Fate of compatible solutes during dilution stress in Ectothiorhodospira marismortui

Abstract The proliferation of murine spleen cells stimulated by a T-cell mitogen such as phytohemagglutinin (PHA) or concanavalin A (ConA) was significantly suppressed when the mice were immunized with either the viable cells or the sonicate of Salmonella typhimurium but not of Escherichia coli . The suppression of T-cell proliferation caused by the sonicate of S. typhimurium was completely restored by addition of phorbol 12-myristate-13-acetate (PMA), an activator of protein kinase C (PKC). Western blots using anti-phosphotyrosine antibodies showed that the mitogen-induced tyrosine phosphorylation of 120-, 106-,94-,76-,68- and 57-kDa proteins in murine splenic T-cells was inhibited in the mice immunized with the viable cells but not the sonicate of S. typhimurium . These results suggest that the inhibition caused by the sonicate involves suppression of PKC activity, whilst that produced by viable cells involves down-regulation of tyrosine phosphorylation, and both inhibitions correlate with the induction of cell-mediated immunity in mice, as evidenced by the induction of delayed-type hypersensitivity reactions.     

Evidence for Nitric Oxide Mediated Effects on Islet Hormone Secretory Phospholipase C Signal Transduction Mechanisms

We have investigated the putative role of nitric oxide (NO) as a modular of islet hormone release, when stimulated by the muscarinic receptor agonist–phospholipase C activator, carbachol, with special regard to whether the IP₃-Ca²⁺ or the diacylglycerol-protein kinase C messenger systems might be involved. It was observed that the NO synthase (NOS) inhibitor N^G-nitro-L-arginine methylester (L-NAME) markedly potentiated insulin release and modestly inhibited glucagon release induced by carbachol. Similarly, insulin release induced by the phorbol ester TPA (protein kinase C activator) was markedly potentiated. Glucagon release, however, was unaffected. Dynamic perifusion experiments with ⁴⁵C²⁺-loaded islets revealed that the inhibitory action of L-NAME on carbachol-stimulated NO-production was reflected in a rapid and sustained increase in insulin secretion above carbachol controls, whereas the ⁴⁵Ca²⁺-efflux pattern was similar in both groups with the exception of a slight elevation of ⁴⁵C²⁺ in the L-NAME-carbachol group during the latter part of the perifusion. No difference in either insulin release or ⁴⁵Ca²⁺-efflux pattern between the carbachol group and L-NAME-carbachol group was seen in another series of experiments with identical design but performed in the absence of extracellular Ca²⁺ . However, it should be noted that in the absence of extracellular Ca²⁺ both ⁴⁵Ca²⁺-efflux and, especially, insulin release were greatly reduced in comparison with experiments in normal Ca²⁺. Further, in the presence of diazoxide, a potent K⁺ _ATP-channel opener, plus a depolarizing concentration of K⁺ the NOS-inhibitor L-NAME still markedly potentiated carbachol-induced insulin release and inhibited glucagon release. The enantiomer D-NAME, which is devoid of NOS-inhibitory properties, did not affect carbachol-induced hormone release. TPA-induced hormone release in depolarized islets was not affected by either L-NAME or D-NAME. The pharmacological intracellular NO donor hydroxylamine dose-dependently inhibited insulin release stimulated by TPA. Furthermore, a series of perifusion experiments revealed that hydroxylamine greatly inhibited carbachol-induced insulin release without affecting the ⁴⁵Ca²⁺-efflux pattern. In summary, our results suggest that the inhibitory effect of NO on carbachol-induced insulin release is not to any significant extent exerted on the IP₃-Ca²⁺ messenger system but rather through S-nitrosylation of critical thiol-residues in protein kinase C and/or other secretion-regulatory thiol groups. In contrast, the stimulating action of NO on carbachol-induced glucagon release was, at least partially, connected to the IP₃-Ca²⁺ messenger system. The main effects of NO on both insulin and glucagon release induced by carbachol were apparently exerted independently of membrane depolarization events.     

Evolutionary Tradeoffs between Economy and Effectiveness in Biological Homeostasis Systems

Biological regulatory systems face a fundamental tradeoff: they must be effective but at the same time also economical. For example, regulatory systems that are designed to repair damage must be effective in reducing damage, but economical in not making too many repair proteins because making excessive proteins carries a fitness cost to the cell, called protein burden. In order to see how biological systems compromise between the two tasks of effectiveness and economy, we applied an approach from economics and engineering called Pareto optimality. This approach allows calculating the best-compromise systems that optimally combine the two tasks. We used a simple and general model for regulation, known as integral feedback, and showed that best-compromise systems have particular combinations of biochemical parameters that control the response rate and basal level. We find that the optimal systems fall on a curve in parameter space. Due to this feature, even if one is able to measure only a small fraction of the system''s parameters, one can infer the rest. We applied this approach to estimate parameters in three biological systems: response to heat shock and response to DNA damage in bacteria, and calcium homeostasis in mammals.     

