a subsequent RVD response is strongly inhibited. In conclusion, the present study supports the notion that LTD4 plays a role in the activation of the RVD response. LTD4 seems to activate K+ and Cl− channels via stimulation of a LTD4 receptor with no need for a detectable increase in [Ca2+]
i
.
Received: 25 September 1995/Revised: 25 January 1996 相似文献
6.
Phylogenetic studies based on DNA sequences typically ignore the potential occurrence of recombination, which may produce different alignment regions with different evolutionary histories. Traditional phylogenetic methods assume that a single history underlies the data. If recombination is present, can we expect the inferred phylogeny to represent any of the underlying evolutionary histories? We examined this question by applying traditional phylogenetic reconstruction methods to simulated recombinant sequence alignments. The effect of recombination on phylogeny estimation depended on the relatedness of the sequences involved in the recombinational event and on the extent of the different regions with different phylogenetic histories. Given the topologies examined here, when the recombinational event was ancient, or when recombination occurred between closely related taxa, one of the two phylogenies underlying the data was generally inferred. In this scenario, the evolutionary history corresponding to the majority of the positions in the alignment was generally recovered. Very different results were obtained when recombination occurred recently among divergent taxa. In this case, when the recombinational breakpoint divided the alignment in two regions of similar length, a phylogeny that was different from any of the true phylogenies underlying the data was inferred. 相似文献
7.
Inward-rectifying potassium channels in plant cells provide important mechanisms for low-affinity K+ uptake and membrane potential control in specific cell types, including guard cells, pulvinus cells, aleurone cells and root
hair cells. K+ channel blockers are potent tools for studying the physiological functions and structural properties of K+ channels. In the present study the structural and biophysical mechanisms of Cs+ and TEA+ block of a cloned Arabidopsis inward-rectifying K+ channel (KAT1) were analyzed. Effects of the channel blockers Cs+ and TEA+ were characterized both extracellularly and intracellularly. Both external Cs+ and TEA+ block KAT1 currents. A mutant of KAT1 (``m2KAT1'; H267T, E269V) was produced by site-directed mutagenesis of two amino acid
residues in the C-terminal portion of the putative pore (P) domain. This mutant channel was blocked less by external Cs+ and TEA+ than the wild-type K+ channel. Internal TEA+ and Cs+ did not significantly block either m2KAT1 or KAT1 channels. Other properties, such as cation selectivity, voltage-dependence
and proton activation did not show large changes between m2KAT1 and KAT1, demonstrating the specificity of the introduced
mutations. These data suggest that the amino acid positions mutated in the inward-rectifying K+ channel, KAT1, are accessible to external blockers and may be located on the external side of the membrane, as has been suggested
for outward-rectifying K+ channels.
Received: 31 July 1995/Revised: 5 January 1996 相似文献
8.
Niji Ohta Naoki Sato Hisayoshi Nozaki Tsuneyoshi Kuroiwa 《Journal of molecular evolution》1997,45(6):688-695
The nucleotide sequence of a cluster of ribosomal protein genes in the plastid genome of a unicellular red alga, Cyanidioschyzon merolae, which has been supposed to be the most primitive alga, was determined. The phylogenetic tree inferred from the amino acid
sequence of ribosomal proteins of two rhodophytes, a chromophyte, a glaucophyte, two chlorophytes (land plants), a cyanobacterium,
and three eubacteria suggested a close relationship between the cyanobacterium Synechocystis PCC6803 and the plastids of various species in the kingdom Plantae, which is consistent with the hypothesis of the endosymbiotic
origin of plastids. In this tree, the two species of rhodophytes were grouped with the chromophyte, and the glaucophyte was
grouped with the chlorophytes. Analysis of the organization of the genes encoding the ribosomal proteins suggested that the
translocation of the str cluster occurred early in the lineage of rhodophytes and chromophytes after these groups had been separated from chlorophytes
and glaucophytes.
Received: 2 June 1997 / Accepted: 15 July 1997 相似文献
9.
