Recent advances in understanding the molecular mechanism of chloroplast photorelocation movement

Plants are photosynthetic organisms that have evolved unique systems to adapt fluctuating environmental light conditions. In addition to well-known movement responses such as phototropism, stomatal opening, and nastic leaf movements, chloroplast photorelocation movement is one of the essential cellular responses to optimize photosynthetic ability and avoid photodamage. For these adaptations, chloroplasts accumulate at the areas of cells illuminated with low light (called accumulation response), while they scatter from the area illuminated with strong light (called avoidance response). Plant-specific photoreceptors (phototropin, phytochrome, and/or neochrome) mediate these dynamic directional movements in response to incident light position and intensity. Several factors involved in the mechanisms underlying the processes from light perception to actin-based movements have also been identified through molecular genetic approach. This review aims to discuss recent findings in the field relating to how chloroplasts move at molecular levels. This article is part of a Special Issue entitled: Dynamic and ultrastructure of bioenergetic membranes and their components.     

Adrenocorticoid action in the spinal cord: Some unique molecular properties of glucocorticoid receptors

1. Glucocorticoid hormones affect several functions of the spinal cord, such as synaptic transmission, biogenic amine content, lipid metabolism, and the activity of some enzymes (ornithine decarboxylase, glycerolphosphate dehydrogenase), indicating that this tissue is a target of adrenal hormones. 2. Corticosterone, the main glucocorticoid of the rat, is detected at all regional levels of the spinal cord, and cold stress increases this steroid, predominantly in the cervical regions. 3. Intracellular glucocorticoid receptors have been found in the spinal cord, with higher concentrations in the cervical and lumbar enlargements. Prima facie, these receptors presented biochemical, stereospecifical, and physicochemical properties similar to those of receptors found in other regions of the nervous system. The prevalent form in the spinal cord is the type II receptor, although type I is also present in small amounts. 4. The type II glucocorticoid receptor of the spinal cord shows an affinity lower (Kd 3.5 nM) than that of the hippocampal type II site (Kd 0.7 nM) when incubated with [3H]dexamethasone. This condition may impair the nuclear translocation of the spinal cord receptor. 5. Another peculiar property of spinal cord type II site is a greater affinity for DNA-cellulose binding than the hippocampal receptor during heat-induced transformation. Also, the spinal cord receptor shows resistance to the action of RNAse A, an enzyme which increases DNA-cellulose binding of the hippocampal receptor, indicating that both receptors may be structurally different. 6. Therefore, it is possible that a different subclass of type II, or "classical glucocorticoid receptor," is present in the spinal cord. This possibility makes the cord a useful system for studying diversity of glucocorticoid receptors of the nervous system, especially the relationship between receptor structure and function.     

Towards understanding molecular mechanisms of action of homeopathic drugs: An overview

The changes in the contents of cyclic AMP, cyclic GMP, ATP, ADP, AMP and fructose-2,6-bisphosphate that occur in the mantle tissue of the mussel Mytilus galloprovincialis Lmk were analysed with regard to the annual gametogenic cycle. Throughout 2 years, the lowest contents of AMP, ADP and ATP were detected during late winter-spring, whereas the maximum appeared in the autumn months. During the second year, fructose-2,6-bisphosphate and cAMP showed a very similar behaviour. The levels of both compounds rose throughout the year until a maximum in September. Their behaviour was also similar to that observed during the first year, but displaced in time. Both in 1998 and in 1999, the highest level of cGMP was detected during the spring-summer months. The results obtained suggest that the glycolytic pathway, with regard to the breeding cycle, might be regulated by fructose-2,6-bisphosphate and cyclic AMP through the activation of 6-phosphofructo-1-kinase, which is the main regulating enzyme of the glycolysis in mantle of M. galloprovincialis.     

Investigating action understanding: inferential processes versus action simulation

In our daily life, we continuously monitor others' behaviors and interpret them in terms of goals, intentions, and reasons. Despite their central importance for predicting and interpreting each other's actions, the functional mechanisms and neural circuits involved in action understanding remain highly controversial. Two alternative accounts have been advanced. Simulation theory assumes that we understand actions by simulating the observed behavior through a direct matching process that activates the mirror-neuron circuit. The alternative interpretive account assumes that action understanding is based on specialized inferential processes activating brain areas with no mirror properties. Although both approaches recognize the central role of contextual information in specifying action intentions, their respective accounts of this process differ in significant respects. Here, we investigated the role of context in action understanding by using functional brain imaging while participants observed an unusual action in implausible versus plausible contexts. We show that brain areas that are part of a network involved in inferential interpretive processes of rationalization and mentalization but that lack mirror properties are more active when the action occurs in an implausible context. However, no differential activation was found in the mirror network. Our findings support the assumption that action understanding in novel situations is primarily mediated by an inferential interpretive system rather than the mirror system.     

Molecular advances in understanding inherited prion diseases

The prion diseases are neurodegenerative disorders that have attracted great interest because of the possible link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (CTD) in humans. Possible transmission of these diseases has been linked to a single protein termed the prion protein. This protein is an abnormal isoform of a normal synaptic glycoprotein. The majority of prion diseases does not appear to be caused by transmission of an infectious agent but occur spontaneously with no known cause. The strongest supporting evidence that the prion protein is the causative agent in prion disease comes from specific inheritable forms of prion disease which are linked to single point mutations in the prion protein gene. Paradoxically, these point mutations, although autosomal dominant with 100% penetrance do not lead to disease until late in life. Molecular techniques are now being used extensively to determine how these point-mutations alter the prion protein’s normal structure and activity. This review deals with the latest insights into how inherited mutations in the prion protein gene lead to neurodegenerative disease.     

Familial thrombosis: inherited deficiency of antithrombin III.

Several members of a family living on the west coast of Scotland and on one of the islands off the coast had serious thrombotic disease. The plasma antithrombin III (ATIII) concentrations were measured by both functional and immunological assay in all available members of the family. Concentrations were 25% to 66% of normal in 12 people, including all seven with thrombotic disease. The inheritance pattern was characteristic of an autosomal dominant disorder. Thrombotic disease generally affected the leg, mesenteric, and axillary veins, although one man who had died before the study began had had severe arterial atheroma. In women the first thrombotic symptoms usually occurred during pregnancy. None of these patients have developed thrombotic symptoms until they were at least 18, so four younger members of the family who have ATIII deficiency but no thrombotic disease may eventually develop symptoms.     

Microsporidia: emerging advances in understanding the basic biology of these unique organisms

Microsporidia are long-known parasites of a wide variety of invertebrate and vertebrate hosts. The emergence of these obligate intracellular organisms as important opportunistic pathogens during the AIDS pandemic and the discovery of new species in humans renewed interest in this unique group of organisms. This review summarises recent advances in the field of molecular biology of microsporidia which (i) contributed to the understanding of the natural origin of human-infecting microsporidia, (ii) revealed unique genetic features of their dramatically reduced genome and (iii) resulted in the correction of their phylogenetic placement among eukaryotes from primitive protozoans to highly evolved organisms related to fungi. Microsporidia might serve as new intracellular model organisms in the future given that gene transfer systems will be developed.