Probing the Structure of Halo Nuclei

Our understanding of halo nuclei has so far relied on high-energy scattering and reactions, but a number of uncertainties remain. I discuss in general terms the new range of observables which will be measured by experiments around the Coulomb barrier, and how some details of the reaction mechanisms still need to be clarified.Comment: Proceedings of FUSION97 conference (March 1997), South Durras, Australia. Submitted to J. Physics G: special issue `Heavy ion collisions at near barrier energies'. No figures; uses IOPConf.sty (included

Chaotic Scattering in Heavy--Ion Reactions

We discuss the relevance of chaotic scattering in heavy--ion reactions at energies around the Coulomb barrier. A model in two and three dimensions which takes into account rotational degrees of freedom is discussed both classically and quantum-mechanically. The typical chaotic features found in this description of heavy-ion collisions are connected with the anomalous behaviour of several experimental data.Comment: 35 pages in RevTex (version 3.0) plus 27 PostScript figures obtainable by anonymous ftp from VAXFCT.CT.INFN.IT in directory kaos. Fig. 1 upon request to the authors. To be published in the October Focus issue on chaotic scattering of CHAO

H3.1K27me1 maintains transcriptional silencing and genome stability by preventing GCN5-mediated histone acetylation

Epigenetic mechanisms play diverse roles in the regulation of genome stability in eukaryotes. In Arabidopsis thaliana, genome stability is maintained during DNA replication by the H3.1K27 methyltransferases ARABIDOPSIS TRITHORAX-RELATED PROTEIN 5 (ATXR5) and ATXR6, which catalyze the deposition of K27me1 on replication-dependent H3.1 variants. The loss of H3.1K27me1 in atxr5 atxr6 double mutants leads to heterochromatin defects, including transcriptional de-repression and genomic instability, but the molecular mechanisms involved remain largely unknown. In this study, we identified the transcriptional co-activator and conserved histone acetyltransferase GCN5 as a mediator of transcriptional de-repression and genomic instability in the absence of H3.1K27me1. GCN5 is part of a SAGA-like complex in plants that requires the GCN5-interacting protein ADA2b and the chromatin remodeler CHR6 to mediate the heterochromatic defects in atxr5 atxr6 mutants. Our results also indicate that Arabidopsis GCN5 acetylates multiple lysine residues on H3.1 variants, but H3.1K27 and H3.1K36 play essential functions in inducing genomic instability in the absence of H3.1K27me1. Finally, we show that H3.1K36 acetylation by GCN5 is negatively regulated by H3.1K27me1 in vitro. Overall, this work reveals a key molecular role for H3.1K27me1 in maintaining transcriptional silencing and genome stability in heterochromatin by restricting GCN5-mediated histone acetylation in plants

Macroscopic quantum superpositions in highly-excited strongly-interacting many-body systems

We demonstrate a break-down in the macroscopic (classical-like) dynamics of wave-packets in complex microscopic and mesoscopic collisions. This break-down manifests itself in coherent superpositions of the rotating clockwise and anticlockwise wave-packets in the regime of strongly overlapping many-body resonances of the highly-excited intermediate complex. These superpositions involve $\sim 10^4$ many-body configurations so that their internal interactive complexity dramatically exceeds all of those previously discussed and experimentally realized. The interference fringes persist over a time-interval much longer than the energy relaxation-redistribution time due to the anomalously slow phase randomization (dephasing). Experimental verification of the effect is proposed.Comment: Title changed, few changes in the abstract and in the main body of the paper, and changes in the font size in the figure. Uses revTex4, 4 pages, 1 ps figur