The RHO1 gene encodes a homolog of mammalian RhoA small GTP binding protein in the yeast Saccharomyces cerevisiae. Rho1p is localized at the growth sites, including the bud tip and the cytokinesis site, and is required for bud formation. We have recently shown that Pkc1p, a yeast homolog of mammalian protein kinase C, and glucan synthase are targets of Rho1p. Using the two‐hybrid screening system, we cloned a gene encoding a protein which interacted with the GTP‐bound form of Rho1p. This gene was identified as BNI1, known to be implicated in cytokinesis or establishment of cell polarity in S.cerevisiae. Bni1p shares homologous domains (FH1 and FH2 domains) with proteins involved in cytokinesis or establishment of cell polarity, including formin of mouse, capu and dia of Drosophila and FigA of Aspergillus. A temperature‐sensitive mutation in which the RHO1 gene was replaced by the mammalian RhoA gene showed a synthetically lethal interaction with the bni1 mutation and the RhoA bni1 mutant accumulated cells with a deficiency in cytokinesis. Furthermore, this synthetic lethality was caused by the incapability of RhoA to activate Pkc1p, but not glucan synthase. These results suggest that Rho1p regulates cytoskeletal reorganization at least through Bni1p and Pkc1p.

A deletion polymorphism of the ACE gene is associated with serum ACE activity and increased risk for CAD in the Japanese.

We puri®ed a novel actin ®lament (F-actin)-binding protein from the soluble fraction of Saccharomyces cerevisiae by successive column chromatographies by use of the 125 I-labeled F-actin blot overlay method. The puri®ed protein showed a minimum M r of about 140 kDa on SDS-polyacrylamide gel electrophoresis and we named it ABP140. A search with the partial amino acid sequences of ABP140 against the Saccharomyces Genome Database revealed that the open reading frame of the ABP140 gene (ABP140) corresponded to YOR239W fused with YOR240W by the +1 translational frame shift. The encoded protein consisted of 628 amino acids with a calculated M r of 71,484. The recombinant protein interacted with F-actin and showed the activity to crosslink F-actin into a bundle. Indirect immuno¯uorescence study demonstrated that ABP140 was colocalized with both cortical actin patches and cytoplasmic actin cables in intact cells. However, elimination of ABP140 by gene disruption did not show a deleterious e ect on cell growth or a ect the organization of F-actin. These results indicate that ABP140 is not required for cell growth but may be involved in the reorganization of F-actin in the budding yeast.

In order to study the thermodynamic properties of brane-antibrane systems, we compute the finite temperature effective potential of tachyon T in this system on the basis of boundary string field theory. At low temperature, the minimum of the potential shifts towards T = 0 as the temperature increases. In the D9-D9 case, the sign of the coefficient of |T | 2 term of the potential changes slightly below the Hagedorn temperature. This means that a phase transition occurs near the Hagedorn temperature. On the other hand, the coefficient is kept negative in the Dp-Dp case with p ≤ 8, and thus a phase transition does not occur. This leads us to the conclusion that only a D9-D9 pair and no other (lower dimensional) braneantibrane pairs are created near the Hagedorn temperature. We also discuss a phase transition in NS9B-NS9B case as a model of the Hagedorn transition of closed strings.As we commented in §4, the calculation based on the canonical ensemble cannot be trusted if the temperature is closed to the Hagedorn temperature. In this appendix, we show that the

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The RHO1 gene encodes a homolog of the mammalian RhoA small GTP-binding protein in the yeast Saccharomyces cerevisiae. Rho1p is localized at the growth site and is required for bud formation. The RHO1(G22S, D125N) mutation is a temperature-sensitive and dominant negative mutation of RHO1, and a multicopy suppressor of RHO1(G22S, D125N), ROM7, was isolated. Nucleotide sequencing of ROM7 revealed that it is identical to the BEM4 gene (GenBank accession number L27816), although its physiological function has not yet been reported. Disruption of BEM4 resulted in the cold-and temperature-sensitive growth phenotypes, and cells of the ⌬bem4 mutant showed abnormal morphology, suggesting that BEM4 is involved in the budding process. The temperature-sensitive growth phenotype was suppressed by overexpression of RHO1, ROM2, which encodes a Rho1p-specific GDP/GTP exchange factor, or PKC1, which encodes a target of Rho1p. Moreover, glucan synthase activity, which is activated by Rho1p, was significantly reduced in the ⌬bem4 mutant. Two-hybrid and biochemical experiments revealed that Bem4p directly interacts with the nucleotide-free form of Rho1p and, to lesser extents, with the GDP-and GTP-bound forms of Rho1p, although Bem4p showed neither GDP/GTP exchange factor, GDP dissociation inhibitor, nor GTPase-activating protein activity toward Rho1p. These results indicate that Bem4p is a novel protein directly interacting with Rho1p and is involved in the RHO1-mediated signaling pathway.

Attenuated total reflectance Fouriertransform infrared (ATR-FTIR) spectra were measured in the region from 4300 t o 400 c m -' f o r a hydrated Na,0-Si02 glass containing 35 wt% water. The Si-OH bending vibration mode was observed. It was found that the incorporated water, molecular water as well as hydroxyls, affected the Si-0 vibrations. The effect of incorporated water upon the glass structure is discussed. [

We present observations of ground deformation at Sakurajima in August 2015 and model the deformation using a combination of GNSS, tilt and strain data in order to interpret a rapid deformation event on August 15, 2015. The pattern of horizontal displacement during the period from August 14 to 16, 2015, shows a WNW-ESE extension, which suggests the opening of a dike. Using a genetic algorithm, we obtained the position, dip, strike length, width and opening of a dislocation source based on the combined data. A nearly vertical dike with a NNE-SSW strike was found at a depth of 1.0 km below sea level beneath the Showa crater. The length and width are 2.3 and 0.6 km, respectively, and a dike opening of 1.97 m yields a volume increase of 2.7 × 10 6 m 3 . 887 volcano-tectonic (VT) earthquakes beside the dike suggest that the rapid opening of the dike caused an accumulation of strain in the surrounding rocks, and the VT earthquakes were generated to release this strain. Half of the total amount of deformation was concentrated between 10:27 and 11:54 on August 15. It is estimated that the magma intrusion rate was 1 × 10 6 m 3 /h during this period. This is 200 times larger than the magma intrusion rate prior to one of the biggest eruptions at the summit crater of Minami-dake on July 24, 2012, and 2200 times larger than the average magma intrusion rate during the period from October 2011 to March 2012. The previous Mogi-type ground deformation is considered to be a process of magma accumulation in preexisting spherical reservoirs. Conversely, the August 2015 event was a dike intrusion and occurred in a different location to the preexisting reservoirs. The direction of the opening of the dike coincides with the T-axes and direction of faults creating a graben structure.