Alpine vascular plant species richness: the importance of daily maximum temperature and pH

Species richness in the alpine zone varies dramatically when communities are compared. We explored (i) which stress and disturbance factors were highly correlated with species richness, (ii) whether the intermediate stress hypothesis (ISH) and the intermediate disturbance hypothesis (IDH) can be applied to alpine ecosystems, and (iii) whether standing crop can be used as an easily measurable surrogate for causal factors determining species richness in the alpine zone. Species numbers and standing crop were determined in 14 alpine plant communities in the Swiss Alps. To quantify the stress and disturbance factors in each community, air temperature, relative air humidity, wind speed, global radiation, UV-B radiation, length of the growing season, soil suction, pH, main soil nutrients, waterlogging, soil movement, number of avalanches, level of denudation, winter dieback, herbivory, wind damage, and days with frost were measured or observed. The present study revealed that 82% of the variance in␣vascular species richness among sites could be explained by just two abiotic factors, daily maximum temperature and soil pH. Daily maximum temperature and pH affect species richness both directly and via their effects on other environmental variables. Some stress and disturbance factors were related to species richness in a monotonic way, others in an unimodal way. Monotonic relationships suggest that the harsher the environment is, the fewer species can survive in such habitats. In cases of unimodal relationships (ISH and IDH) species richness decreases at both ends of the gradients due to the harsh environment and/or the interaction of other environmental factors. Competition and disturbance seemed only to play a secondary role in the form of fine-tuning species richness in specific communities. Thus, we concluded that neither the ISH nor the IDH can be considered useful conceptual models for the alpine zone. Furthermore, we found that standing crop can be used as an easily measurable surrogate for causal factors determining species richness in the alpine zone, even though there is no direct causality.     

Solubilization of the bovine cardiac sarcolemmal binding sites for calcium channel blockers

Nonionic and ionic detergents were used to solubilize the bovine cardiac sarcolemmal binding sites for nimodipine and (-)desmethoxyverapamil in the absence of added ligand. Only Chaps, digitonin and sucrose monolauryl ester were able to solubilize the binding sites in a form that bound radioligands. About 45% of each of the membrane-bound high-affinity site was solubilized by 0.4% Chaps (w/v) in the presence of 48% (w/v) glycerol. The solubilized binding sites were destroyed by trypsin or by a 10-min incubation at 50 degrees C. Calcium stimulated nimodipine binding slightly at 0.3 mM and inhibited (-)desmethoxyverapamil binding completely with an IC50 of 1.2 mM. Nimodipine binding was reduced by 20% in the presence of EGTA. The solubilized receptors sedimented in sucrose density gradients with an apparent s20,w of 21 S. An identical sedimentation value was obtained for the cardiac sarcolemmal and skeletal transverse tubulus receptor which were prelabeled with nitrendipine and solubilized by digitonin. Solubilization reduced the affinity of nimodipine for its high-affinity site slightly from 0.35 nM to 1.2 nM and that for its low-affinity site from 33 nM to 130 nM. Solubilization did not affect significantly the specific density of these sites. Binding of nimodipine to the low-affinity site was completely abolished by 0.1 microM nitrobenzylthioinosine. After solubilization only the high-affinity site for (-)desmethoxyverapamil could be measured with tenfold reduced affinity (Kd = 15.3 nM) but unchanged specific density. Binding to the solubilized high-affinity site for nimodipine and (-)desmethoxyverapamil was stereospecific and showed a similar rank order as the particulate binding sites. Binding of nimodipine was inhibited allosterically by phenylalkylamines. Similarly, (+)PN200-110 inhibited allosterically (-)desmethoxyverapamil binding. d-cis-Diltiazem stimulated nimodipine binding at 20 degrees C 1.2-fold, reduced the dissociation rate from 0.018 min-1 to 0.0083 min-1 and had no effect on the association rate (0.173 min-1. nM-1). The Kd calculated from the rate constants was 0.1 nM and in close agreement with the value of 0.49 nM measured under equilibrium conditions in the presence of nitrobenzylthioinosine. In contrast, desmethoxyverapamil increased the dissociation rate of nimodipine to 0.03 min-1. The association and dissociation rate constants for (-)desmethoxyverapamil were 0.024 min-1. nM-1 and 0.025 min-1, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)     