The current-voltage (I/V) profiles of Ventricaria (formerly Valonia) membranes were measured at a range of external potassium concentrations, [K+]
o
, from 0.1 to 100 mm. The conductance-voltage (G/V) characteristics were computed to facilitate better resolution of the profile change with time after exposure to different
[K+]
o
. The resistance-voltage (R/V) characteristics were computed to attempt resolution of plasmalemma and tonoplast. Four basic electrophysiological stages
emerged: (1) Uniform low resistance between −60 and +60 mV after the cell impalement. (2) High resistance between +50 and
+150 for [K+]
o
from 0.1 to 1.0 mm and hypotonic media. (3) High resistance between −150 and −20 mV for [K+]
o
of 10 mm (close to natural seawater) and hypertonic media. (4) High resistance between −150 and +170 mV at [K+]
o
of 100 mm.
The changes between these states were slow, requiring minutes to hours and sometimes exhibiting spontaneous oscillations of
the membrane p.d. (potential difference). Our analysis of the I/V data supports a previous hypothesis, that Ventricaria tonoplast is the more resistive membrane containing a pump, which transports K+ into the vacuole to regulate turgor. We associate state (1) with the plasmalemma conductance being dominant and the K+ pump at the tonoplast short-circuited probably by a K+ channel, state (2) with the K+ pump ``off' or short-circuited at p.d.s more negative than +50 mV, state (3) with the K+ pump ``on,' and state (4) with the pump dominant, but affected by high K+. A model for the Ventricaria membrane system is proposed.
Received: 5 November 1998/Revised: 11 May 1999 相似文献
10.
Péter M Varga Z Hajdu P Gáspár R Damjanovich S Horjales E Possani LD Panyi G 《The Journal of membrane biology》2001,179(1):13-25
We investigated the cytosolic free Ca2+ concentration ([Ca2+]i) of leech Retzius neurons in situ while varying the extracellular and intracellular pH as well as the extracellular ionic
strength. Changing these parameters had no significant effect on [Ca2+]i when the membrane potential of the cells was close to its resting value. However, when the cells were depolarized by raising
the extracellular K+ concentration or by applying the glutamatergic agonist kainate, extracellular pH and ionic strength markedly affected [Ca2+]i, whereas intracellular pH changes appeared to have virtually no effect. An extracellular acidification decreased [Ca2+]i, while alkalinization or reduction of the ionic strength increased it. Correspondingly, [Ca2+]i also increased when the kainate-induced extracellular acidification was reduced by raising the pH-buffering capacity. At
low extracellular pH, the membrane potential to which the cells must be depolarized to evoke a detectable [Ca2+]i increase was shifted to more positive values, and it moved to more negative values at high pH. We conclude that in leech
Retzius neurons extracellular pH, but not intracellular pH, affects [Ca2+]i by modulating Ca2+ influx through voltage-dependent Ca2+ channels. The results suggest that this modulation is mediated primarily by shifts in the surface potential at the extracellular
side of the plasma membrane.
Received: 23 January 2001/Revised: 15 June 2001 相似文献
11.
Electrical breakdown of erythrocytes induces hemoglobin release which increases markedly with decreasing conductivity of
the pulse medium. This effect presumably results from the transient, conductivity-dependent deformation forces (elongation
or compression) on the cell caused by Maxwell stress. The deformation force is exerted on the plasma membrane of the cell,
which can be viewed as a transient dipole induced by an applied DC electric field pulse. The induced dipole arises from the
free charges that accumulate at the cell interfaces via the Maxwell-Wagner polarization mechanism. The polarization response
of erythrocytes to a DC field pulse was estimated from the experimental data obtained by using two complementary frequency-domain
techniques. The response is very rapid, due to the highly conductive cytosol. Measurements of the electrorotation and electrodeformation
spectra over a wide conductivity range yielded the information and data required for the calculation of the deformation force
as a function of frequency and external conductivity and for the calculation of the transient development of the deformation
forces during the application of a DC-field pulse. These calculations showed that (i) electric force precedes and accompanies
membrane charging (up to the breakdown voltage) and (ii) that under low-conductivity conditions, the electric stretching force
contributes significantly to the enlargement of ``electroleaks' in the plasma membrane generated by electric breakdown.
Received: 12 December 1997/Revised: 13 March 1998 相似文献
12.
