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This study aimed to map and analyze the spatial pattern of the surface deformation associated with the 2024 Noto Peninsula earthquake (Mw7.5) using structure-from-motion/multi-view-stereo (SfM–MVS), an advanced photogrammetric technique. The analysis was conducted using digital aerial photographs with a ground pixel dimension of 0.2 m (captured the day after the earthquake). Horizontal locations of GCPs were determined using pre-earthquake data to remove the wide-area horizontal crustal deformation component. The elevations of the GCPs were corrected by incorporating quasi-vertical values derived from a 2.5-dimensional analysis of synthetic aperture radar (SAR) results. In the synclinorium structure area, where no active fault had previously been identified, we observed a 5 km long uplift zone (0.1 to 0.2 km in width), along with multiple scarps that reached a maximum height of 2.2 m. The area and shape of the surface deformation suggested that the induced uplift and surrounding landslides were related to fold structures and their growth. Thus, our study shows the efficacy of SfM–MVS with respect to accurately mapping earthquake-induced deformations, providing crucial data for understanding seismic activity and informing disaster-response strategies. [ABSTRACT FROM AUTHOR]

Huntington's disease (HD) is a polyglutamine (polyQ) disease caused by aberrant expansion of the polyQ tract in Huntingtin (HTT). While motor impairment mediated by polyQ-expanded HTT has been intensively studied, molecular mechanisms for nonmotor symptoms in HD, such as psychiatric manifestations, remain elusive. Here we have demonstrated that HTT forms a ternary protein complex with the scaffolding protein DISC1 and cAMP-degrading phosphodiesterase 4 (PDE4) to regulate PDE4 activity. We observed pathological cross-seeding between DISC1 and mutant HTT aggregates in the brains of HD patients as well as in a murine model that recapitulates the polyQ pathology of HD (R6/2 mice). In R6/2 mice, consequent reductions in soluble DISC1 led to dysregulation of DISC1-PDE4 complexes, aberrantly increasing the activity of PDE4. Importantly, exogenous expression of a modified DISC1, which binds to PDE4 but not mutant HTT, normalized PDE4 activity and ameliorated anhedonia in the R6/2 mice. We propose that cross-seeding of mutant HTT and DISC1 and the resultant changes in PDE4 activity may underlie the pathology of a specific subset of mental manifestations of HD, which may provide an insight into molecular signaling in mental illness in general., Introduction Huntington's disease (HD) is a hereditary brain disease characterized by both motor and nonmotor manifestations. Identification of the causal gene for HD, huntingtin (HTT), has facilitated our understanding of [...]

Sphingobium japonicum UT26 utilizes [gamma]-hexachloroeyclohexane ([gamma]/-HCH) as its sole source of carbon and energy. In our previous studies, we cloned and characterized genes encoding enzymes for the conversion of [gamma]-HCH to [beta]-ketoadipate in UT26. In this study, we analyzed a mutant obtained by transposon mutagenesis and identified and characterized new genes encoding a putative ABC-type transporter essential for the utilization of [gamma]-HCH in strain UT26. This putative ABC transporter consists of four components, permease, ATPase, periplasmic protein, and lipoprotein, encoded by linK, linL, linM, and linN, respectively. Mutation and complementation analyses indicated that all the linKLMN genes are required, probably as a set, for [gamma]-HCH utilization in UT26. Furthermore, the mutant cells deficient in this putative ABC transporter showed (i) higher [gamma]-HCH degradation activity and greater accumulation of the toxic dead-end product 2,5-dichlorophenol (2,5-DCP), (ii) higher sensitivity to 2,5-DCP itself, and (iii) higher permeability of hydrophobic compounds than the wild-type cells. These results strongly suggested that LinKLMN are involved in [gamma]-HCH utilization by controlling membrane hydrophobicity. This study clearly demonstrated that a cellular factor besides catabolic enzymes and transcriptional regulators is essential for utilization of xenobiotic compounds in bacterial cells. doi:10.1128/JB.01883-06

Sphingomonas paucimobilis UT26 utilizes [gamma]-hexachiorocyclohexane ([gamma]-HCH) as a sole source of carbon and energy. In our previous study, we cloned and characterized genes that are involved in the conversion of [gamma]-HCH to maleylacetate (MA) via chlorohydroquinone (CHQ) in UT26. In this study, we identified and characterized an MA reductase gene, designated linF, that is essential for the utilization of [gamma]-HCH in UT26. A gene named linEb, whose deduced product showed significant identity to LinE (g3%), was located close to linF. LinE is a novel type of ring cleavage dioxygenase that catalyzes the conversion of CHQ to MA. LinEb expressed in Escherichia coli transformed CHQ and 2,6-dichlorohydroquinone to MA and 2-chloromaleylacetate, respectively. Our previous and present results indicate that UT26 (i) has two gene clusters for degradation of chlorinated aromatic compounds via hydroquinone-type intermediates and (ii) uses at least parts of both clusters for [gamma]-HCH utilization.