Cardiac sarcoplasmic reticulum contains a low-affinity site for phenylalkylamines

The distribution of the bovine cardiac binding sites for the organic calcium-channel blockers was studied. Crude microsomal membranes were separated into three fractions, which contained mainly membranes derived from sarcolemma, 'junctional' sarcoplasmic reticulum containing transversal tubuli, and free sarcoplasmic reticulum. The high-affinity binding site for the dihydropyridines, determined in the presence of nitrobenzylthioinosine, was enriched 12-fold and 17-fold in sarcolemma and junctional sarcoplasmic reticulum. The binding sites for the phenylalkylamines, determined with [3H]verapamil or [3H](-)desmethoxyverapamil, were enriched 1.5-3.4-fold in sarcolemma and junctional sarcoplasmic reticulum but 6-10-fold in free sarcoplasmic reticulum. The phenylalkylamine-binding site, present in free sarcoplasmic reticulum, was partially destroyed by chymotrypsin or phospholipase A2 and C treatment. Specific binding was proportional to the concentration of the added membrane protein. The binding of (-)desmethoxyverapamil was half-maximally inhibited by 6.5 mM calcium chloride and was optimal in the presence of 5 mM EGTA. In three out of five preparations (-)desmethoxyverapamil bound to a single site with an apparent Kd value of 191 +/- 42.8 nM and a density of 34.5 +/- 7.7 pmol/mg protein. In two out of five preparations an additional high-affinity site (Kd approximately 0.67 nM) was detected. The low-affinity site bound other phenylalkylamines, but stereospecific binding of phenylalkylamines was not observed. Binding of phenylalkylamines to the low-affinity site was inhibited by some but not all calmodulin 'antagonists'. Furthermore dihydropyridines did not affect the binding of (--)desmethoxyverapamil suggesting that the low-affinity site differs considerably from the high-affinity sarcolemmal site. These results suggest that free sarcoplasmic reticulum contains a binding site for phenylalkylamines at a relative high density, which is not related to the high-affinity site present in the voltage-dependent calcium channel.     

Characterization of the binding sites for nimodipine and (-)-desmethoxyverapamil in bovine cardiac sarcolemma

The bovine cardiac sarcolemmal binding sites for the dihydropyridine nimodipine and the phenylalkylamine (-)-desmethoxyverapamil were studied. The density of the nimodipine and (-)-desmethoxyverapamil binding sites increased 8.3-fold and 3.4-fold with the sarcolemma. The binding sites for both compounds were destroyed by trypsin. Nimodipine bound in the presence of 1 mM free calcium to a high-affinity and a low-affinity site with apparent Kd values of 0.35 +/- 0.09 nM (n = 9) and 33 +/- 6.0 nM (n = 9) and with apparent densities of 0.3 +/- 0.05 pmol/mg (n = 9) and 8.2 +/- 1.0 pmol/mg (n = 9). The binding to the high-affinity site was abolished by 1 mM EGTA. The binding sites were specific for dihydropyridines. The (-)-isomers of several phenylalkylamines inhibited nimodipine binding by an apparent allosteric mechanism. (-)-Desmethoxyverapamil bound in the presence of 5 mM EGTA to a high-affinity and a low-affinity site with apparent Kd values of 1.4 +/- 0.3 nM (n = 6) and 171 +/- 26 nM (n = 6) and with apparent densities of 0.16 +/- 0.02 pmol/mg (n = 6) and 13.6 +/- 2.7 pmol/mg (n = 6). The binding to both sites was inhibited by calcium with a half-maximal concentration of 4.3 mM. The binding sites were specific for the other phenylalkylamines and had a higher affinity for the (-)-isomers than for the (+)-isomers. Nimodipine inhibited the binding of (-)-desmethoxyverapamil by an apparent allosteric mechanism. d-cis-Diltiazem inhibited non-competitively the binding of (-)-[3H]desmethoxyverapamil with a Ki of 3.7 microM. Diltiazem up to concentrations of 10 microM did not affect the amount of nimodipine bound at equilibrium at 20 degrees C. However, but in agreement with this result, diltiazem decreased threefold at 20 degrees C the dissociation and association rates for the high-affinity nimodipine receptor. These rates were only marginally affected at 4 degrees C and 37 degrees C. d-cis-Diltiazem reversed in a competitive manner the inhibition of nimodipine binding elicited by the addition of (-)-desmethoxyverapamil with a Ka value of 1.6 microM. The amount of nimodipine bound was inhibited by 50% by the adenosine uptake inhibitors nitrobenzylthioinosine and hexobendine with apparent median inhibitory concentrations of 1 nM and 3 nM, respectively. Nitrobenzylthioinosine completely abolished binding of nimodipine to the low-affinity site, but did not affect binding to the high-affinity site.(ABSTRACT TRUNCATED AT 400 WORDS)     