We investigated the cytosolic free calcium concentration ([Ca2+]i) of leech Retzius neurons in situ while varying the extracellular Ca2+ concentration via the bathing solution ([Ca2+]B). Changing [Ca2+]B had only an effect on [Ca2+]i if the cells were depolarized by raising the extracellular K+ concentration. Surprisingly, raising [Ca2+]B from 2 to 10 mm caused a decrease in [Ca2+]i, and an increase was evoked by reducing [Ca2+]B to 0.1 mm. These changes were not due to shifts in membrane potential. At low [Ca2+]B moderate membrane depolarizations were sufficient to evoke a [Ca2+]i increase, while progressively larger depolarizations were necessary at higher [Ca2+]B. The changes in the relationship between [Ca2+]i and membrane potential upon varying [Ca2+]B could be reversed by changing extracellular pH. We conclude that [Ca2+]B affects [Ca2+]i by modulating Ca2+ influx through voltage-dependent Ca2+ channels via the electrochemical Ca2+ gradient and the surface potential at the extracellular side of the plasma membrane. These two parameters are affected in
a counteracting way: Raising the extracellular Ca2+ concentration enhances the electrochemical Ca2+ gradient and hence Ca2+ influx, but it attenuates Ca2+ channel activity by shifting the extracellular surface potential to the positive direction, and vice versa.
Received: 23 January 2001/Revised: 23 June 2001 相似文献
13.
K-Cl cotransport is abnormally active in erythrocytes containing positively charged hemoglobins such as Hb S (SS: β6 Glu
→ Val) or Hb C (CC: β6 Glu → Lys). The relatively younger age of erythrocytes in these diseases cannot completely account
for the increased K-Cl cotransport activity. It has been suggested that these positively charged Hb may interact with the
K-Cl cotransport system or one of its regulators and induce changes in its functional activity. We report here data on the
volume- and pH-dependence of K-Cl cotransport in ghosts obtained from normal and sickle erythrocytes, and on the effect of
addition of either Hb A or Hb S before resealing. In erythrocyte ghosts prepared with the gel column method to contain minimal
amounts of Hb, (white ghosts, WG), K-Cl cotransport has similar magnitude in normal and sickle erythrocytes, is not inhibited
by alkaline pH and it is volume-independent. Addition of low concentrations of Hb A to WG from normal erythrocytes decreases
the magnitude of K-Cl cotransport and restores its volume dependency, but not its pH sensitivity. Addition of Hb S to WG from
either normal or sickle erythrocytes restores the volume-dependent component of K-Cl cotransport and increases the magnitude
of flux mediated by this transporter. Thus, Hb A and Hb S seem to affect in different manners the functional properties of
K-Cl cotransport.
Received: 29 May 1998/Revised: 3 November 1998 相似文献
14.
N.K. Jørgensen S. Christensen H. Harbak A.M. Brown I.H. Lambert E.K. Hoffmann L.O. Simonsen 《The Journal of membrane biology》1997,157(3):281-299
The putative role for Ca2+ entry and Ca2+ mobilization in the activation of the regulatory volume decrease (RVD) response has been assessed in Ehrlich cells. Following
hypotonic exposure (50% osmolarity) there is: (i) no increase in cellular Ins(1,4,5)P3 content, as measured in extracts from [2-3H]myoinositol-labeled cells, a finding at variance with earlier reports from our group; (ii) no evidence of Ca2+-signaling recorded in a suspension of fura-2-loaded cells; (iii) Ca2+-signaling in only about 6% of the single, fura-2-loaded cells at 1-mm Ca2+ (1% only at 0.1-mm Ca2+ and in Ca2+-free medium), as monitored by fluorescence-ratio imaging; (iv) no effect of removing external Ca2+ upon the volume-induced K+ loss; (v) no significant inhibition of the RVD response in cells loaded with the Ca2+ chelator BAPTA when the BAPTA-loading is performed in K+ equilibrium medium; (vi) an inhibition of the swelling-induced K+ loss (about 50%) at 1-mm Ba2+, but almost no effect of charybdotoxin (100 nm) or of clotrimazole (10 μm), reported inhibitors of the K+ loss induced by Ca2+-mobilizing agonists. Thus, Ca2+signaling by Ca2+ release or Ca2+ entry appears to play no role in the activation mechanism for the RVD response in Ehrlich cells.
