Search

A railway is organized by a variety of individual technologies, and functions safely and properly as a system, therefore it is necessary for the system safety to study each potential unsafe case caused due to large earthquakes. Recent reports indicate that railway vehicles could be derailed by earthquake ground motions with no fatal damages of vehicles or tracks. Thus, we should further study the derailment mechanism to pursue to minimize the risk of railway system safety against large earthquakes. Particularly, for more comprehensive understanding on the derailment mechanism of high speed railway vehicle, the derailment process of the case should be directly verified. Therefore, in this study, we arrange an experimental setup with 1/10 scale vehicle and roller rig providing both conditions of high speed wheel/rail rolling contact and large amplitude excitations. Through the experiment, we obtained the outcomes. (1) Two types of vehicle derailment motions are observed; one is rocking derailment and the other is sliding derailment. Derailment motions are similar regardless of vehicle speed. (2) By contrast, the excitation amplitudes for derailment decrease according to the increase of vehicle speed particularly by low frequency excitations. (3) The excitation amplitudes for wheel lift of flange height are relatively independent of vehicle speed. (4) Based on the similarity of fundamental vehicle dynamics between the 1/10 and full scale vehicles, those observed mechanisms in the scaled test should be applicable to that of full scale vehicle.

The APSES protein family includes important transcriptional regulators of morphological processes in ascomycetes. We identified a deletion mutant of the APSES protein Mstu1 in Magnaporthe grisea that showed reduced conidiation and mycelial growth. Mstu1 formed a number of appressoria comparable to the wild type, although appressorium formation was delayed. In M. grisea, rapid transfer of conidial glycogen and lipid droplets to incipient appressoria is required for appressorial turgor generation, which the fungus uses to penetrate plant cuticles. Appressorial turgor was low in mstu1 and the mutant was deficient in appressorium-mediated invasion of rice leaves. The transfer of conidial glycogen and lipid droplets was remarkably delayed in mstu1, and a consequent delay in degradation of these conidial reserves was observed. Our results indicate that Mstu1 is required for appressorium-mediated infection due to its involvement in the mobilization of lipids and glycogen.

Coprinopsis phlyctidospora (syn: Coprinus phlyctidosporus) from the Netherlands, Japan, New Zealand, and Australia can be segregated into two groups, northern and southern, based on the nucleotide sequences of their ITS regions. The mating type of a C. phlyctidospora isolate was tetrapolar. Mating reactions were compatible between monokaryotic testers derived from basidiospores of a Japanese isolate and dikaryotic isolates obtained from a wide geographic area in Japan. In contrast, mating between the Japanese monokaryotic and dikaryotic isolates from Australia and New Zealand were incompatible. These results indicated that C. phlyctidospora was complex and individuals currently recognized as C. phlyctidospora in the Northern Hemisphere and those in the Southern Hemisphere are distinct taxa. The relationship between the clades and the biogeography of the C. phlyctidospora complex are also discussed.

Polyphosphate accumulating organisms (PAOs) belong mostly to Proteobacteria and Actinobacteria and are quite divergent. Under aerobic conditions, they accumulate intracellular polyphosphate (polyP), while they typically synthesize polyhydroxyalkanoates (PHAs) under anaerobic conditions. Many ecological, physiological, and genomic analyses have been performed with proteobacterial PAOs, but few with actinobacterial PAOs. In this study, the whole genome sequence of an actinobacterial PAO, Microlunatus phosphovorus NM-1(T) (NBRC 101784(T)), was determined. The number of genes for polyP metabolism was greater in M. phosphovorus than in other actinobacteria; it possesses genes for four polyP kinases (ppks), two polyP-dependent glucokinases (ppgks), and three phosphate transporters (pits). In contrast, it harbours only a single ppx gene for exopolyphosphatase, although two copies of ppx are generally present in other actinobacteria. Furthermore, M. phosphovorus lacks the phaABC genes for PHA synthesis and the actP gene encoding an acetate/H(+) symporter, both of which play crucial roles in anaerobic PHA accumulation in proteobacterial PAOs. Thus, while the general features of M. phosphovorus regarding aerobic polyP accumulation are similar to those of proteobacterial PAOs, its anaerobic polyP use and PHA synthesis appear to be different.

Ubiquitin-dependent degradation is implicated in various cellular regulatory mechanisms. The SCF Cdc4 (Skp1, Cullin/Cdc53, and the F-box protein Cdc4) complex is an ubiquitin ligase complex that acts as a regulator of cell cycle, signal transduction, and transcription. These regulatory mechanisms are not well defined because of the difficulty in identifying the interaction between ubiquitin ligases and their substrates. To identify substrates of the yeast SCF Cdc4 ubiquitin ligase complex, we refined the yeast two-hybrid system to allow screening Cdc4-substrate interactions under conditions of substrate stabilization, and identified Swi5 as a substrate of the SCF Cdc4 complex. Swi5 is the transcriptional activator of Sic1, the inhibitor of S phase cyclin-dependent kinases (CDKs). We showed that Swi5 is indeed ubiquitinated and degraded through the SCF Cdc4 complex. Furthermore, the SCF Cdc4 -dependent degradation of Swi5 was required to terminate SIC1 transcription at early G 1 phase, which ensured efficient entry into S phase: Hyperaccumulation of Sic1 was noted in cells expressing stabilized Swi5, and expression of stabilized Swi5 delayed S phase entry, which was dominantly suppressed by SIC1 deletion. These findings indicate that the SCF Cdc4 complex regulates S phase entry not only through degradation of Sic1, but also through degradation of Swi5.