S-Nitrosylation of Drp1 links excessive mitochondrial fission to neuronal injury in neurodegeneration

Neurons are known to use large amounts of energy for their normal function and activity. In order to meet this demand, mitochondrial fission, fusion, and movement events (mitochondrial dynamics) control mitochondrial morphology, facilitating biogenesis and proper distribution of mitochondria within neurons. In contrast, dysfunction in mitochondrial dynamics results in reduced cell bioenergetics and thus contributes to neuronal injury and death in many neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease, and Huntington’s disease. We recently reported that amyloid-β peptide, thought to be a key mediator of AD pathogenesis, engenders S-nitrosylation and thus hyperactivation of the mitochondrial fission protein Drp1. This activation leads to excessive mitochondrial fragmentation, bioenergetic compromise, and synaptic damage in models of AD. Here, we provide an extended commentary on our findings of nitric oxide-mediated abnormal mitochondrial dynamics.     

Ca signaling and STIM1

An increase in the intracellular calcium ion concentration ([Ca²⁺]) impacts a diverse range of cell functions, including adhesion, motility, gene expression and proliferation. Elevation of intracellular calcium ion (Ca²⁺) regulates various cellular events after the stimulation of cells. Initial increase in Ca²⁺ comes from the endoplasmic reticulum (ER), intracellular storage space. However, the continuous influx of extracellular Ca²⁺ is required to maintain the increased level of Ca²⁺ inside cells. Store-operated Ca²⁺ entry (SOCE) manages this process, and STIM1, a newly discovered molecule, has a unique and essential role in SOCE. STIM1 can sense the exhaustion of Ca²⁺ in the ER, and activate the SOC channel in the plasma membrane, leading to the continuous influx of extracellular Ca²⁺. STIM1 senses the status of the intracellular Ca²⁺ stores via a luminal N-terminal Ca²⁺-binding EF-hand domain. Dissociation of Ca²⁺ from this domain induces the clustering of STIM1 to regions of the ER that lie close to the plasma membrane, where it regulates the activity of the store-operated Ca²⁺ channels/entry (calcium-release-activated calcium channels/entry). In this review, we summarize the mechanism by which STIM1 regulates SOCE, and also its role in the control of mast cell functions and allergic responses.     

Genetic relationships between resistances to Fusarium head blight and crown rot in bread wheat (Triticum aestivum L.)

Fusarium head blight (FHB) and crown rot (CR) are two wheat diseases caused by the same Fusarium pathogens. Progress towards CR resistance could benefit from FHB-resistant germplasm if the same genes are involved in resistance to these two different diseases. Two independent studies were conducted to investigate the relationship between host resistances to these two diseases. In the first study 32 genotypes were assessed and no significant correlation between their reactions to FHB and CR was detected. The second study was based on a QTL analysis of a doubled haploid population derived from a variety with resistance to both diseases. Results from this study showed that loci conferring resistance to FHB and CR are located on different chromosomes. Together, these results suggest that, despite a common aetiology, different host genes are involved in the resistance against FHB and CR in wheat. Thus, although it is possible that genes affecting both diseases may exist in other germplasm or under different conditions, separate screening seems to be needed in identifying sources of CR resistance.     

Decomposition Analysis of Waste Generation From Stocks in a Dynamic System

We conducted a decomposition analysis of material flows in a dynamic system, focusing on factors in the generation of waste consumer durables. A methodology for the analysis of consumer durables was developed and applied to three common consumer durables: cathode ray tube TVs, refrigerators, and passenger cars. The methodology decomposed changes in the numbers of waste products into three factors: changes in lifespan distribution, past trends in replacement sales, and past trends in sales for additional purchases. The decomposed equation clearly showed that the number of waste products would not necessarily be reduced by lifespan extension alone. This is because the number of waste products generated is affected not only by current lifespan distribution but also by past trends in sales for replacement and in additional purchases. The results show that changes in past replacement sales influence the current generation of waste, even if current replacement sales are declining. To reduce the generation of waste products on a short‐term basis, lifespan must be extended until the waste‐reducing effect of lifespan extension exceeds the waste‐increasing effect of the other two factors. From a long‐term perspective, controlling current replacement and additional purchases can be used to prevent future waste product generation.     

Monolayers assembled from a glycolipid biosurfactant from <Emphasis Type="Italic">Pseudozyma</Emphasis> (<Emphasis Type="Italic">Candida</Emphasis>) <Emphasis Type="Italic">antarctica</Emphasis> serve as a high-affinity ligand system for immunoglobulin G and M

A carbohydrate ligand system has been developed which is composed of self-assembled monolayers (SAMs) of mannosylerythritol lipid-A (MEL-A) from Pseudozyma antarctica, serving for human immunoglobulin G and M (HIgG and HIgM). The estimated binding constants from surface plasmon resonance (SPR) measurement were K _a = 9.4 × 10⁶ M⁻¹ for HIgG and 5.4 × 10⁶ M⁻¹ for HIgM, respectively. The binding site was not in the Fc region of immunoglobulin but in the Fab region. Large amounts of HIgG and HIgM bound to MEL-A SAMs were directly observed by atomic force microscopy.