Received: 8 December 1996/Revised: 14 January 1997 相似文献
15.
The polyamine secretagogue, aminoethyldextran (AED), causes a cortical [Ca2+] transient in Paramecium cells, as analyzed by fluorochrome imaging. Our most essential findings are: (i) Cortical Ca2+ signals also occur when AED is applied in presence of the fast Ca2+ chelator, BAPTA. (ii) Extracellular La3+ application causes within seconds a rapid, reversible fluorescence signal whose reversibility can be attributed to a physiological
[Ca2+]
i
transient (while injected La3+ causes a sustained fluorescence signal). (iii) Simply increasing [Ca2+]
o
causes a similar rapid, short-lived [Ca2+]
i
transient. All these phenomena, (i–iii), are compatible with activation of an extracellular ``Ca2+/(polyvalent cation)-sensing receptor' known from some higher eukaryotic systems, where this sensor (responding to Ca2+, La3+ and some multiply charged cations) is linked to cortical calcium stores which, thus, are activated. In Paramecium, such subplasmalemmal stores (``alveolar sacs') are physically linked to the cell membrane and they can also be activated
by the Ca2+ releasing agent, 4-chloro-m-cresol, just like in Sarcoplasmic Reticulum. Since this drug causes a cortical Ca2+ signal also in absence of Ca2+
o
we largely exclude a ``Ca2+-induced Ca2+ release' (CICR) mechanism. Our finding of increased cortical Ca2+ signals after store depletion and re-addition of extracellular Ca2+ can be explained by a ``store-operated Ca2+ influx' (SOC), i.e., a Ca2+ influx superimposing store activation. AED stimulation in presence of Mn2+
o
causes fluorescence quenching in Fura-2 loaded cells, indicating involvement of unspecific cation channels. Such channels,
known to occur in Paramecium, share some general characteristics of SOC-type Ca2+ influx channels. In conclusion, we assume the following sequence of events during AED stimulated exocytosis: (i) activation
of an extracellular Ca2+/polyamine-sensing receptor, (ii) release of Ca2+ from subplasmalemmal stores, (iii) and Ca2+ influx via unspecific cation channels. All three steps are required to produce a steep cortical [Ca2+] signal increase to a level required for full exocytosis activation. In addition, we show formation of [Ca2+] microdomains (≤0.5 μm, ≤33 msec) upon stimulation.
Received: 30 August 1999/Revised: 1 December 1999 相似文献
16.
K.D. Clark T.M. Hennessey D.L. Nelson R.R. Preston 《The Journal of membrane biology》1997,157(2):159-167
Paramecium tetraurelia responds to extracellular GTP (≥ 10 nm) with repeated episodes of prolonged backward swimming. These backward swimming events cause repulsion from the stimulus
and are the behavioral consequence of an oscillating membrane depolarization. Ion substitution experiments showed that either
Mg2+ or Na+ could support these responses in wild-type cells, with increasing concentrations of either cation increasing the extent of
backward swimming. Applying GTP to cells under voltage clamp elicited oscillating inward currents with a periodicity similar
to that of the membrane-potential and behavioral responses. These currents were also Mg2+- and Na+-dependent, suggesting that GTP acts through Mg2+-specific (I
Mg) and Na+-specific (I
Na) conductances that have been described previously in Paramecium. This suggestion is strengthened by the finding that Mg2+ failed to support normal behavioral or electrophysiological responses to GTP in a mutant that specifically lacks I
Mg (``eccentric'), while Na+ failed to support GTP responses in ``fast-2,' a mutant that specifically lacks I
Na. Both mutants responded normally to GTP if the alternative cation was provided. As I
Mg and I
Na are both Ca2+-dependent currents, the characteristic GTP behavior could result from oscillations in intracellular Ca2+ concentration. Indeed, applying GTP to cells in the absence of either Mg2+ or Na+ revealed a minor inward current with a periodicity similar to that of the depolarizations. This current persisted when known
voltage-dependent Ca2+ currents were blocked pharmacologically or genetically, which implies that it may represent the activation of a novel purinergic-receptor–coupled
Ca2+ conductance.
