RESUMO
The new Japanese x-ray astronomy satellite, ASTRO-H, will carry two identical hard x-ray telescopes (HXTs), which cover the energy range of 5 to 80 keV. The HXT mirrors employ tightly nested, conically approximated thin-foil Wolter-I optics, and the mirror surfaces are coated with Pt/C depth-graded multilayers to enhance the hard x-ray effective area by means of Bragg reflection. The HXT comprises foils 120-450 mm in diameter and 200 mm in length, with a focal length of 12 m. To obtain a large effective area, 213 aluminum foils 0.2 mm in thickness are tightly nested confocally. The requirements for HXT are a total effective area of >300 cm2 at 30 keV and an angular resolution of <1.7' in half-power diameter (HPD). Fabrication of two HXTs has been completed, and the x-ray performance of each HXT was measured at a synchrotron radiation facility, SPring-8 BL20B2 in Japan. Angular resolutions (HPD) of 1.9' and 1.8' at 30 keV were obtained for the full telescopes of HXT-1 and HXT-2, respectively. The total effective area of the two HXTs at 30 keV is 349 cm2.
Assuntos
Lentes , Astronave/instrumentação , Telescópios , Difração de Raios X/instrumentação , Desenho Assistido por Computador , Desenho de Equipamento , Análise de Falha de EquipamentoRESUMO
Nucleosome positioning has been proposed as a mechanism of transcriptional repression. Here, we examined whether nucleosome positioning affects activator binding in living yeast cells. We introduced the cognate Hap1 binding site (UAS1) at a location 24-43 bp, 29-48 bp, or 61-80 bp interior to the edge of a nucleosome positioned by alpha2/Mcm1 in yeast minichromosomes. Hap1 binding to the UAS1 was severely inhibited, not only at the pseudo-dyad but also in the peripheral region of the positioned nucleosome in alpha cells, while it was detectable in a cells, in which the nucleosomes were not positioned. Hap1 binding was restored in alpha cells with tup1 or isw2 mutations, which caused the loss of nucleosome positioning. These results support the mechanism in which alpha2/Mcm1-dependent nucleosome positioning has a regulatory function to limit the access of transcription factors.
Assuntos
Proteínas de Ligação a DNA/genética , Nucleossomos/fisiologia , Nucleossomos/ultraestrutura , Proteínas de Saccharomyces cerevisiae/genética , Saccharomyces cerevisiae/genética , Transativadores/genética , Fatores de Transcrição/genética , Ativação Transcricional/genética , Proteína 1 de Manutenção de Minicromossomo , Ligação ProteicaRESUMO
Triplet repeat sequences that cause human hereditary diseases can form a variety of DNA conformations. Since DNA structures act as determinants of chromatin structure, chromatin may be involved in mechanisms of these diseases. To address this issue, we examined effects of triplet repeat sequences on chromatin structure and gene expression in Saccharomyces cerevisiae. We show here that (1) (CTG)12 promotes nucleosome formation, (2) (CGG)12 disrupts an array of positioned nucleosomes, and (3) (GAA)12 has little effect on nucleosome formation. Also, we show that insertion of (CGG)12 increases gene expression of a UAS-less promoter about 10-fold, while (CTG)12 and (GAA)12 have no effect. Thus, expansion of triplet repeat sequences may cause improper expression of disease related genes, through their effects on chromatin structure.