Contributions of Histone H3 Nucleosome Core Surface Mutations to Chromatin Structures, Silencing and DNA Repair

Histone H3 mutations in residues that cluster in a discrete region on the nucleosome surface around lysine 79 of H3 affect H3-K79 methylation, impair transcriptional silencing in subtelomeric chromatin, and reveal distinct contributions of histone H3 to various DNA-damage response and repair pathways. These residues might act by recruitment of silencing and DNA-damage response factors. Alternatively, their location on the nucleosome surface suggests a possible involvement in nucleosome positioning, stability and nucleosome interactions. Here, we show that the yeast H3 mutants hht2-T80A, hht2-K79E, hht2-L70S, and hht2-E73D show normal nucleosome positioning and stability in minichromosomes. However, loss of silencing in a subtelomeric URA3 gene correlates with a shift of the promoter nucleosome, while nucleosome positions and stability in the coding region are maintained. Moreover, the H3 mutants show normal repair of UV lesions by photolyase and nucleotide excision repair in minichromosomes and slightly enhanced repair in the subtelomeric region. Thus, these results support a role of those residues in the recruitment of silencing proteins and argue against a general role in nucleosome organization

Modification of the ω\omega-Meson Lifetime in Nuclear Matter

The photo production of $\omega$ mesons on the nuclei C, Ca, Nb and Pb has been measured using the Crystal Barrel/TAPS detector at the ELSA tagged photon facility in Bonn. The dependence of the $\omega$ meson cross section on the nuclear mass number has been compared with three different types of models, a Glauber analysis, a BUU analysis of the Giessen theory group and a calculation by the Valencia theory group. In all three cases, the inelastic $\omega$ width is found to be $130-150 \rm{MeV/c^2}$ at normal nuclear matter density for an average 3-momentum of 1.1 GeV/c. In the restframe of the $\omega$ meson, this inelastic $\omega$ width corresponds to a reduction of the $\omega$ lifetime by a factor $\approx 30$. For the first time, the momentum dependent $\omega$N cross section has been extracted from the experiment and is in the range of 70 mb.Comment: 5 pages, 4 figure

First observation of in-medium modifications of the omega meson

The photoproduction of omega mesons on nuclei has been investigated using the Crystal Barrel/TAPS experiment at the ELSA tagged photon facility in Bonn. The aim is to study possible in-medium modifications of the omega meson via the reaction A(gamma, omega)X. Results obtained for Nb are compared to a reference measurement on a liquid hydrogen target. While for recoiling, long-lived mesons (pi, eta and etaprime), which decay outside of the nucleus, a difference in the lineshape for the two data samples is not observed, we find a significant enhancement towards lower masses for omega mesons with low momenta produced on the Nb target.Comment: Latex, 4 pages, 4 figures, accepted by Phys. Rev. Lett; references re-arranged, now references in chronological order in first paragrap

RNA Polymerase I Transcription Factors in Active Yeast rRNA Gene Promoters Enhance UV Damage Formation and Inhibit Repair

UV photofootprinting and repair of pyrimidine dimers by photolyase was used to investigate chromatin structure, protein-DNA interactions, and DNA repair in the spacer and promoter of Saccharomyces cerevisiae rRNA genes. Saccharomyces cerevisiae contains about 150 copies of rRNA genes separated by nontranscribed spacers. Under exponential growth conditions about half of the genes are transcribed by RNA polymerase I (RNAP-I). Initiation of transcription requires the assembly of the upstream activating factor (UAF), the core factor (CF), TATA binding protein, and RNAP-I with Rrn3p on the upstream element and core promoter. We show that UV irradiation of wild-type cells and transcription factor mutants generates photofootprints in the promoter elements. The core footprint depends on UAF, while the UAF footprint was also detected in absence of the CFs. Fractionation of active and inactive promoters showed the core footprint mainly in the active fraction and similar UAF footprints in both fractions. DNA repair by photolyase was strongly inhibited in active promoters but efficient in inactive promoters. The data suggest that UAF is present in vivo in active and inactive promoters and that recruitment of CF and RNAP-I to active promoters generates a stable complex which inhibits repair

Taq DNA Polymerase Blockage at Pyrimidine Dimers

ISSN:1362-4962ISSN:0301-561