Received: 28 October 1996/Revised: 24 December 1996 相似文献
17.
The AAA proteins (ATPases Associated with a variety of cellular Activities) are found in eubacterial, archaebacterial, and eukaryotic species and participate in a large number of cellular
processes, including protein degradation, vesicle fusion, cell cycle control, and cellular secretory processes. The AAA proteins
are characterized by the presence of a 230 to 250-amino acid ATPase domain referred to as the Conserved ATPase Domain or CAD. Phylogenetic analysis of 133 CAD sequences from 38 species reveal that AAA CADs are organized into discrete
groups that are related not only in structure but in cellular function. Evolutionary analyses also indicate that the CAD was
present in the last common ancestor of eubacteria, archaebacteria, and eukaryotes. The eubacterial CADs are found in metalloproteases,
while CAD-containing proteins in the archaebacterial and eukaryotic lineages appear to have diversified by a series of gene
duplication events that lead to the establishment of different functional AAA proteins, including proteasomal regulatory,
NSF/Sec, and Pas proteins. The phylogeny of the CADs provides the basis for establishing the patterns of evolutionary change
that characterize the AAA proteins.
Received: 28 January 1997 / Accepted: 8 May 1997 相似文献
18.
David Posada 《Journal of molecular evolution》2001,52(5):434-444
Models of sequence evolution play an important role in molecular evolutionary studies. The use of inappropriate models of
evolution may bias the results of the analysis and lead to erroneous conclusions. Several procedures for selecting the best-fit
model of evolution for the data at hand have been proposed, like the likelihood ratio test (LRT) and the Akaike (AIC) and
Bayesian (BIC) information criteria. The relative performance of these model-selecting algorithms has not yet been studied
under a range of different model trees. In this study, the influence of branch length variation upon model selection is characterized.
This is done by simulating sequence alignments under a known model of nucleotide substitution, and recording how often this
true model is recovered by different model-fitting strategies. Results of this study agree with previous simulations and suggest
that model selection is reasonably accurate. However, different model selection methods showed distinct levels of accuracy.
Some LRT approaches showed better performance than the AIC or BIC information criteria. Within the LRTs, model selection is
affected by the complexity of the initial model selected for the comparisons, and only slightly by the order in which different
parameters are added to the model. A specific hierarchy of LRTs, which starts from a simple model of evolution, performed
overall better than other possible LRT hierarchies, or than the AIC or BIC.
Received: 2 October 2000 / Accepted: 4 January 2001 相似文献
19.
20.
Osmotic swelling of fish erythrocytes activates a broad-specificity permeation pathway that mediates the volume-regulatory
efflux of taurine and other intracellular osmolytes. This pathway is blocked by inhibitors of the erythrocyte band 3 anion
exchanger, raising the possibility that band 3 is involved in the volume-regulatory response. In this study of eel erythrocytes,
a quantitative comparison of the pharmacology of swelling-activated taurine transport with that of band 3-mediated SO2−
4 transport showed there to be significant differences between them. N-ethylmaleimide and quinine were effective inhibitors of swelling-activated taurine transport but caused little, if any, inhibition
of band 3. Conversely, DIDS was a more potent inhibitor of band 3-mediated SO2−
4 flux than of swelling-activated taurine transport. In cells in isotonic medium, pretreated then co-incubated with 0.1 mm DIDS, the band 3-mediated transport of SO2−
4 and Cl− was reduced to a low level. Exposure of these cells to a hypotonic medium containing 0.1 mm DIDS was followed by the activation of a Cl− permeation pathway showing the same inhibitor sensitivity as swelling-activated taurine transport. The data are consistent
with swelling-activated transport of taurine and Cl− being via a common pathway. A comparison of the swelling-activated transport rates for taurine and Cl− with those for several other solutes was consistent with the hypothesis that this pathway is an anion-selective channel,
similar to those that mediate the volume-regulatory efflux of Cl− and organic osmolytes from mammalian cells.
Received: 7 July 1995/Revised: 2 September 1995 相似文献