Super-resolution microscopy reveals the number and distribution of topoisomerase IIα and CENH3 molecules within barley metaphase chromosomes

Chromosoma - Topoisomerase IIα (Topo IIα) and the centromere-specific histone H3 variant CENH3 are key proteins involved in chromatin condensation and centromere determination,...     

Phytochrome Control of Its Own Synthesis in Pisum sativum

An analysis of phytochrome synthesis in Pisum seedlings by measuringthe activity of polysomal polyadenylated RNA (poly-A⁺-RNA) codingfor phytochrome apoprotein showed phytochrome control of itsown synthesis; brief red-light irradiation of pea seedlingsinhibited the activity of the RNA, and the red-light effectwas red/far-red reversible. ⁴ Permanent address: Biology Department, Faculty of Science,University of Tokyo, Hongo, Tokyo 113, Japan. (Received August 13, 1984; Accepted September 17, 1984)     

Activated T lymphocytes resist the toxic effects of the adenosine deaminase inhibitor, 2-deoxycoformycin

Tonsil lymphocytes from three adults and three children were examined for immunoglobulin (Ig) production before and after Epstein-Barr virus (EBV) transformation. T-cell depletion was required to obtain cell lines from EBV-seropositive individuals. Cytoplasmic Ig was mainly IgG in adult lymphocytes before and after transformation; IgA and IgM were more prominent after than before. IgM and IgG predominated in lymphocytes of children before and after transformation; IgA was more prominent after than before. Cytoplasmic Ig of peripheral blood lymphocytes from these individuals was mainly IgM. Secreted Ig from tonsil lymphocytes was mainly IgA or IgG; after transformation IgM predominated with adult cell lines, and IgG or IgM with cell lines from children. IgE was consistently sparse in spite of ragweed and/or grass allergies of the adults.     

Immunoregulatory activity of culture-induced suppressor macrophages

Rat splenic cells precultured in vitro for 5 days exhibited marked suppressive activity on the secondary cytotoxic T lymphocyte (CTL) response to a Gross virus-induced lymphoma. Suppressive activity was produced by macrophages (MØ) rather than lymphocytes and as low as 1% MØ content was sufficient to achieve completely inhibited CTL responses. Aspirin, indomethacin, and d,l-6-chloro-2-methylcarbazole-2-acetic acid prevented cultured splenic MØ from exerting their inhibitory effect, thereby suggesting a role for prostaglandins in suppression. Events which occurred within the first 24 to 48 hr of the CTL response were susceptible to the suppressive action of MØ since normal CTL responses were obtained if suppressive MØ were added later than Day 2 or if indomethacin was added within the first 24 to 48 hr of culture. Two processes of lymphocyte activation, namely blast transformation and DNA synthesis, were inhibited in the presence of suppressive MØ. However, suppression of these processes did not result in the loss of CTL progenitor cells since CTL responses that were inhibited in the presence of suppressive MØ proceeded normally following their removal.