Repair of DNA double-strand breaks (DSBs) protects cells and organisms, as well as their genome integrity. Since DSB repair occurs in the context of chromatin, chromatin must be modified to prevent it from inhibiting DSB repair. Evidence supports the role of histone modifications and ATP-dependent chromatin remodeling in repair and signaling of chromosome DSBs. The key questions are, then, what the nature of chromatin altered by DSBs is and how remodeling of chromatin facilitates DSB repair. Here we report a chromatin alteration caused by a single HO endonuclease-generated DSB at the Saccharomyces cerevisiae MAT locus. The break induces rapid nucleosome migration to form histone-free DNA of a few hundred base pairs immediately adjacent to the break. The DSB-induced nucleosome repositioning appears independent of end processing, since it still occurs when the 5-to-3 degradation of the DNA end is markedly reduced. The tetracyclinecontrolled depletion of Sth1, the ATPase of RSC, or deletion of RSC2 severely reduces chromatin remodeling and loading of Mre11 and Yku proteins at the DSB. Depletion of Sth1 also reduces phosphorylation of H2A, processing, and joining of DSBs. We propose that RSC-mediated chromatin remodeling at the DSB prepares chromatin to allow repair machinery to access the break and is vital for efficient DSB repair.

The photocatalytic degradation of polychlorinated dibenzo-p-dioxins (PCDDs), which include mono-, tetra-, hepta-, and octachlorinated congeners (MCDD, TCDD, HpCDD and OCDD), was carried out on TiO2 films under UV (λ > 300 nm) or solar light irradiation in the air. All the dioxin congeners tested were successfully degraded on TiO2 while the direct photolysis of them in the absence of TiO2 was negligible. The photocatalytic degradation rates of PCDDs decreased with the number of chlorines and were described by the first-order reaction kinetics with half-lives of 5.8, 3.9, 0.71, and 0.38 h for OCDD, HpCDD, TCDD, and MCDD, respectively. The degradation rates increased with light intensity and TiO2 coating weights up to 2 mW/cm2 (300 < λ < 400 nm) and 200 μg of TiO2/cm2, respectively. Further increases in either the light intensity or the TiO2 coating mass did not much affect the degradation rate. The natural solar light under clear sky conditions was as effective as a 200-W mercury lamp irradiation (filtered through a Pyrex filter) in degrading OCDD on TiO2. The photocatalytic degradation of PCDDs seems to be initiated by OH radical attack and not by conduction band electron transfer. From a diffuse reflectance FTIR study, the degradation of OCDD was found to involve the cleavage of the aromatic ring. Neither stable intermediates nor dechlorinated PCDDs were detected during the photocatalytic degradation.

Artículo de publicación ISIGiven a factor code pi from a shift of finite type X onto a sofic shift Y, the class degree of pi is defined to be the minimal number of transition classes over the points of Y. In this paper, we investigate the structure of transition classes and present several dynamical properties analogous to the properties of fibers of finite-to-one factor codes. As a corollary, we show that for an irreducible factor triple, there cannot be a transition between two distinct transition classes over a right transitive point, answering a question raised by Quas.Fondecyt; Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Educatio

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Background and Purpose-The etiology of moyamoya disease (MMD) remains obscure. This study was undertaken to identify specific proteins associated with the pathogenesis of MMD. Methods-We studied cerebrospinal fluid (CSF) from 20 patients with angiographically confirmed MMD (4 boys and 16 girls; age range, 3 to 13 years; mean, 7.5 years) and 4 control patients with cerebral palsy who underwent selective dorsal rhizotomy (2 boys and 2 girls; age range, 5 to 10 years; mean, 7.3 years). CSF proteins were analyzed by 2-dimensional polyacrylamide gel electrophoresis, and protein identification was performed by matrix-assisted laser desorption/ ionization time-of-flight mass spectrometry. The presence of specific CSF protein in patients with MMD was confirmed by Western blotting. In addition, cerebral CSF was also tested in 7 patients who had other brain diseases but no MMD (2 boys and 5 girls; age range, 1 to 12 years; mean, 6.9 years). Results-We identified 1 polypeptide spot (M r of 13 to 15 kDa and isoelectric point of 5 to 5.5) that was differentially expressed in the CSF samples of MMD patients (mean optical density intensity, 0.36Ϯ0.24; range, 0.05 to 0.92) and control spinal CSF samples (mean, 0.03Ϯ0.04; range, 0 to 0.08; Pϭ0.002). This polypeptide was identified as cellular retinoic acid-binding protein (CRABP)-I. High levels of expression of CRABP-I in the CSF from 17 MMD children were confirmed by Western blotting. Conclusions-The analysis of the CSF of MMD patients reveals high CRABP-I expression. The present study suggests that the elevation of CRABP-I in CSF may be a candidate for pathogenesis of MMD.