Proteasome plasticity

The 26S proteasome is responsible for regulated proteolysis of most intracellular proteins yet the focus of intense regulatory action itself. Proteasome abundance is responsive to cell needs or stress conditions, and dynamically localized to concentrations of substrates. Proteasomes are continually assembled and disassembled, and their subunits subject to a variety of posttranslational modifications. Furthermore, as robust and multi-tasking as this complex is, it does not function alone. A spattering of closely associating proteins enhances complex stability, fine-tunes activity, assists in substrate-binding, recycling of ubiquitin, and more. HEAT repeat caps activate proteasomes, yet share remarkable features with nuclear importins. Fascinating cross talk even occurs with ribosomes through common maturation factors. The dynamics of proteasome configurations and how they relate to diverse activities is the topic of this review.     

Thrombin plasticity

Thrombin is the final protease generated in the blood coagulation cascade. It has multiple substrates and cofactors, and serves both pro- and anti-coagulant functions. How thrombin activity is directed throughout the evolution of a clot and the role of conformational change in determining thrombin specificity are issues that lie at the heart of the haemostatic balance. Over the last 20 years there have been a great number of studies supporting the idea that thrombin is an allosteric enzyme that can exist in two conformations differing in activity and specificity. However, recent work has shown that thrombin in its unliganded state is inherently flexible in regions that are important for activity. The effect of flexibility on activity is discussed in this review in context of the zymogen-to-protease conformational transition. Understanding thrombin function in terms of 'plasticity' provides a new conceptual framework for understanding regulation of enzyme activity in general. This article is part of a Special Issue entitled: Proteolysis 50 years after the discovery of lysosome.     

Spinal-cord plasticity

Plasticity is one of the most extensively studied aspects in neuroscience. Interest in it has primarily been related to its proposed role in learning and memory and its relevance to adaptive changes following injury. Plasticity can be evoked by changes in molecular, cellular, and synaptic properties, either as a result of activity-dependent effects, or by relatively slow-acting neuromodulatory transmitters. In addition, it is increasingly recognized that the plasticity evoked by these individual effects can be altered by previous inputs and is thus itself plastic. Here, I will review studies in the lamprey spinal cord that have examined individual and interactive activity-dependent and neuromodulator-mediated plasticity. The results show that activity-dependent and neuromodulator-mediated plasticity evoke neuron-and synapse-specific effects at different levels in the spinal cord, and that interactions within and between these effects can evoke dynamic changes in cellular, synaptic, and network plasticity.     

Thrombin plasticity

Thrombin is the final protease generated in the blood coagulation cascade. It has multiple substrates and cofactors, and serves both pro- and anti-coagulant functions. How thrombin activity is directed throughout the evolution of a clot and the role of conformational change in determining thrombin specificity are issues that lie at the heart of the haemostatic balance. Over the last 20 years there have been a great number of studies supporting the idea that thrombin is an allosteric enzyme that can exist in two conformations differing in activity and specificity. However, recent work has shown that thrombin in its unliganded state is inherently flexible in regions that are important for activity. The effect of flexibility on activity is discussed in this review in context of the zymogen-to-protease conformational transition. Understanding thrombin function in terms of ‘plasticity’ provides a new conceptual framework for understanding regulation of enzyme activity in general. This article is part of a Special Issue entitled: Proteolysis 50 years after the discovery of lysosome.     

Synaptic plasticity: the subcellular location of CaMKII controls plasticity

In a neuron's dendritic spine, the location of CaMKII is controlled by a number of interacting factors, including its ability to bind calcium/calmodulin, its phosphorylation state and the synthesis of new subunits in the dendrites.New studies have shown that the exact location of CaMKII is crucial for the form and endurance of synaptic plasticity.     

Dendritic structural plasticity

Dendrites represent the compartment of neurons primarily devoted to collecting and computating input. Far from being static structures, dendrites are highly dynamic during development and appear to be capable of plastic changes during the adult life of animals. During development, it is a combination of intrinsic programs and external signals that shapes dendrite morphology; input activity is a conserved extrinsic factor involved in this process. In adult life, dendrites respond with more modest modifications of their structure to various types of extrinsic information, including alterations of input activity. Here, the author reviews classical and recent evidence of dendrite plasticity in invertebrates and vertebrates and current progress in the understanding of the molecular mechanisms that underlie this plasticity. Importantly, some fundamental questions such as the functional role of dendrite remodeling and the causal link between structural modifications of neurons and plastic processes, including learning, are still open.     