On the relation between the instability of ESS in discrete dynamics and segregation distortion

There is a simple correspondence between discrete dynamical systems associated with evolutionary game dynamics and general locus multiallele selection models with non-Mendelian segregation. When interpreted properly the payoff matrix has two components, a fitness matrix component and a segregation matrix component. The presence of segregation distortion which corresponds to a non-symmetric payoff matrix, is a source of instability. With non-symmetric payoff an ESS does not usually correspond to a stable equilibrium. It is always externally stable but does not necessarily have an internally stable equilibrium.     

Northern genetic richness and southern purity,but just one species in the Chelonoidis chilensis complex

Fritz, U., Alcalde, L., Vargas‐Ramírez, M., Goode, E.V., Fabius‐Turoblin, D.U. & Praschag, P. (2012). Northern genetic richness and southern purity, but just one species in the Chelonoidis chilensis complex. —Zoologica Scripta, 41, 220–232. The Chelonoidis chilensis complex, the sister group of the famous Galápagos tortoises, is a widely distributed group of South American land tortoises, ranging from the dry Chaco of Bolivia, Paraguay and northern Argentina to northern Patagonia. Within this complex, up to three distinct species have been recognized. Using sequence data of the mitochondrial cytochrome b gene and length polymorphisms of 10 microsatellite loci, we investigate genetic differentiation among all three nominal species. We find only negligible differentiation, with decreasing genetic diversity from north to south. We conclude that only one species, Chelonoidis chilensis (Gray, 1870), is valid, with C. donosobarrosi ( Freiberg, 1973 ) and C. petersi ( Freiberg, 1973 ) as its junior synonyms. Morphological variation within C. chilensis sensu lato is in accord with the observation that size variation in chelonians follows Bergmann’s rule, with body size increasing with latitude. The observed phylogeographic differentiation inverses the well‐known pattern of southern genetic richness and northern purity from the northern hemisphere, resulting from dispersal from glacial refugia. This implies that in higher latitudes of both hemispheres genetic diversity may decrease with increasing distance from the refugium. For C. chilensis sensu lato, it seems likely that long‐distance dispersal via rafting on the Desaguadero River led to the foundation of the southernmost populations in northern Patagonia during the Holocene.     

Osmoregulatory traits of broad-toothed field mouse (Apodemus mystacinus) populations from different habitats

One mechanism for physiological adjustment of small mammals to different habitats and different seasons is by seasonal acclimatization of their osmoregulatory system. We examined the abilities of broad-toothed field mice (Apodemus mystacinus) from different ecosystems (‘sub-alpine’ and ‘Mediterranean’) to cope with salinity stress under short day (SD) and long day (LD) photoperiod regimes. We compared urine volume, osmolarity, urea and electrolyte (sodium, potassium and chloride) concentrations. Significant differences were noted in the abilities of mice from the two ecosystems to deal with salinity load; in particular sub-alpine mice produced less concentrated urine than Mediterranean mice with SD− sub-alpine mice seeming to produce particularly dilute urine. Urea concentration generally decreased with increasing salinity, whereas sodium and potassium levels increased, however SD− sub-alpine mice behaved differently and appeared not to be able to excrete electrolytes as effectively as the other groups of mice. Differences observed provide an insight into the kinds of variability that are present within populations inhabiting different ecosystems, thus how populations may be able to respond to potential changes in their environment. Physiological data pertaining to adaptation to increased xeric conditions, as modelled by A. mystacinus, provides valuable information as to how other species may cope with potential climatic challenges.     

On the limited recognition of inorganic surfaces by short peptides compared with antibodies

The vast potential applications of biomolecules that bind inorganic surfaces led mostly to the isolation of short peptides that target selectively specific materials. The demonstrated differential affinity toward certain surfaces created the impression that the recognition capacity of short peptides may match that of rigid biomolecules. In the following, we challenge this view by comparing the capacity of antibody molecules to discriminate between the (100) and (111A) facets of a gallium arsenide semiconductor crystal with the capacity of short peptides to do the same. Applying selection from several peptide and single chain phage display libraries, we find a number of antibody molecules that bind preferentially a given crystal facet but fail to isolate, in dozens of attempts, a single peptide capable of such recognition. The experiments underscore the importance of rigidity to the recognition of inorganic flat targets and therefore set limitations on potential applications of short peptides in biomimetics. Copyright © 2014 European Peptide Society and John Wiley & Sons, Ltd.     

Modification of chloroplast CF1 by fluoresceinisothiocyanate

Incubation of the chloroplast coupling factor with fluorescein isothiocyanate inhibits the Ca-ATPase activity of the enzyme and results in incorporation of fluorescein into the α and β subunits. High concentrations of ATP prevent the inhibition and reduce the incorporation of fluorescein into the α and β subunits. Ca and Mg ions increase fluorescein isothiocyanate inhibition and fluorescein incorporation into the α, β and γ subunits. It is suggested that fluorescein isothiocyanate modifies the catalytic site of the enzyme by blocking lysine residues in the α and β subunits which are involved in the binding of ATP.