Ca2+ signaling in prokaryotes

The role of Ca²⁺ ions in the regulation of motility, cell cycle, and division of prokaryotes is discussed, as well as their involvement in the pathogenesis of some infectious diseases. The structural and functional organization of the prokaryotic Ca²⁺ signaling system and the mechanisms of Ca²⁺ membrane transport and homeostasis are described. Special attention is paid to the role of Ca²⁺ cation channels, Ca²⁺ transporters, and Ca²⁺-binding proteins in the regulation of the intercellular Ca²⁺ concentration.     

Evolution of mechanisms of Ca<Superscript>2+</Superscript>-signaling. Role of Ca<Superscript>2+</Superscript> in regulation of fundamental cell functions

The review considers mechanisms of Ca²⁺-dependent regulation of cell growth, differentiation, and apoptosis in cells of the higher eukaryotes by modulation of the signal Ras-MAPK pathway.     

Sodium Ions in the Electromechanical Coupling System of Myocardium and Skeletal Muscles of the Frog Rana temporaria

The role of the transsarcolemmal Na⁺ gradient in providing phasic contraction of myocardium and skeletal muscles of the common frog Rana temporaria was studied. It was shown that a decrease of the gradient by means of total or partial substitution of Na⁺ for Ch⁺ or Li⁺ produced a tissue-specific reduction of the isometric tension developed by the muscles as well as of the maximum rate of its development. The functional mechanisms of use of the Na⁺-gradient for intracellular mobilization of activator of the muscle contraction, Ca²⁺ ions, are considered, and the experimental evidences for significance of this gradient increase to provide intensification of the process of activation of the discrete (single, rhythmic) contraction of vertebrate phasic muscles are presented. The revealed differences between the studied muscles reflect adaptive rearrangement levels of ionic mechanisms of the electromechanical coupling system in these muscles, which are achieved in the course of evolution of their contractile function.     

Ultrastructural changes in the plasma membrane of A-431 cells exposed to epidermal growth factor

The plasma membrane ultrastructural changes after the action of epidermal growth factor were studied in A-431 cells using freeze-fracture methods. The incubation with EGF (100 ng/ml, 0 degree C, 60 min) led to a decrease in density of intramembrane particles on the P surface of ventral cell membrane, while the number of coated pits increased there. The revealed effects of EGF may be related to direct consequences of EGF-receptor complex formation, because all the temperature dependent steps of its processing were blocked. The data obtained testify to an active involvement of the membrane ventral surface in the formation of cell response towards growth factors.     

Effect of oxidative processes in mitochondria on contractility of heart muscle of the frog <Emphasis Type="Italic">Rana temporaria</Emphasis>. Actions of Cd<Superscript>2+</Superscript>

The inotropic Cd²⁺ action on frog heart is studied with taking into account its toxic effects upon mitochondria. Cd²⁺ at concentrations of 1, 10, and 20 mM is established to decrease dose dependently (21.3, 50.3, and 72.0%, respectively) the muscle contraction amplitude; this is explained by its competitive action on the potential-controlled Na²⁺-channels of the L-type (Ca_v 1.2). In parallel experiments on isolated rat heart mitochondria (RHM) it was shown that Cd²⁺ at concentrations of 15 and 25 mM produces swelling of non-energized and energized mitochondria in isotonic (with KNO₂ and NH₂NO₃) and hypoosmotic (with 25 mM CH₃COOK) media. Study of oxidative processes in RHM by polarographic method has shown 20 mM Cd²⁺ to disturb activity of respiratory mitochondrial chain. The rate of endogenous respiration of isolated mitochondria in the medium with Cd²⁺ in the presence of malate and succinate was approximately 5 times lower than in control. In experimental preparations, addition into the medium of DNP—uncoupler of oxidation and phosphorylation did not cause an increase of the oxygen consumption rate. Thus, the obtained data indicate that a decrease in the cardiac muscle contractility caused by Cd²⁺ is due not only to its direct blocking action on Ca²⁺-channels, but also is mediated by toxic effect on rat heart mitochondria, which was manifested as an increase in ion permeability of the inner mitochondrial membrane (IMM), acceleration of the energy-dependent K⁺ transport into the matrix of mitochondria, and inhibition of their respiratory chain.     

Gene angora enhances the effects of gene waved alopecia in mouse

Interaction between the mutant gene angora-Y (Fgf5 ^go-Y ) and the mutant gene waved alopecia (wal) in mice has been studied. Gene Fgf5 ^go-Y in a homozygous state increases the length of hair of all types, whereas the homozygotes for the wal gene display a waved hair with subsequent development of partial alopecia. Crosses between Fgf5 ^go-Y /Fgf5 ^go-Y and wal/wal mice gave the animals displaying the genotypes +/Fgf5 ^go-Y wal/wal and Fgf5 ^go-Y /Fgf5 ^go-Y wal/wal as well as F₂ +/+ wal/wal mice. The first signs of alopecia in F₂ +/+ wal/wal appear at the same time as in the mutant wal/wal BALB/c mice. This demonstrates that the genetic background has no effect on the expression of mutant gene wal. A single dose of gene +/Fgf5 ^go-Y in +/Fgf5 ^go-Y wal/wal mice causes a considerably earlier appearance of the first signs of alopecia compared with the +/+ wal/wal single homozygotes. The signs of alopecia in double homozygotes Fgf5 ^go-Y /Fgf5 ^go-Y wal/wal appear earlier than in the mice +/Fgf5 ^go-Y wal/wal. By the end of the first month after birth, the majority of double homozygotes have a virtually bold back with preserved scarce long hairs, guard hairs. Alopecia covers also the sides and belly. However, the head retains its hair and the regions of thinned long hairs remain on the limbs and near the tail base. The data obtained demonstrate that gene Fgf5 ^go-Y is a modifier of gene wal, as it enhances considerably the effect of gene wal. This appears in an earlier development of alopecia and its more pronounced progress in the mice with genotypes +/Fgf5 ^go-Y wal/wal and, particularly, Fgf5 ^go-Y /Fgf5 ^go-Y wal/wal.