Genome plasticity inPlasmodium

Extensive genome plasticity inPlasmodium involves frequent loss of dispensable functions under non-selective conditions, polymorphisms in subtelomeric repetitive regions, as well as rapid and apparently concerted variation in the intra-genic repetitive arrays that are typical of plasmodial antigen genes. As an example of the latter type of variation, the region of the merozoite surface antigen gene MSA-1 ofPlasmodium falciparum, which encodes a tri-peptide repeat, is analysed in detail. The example illustrates how evasion of the immune defenses of the vertebrate host can be achieved through repeat homogenization mechanisms, acting at the DNA level, and leading to rapid fixation of variant epitopes. The remarkable ability of Plasmodia to utilize mechanisms which operate on its own nuclear DNA in the course of mitotic multiplication is discussed against the need of life cycle closure as a haploid unicellular. The possibility is suggested that active genomic diversification in a (clonal) multicellular population evolved as an adaptive tool.     

Short-term presynaptic plasticity

Different types of synapses are specialized to interpret spike trains in their own way by virtue of the complement of short-term synaptic plasticity mechanisms they possess. Numerous types of short-term, use-dependent synaptic plasticity regulate neurotransmitter release. Short-term depression is prominent after a single conditioning stimulus and recovers in seconds. Sustained presynaptic activation can result in more profound depression that recovers more slowly. An enhancement of release known as facilitation is prominent after single conditioning stimuli and lasts for hundreds of milliseconds. Finally, tetanic activation can enhance synaptic strength for tens of seconds to minutes through processes known as augmentation and posttetantic potentiation. Progress in clarifying the properties, mechanisms, and functional roles of these forms of short-term plasticity is reviewed here.     

植物养分捕获的菌根塑性——外生菌根的塑性

植物根资源捕获塑性是地下生态学研究的重点之一, 在过去二三十年间有长足的进步。菌根塑性是根资源捕获塑性的重要方面, 但由于研究手段的限制, 目前仅有概念上的探讨。缺乏菌根塑性的根塑性研究至少是不全面的。菌根生物学的迅速发展, 尤其是分子生物学手段的介入, 使对菌根塑性进行深入研究成为可能。该文对外生菌根塑性进行讨论, 在简要介绍了外生菌根的生物学基本知识后, 着重讨论了外生菌根形态塑性和生理塑性的定义与内涵。通过文献综述, 分析讨论了外生菌根塑性的研究现状: 很少有研究聚焦在菌根塑性本身, 现有的材料多为其他研究的隐示或研究结果的引申, 并多在形态塑性方面。外生菌根的生理塑性未见有直接的实验数据。该文还对外生菌根研究中发展的、可用于菌根塑性研究的方法进行了综述。由于外生菌根塑性的复杂性, 对菌根塑性的研究会较植物根本身塑性的研究复杂得多, 问题也会相对复杂, 比如植物和外生菌根菌之间的营养需求关系、植物外生菌根塑性的生态意义、实验方法的缺陷等等。对今后外生菌根塑性研究的方向进行了探讨。     

Adult visual cortical plasticity

The visual cortex has the capacity for experience-dependent change, or cortical plasticity, that is retained throughout life. Plasticity is invoked for encoding information during perceptual learning, by internally representing the regularities of the visual environment, which is useful for facilitating intermediate-level vision-contour integration and surface segmentation. The same mechanisms have adaptive value for functional recovery after CNS damage, such as that associated with stroke or neurodegenerative disease. A common feature to plasticity in primary visual cortex (V1) is an association field that links contour elements across the visual field. The circuitry underlying the association field includes a plexus of long-range horizontal connections formed by cortical pyramidal cells. These connections undergo rapid and exuberant sprouting and pruning in response to removal of sensory input, which can account for the topographic reorganization following retinal lesions. Similar alterations in cortical circuitry may be involved in perceptual learning, and the changes observed in V1 may be representative of how learned information is encoded throughout the cerebral cortex.     

Cell fusion and plasticity

Cell plasticity is a central issue in stem cell biology. In many recent discussions, observation of cell fusion has been seen as a confounding factor which calls into question published results concerning cell plasticity of, particularly, adult stem cells. An examination of the voluminous literature of "somatic cell fusion" suggests the relatively frequent occurrence of "spontaneous" cell fusion and shows that the complicated cellular phenotypes which it can give rise to have long been recognized. Here, a brief overview of this field is presented, with emphasis on studies of special relevance to current work on cell plasticity. This revised version was published online in July 2006 with corrections to the Cover Date.