11 research outputs found

    Three-Nucleon Electroweak Capture Reactions

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    Recent advances in the study of the p-d radiative and mu-3he weak capture processes are presented and discussed. The three-nucleon bound and scattering states are obtained using the correlated-hyperspherical-harmonics method, with realistic Hamiltonians consisting of the Argonne v14 or Argonne v18 two-nucleon and Tucson-Melbourne or Urbana IX three-nucleon interactions. The electromagnetic and weak transition operators include one- and two-body contributions. The theoretical accuracy achieved in these calculations allows for interesting comparisons with experimental data.Comment: 12 pages, 4 figures, invited talk at the CFIF Fall Workshop: Nuclear Dynamics, from Quarks to Nuclei, Lisbon, 31st of October - 1st of November 200

    Mutability and mutational spectrum of chromosome transmission fidelity genes

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    It has been more than two decades since the original chromosome transmission fidelity (Ctf) screen of Saccharomyces cerevisiae was published. Since that time the spectrum of mutations known to cause Ctf and, more generally, chromosome instability (CIN) has expanded dramatically as a result of systematic screens across yeast mutant arrays. Here we describe a comprehensive summary of the original Ctf genetic screen and the cloning of the remaining complementation groups as efforts to expand our knowledge of the CIN gene repertoire and its mutability in a model eukaryote. At the time of the original screen, it was impossible to predict either the genes and processes that would be overrepresented in a pool of random mutants displaying a Ctf phenotype or what the entire set of genes potentially mutable to Ctf would be. We show that in a collection of 136 randomly selected Ctf mutants, >65% of mutants map to 13 genes, 12 of which are involved in sister chromatid cohesion and/or kinetochore function. Extensive screening of systematic mutant collections has shown that ~350 genes with functions as diverse as RNA processing and proteasomal activity mutate to cause a Ctf phenotype and at least 692 genes are required for faithful chromosome segregation. The enrichment of random Ctf alleles in only 13 of ~350 possible Ctf genes suggests that these genes are more easily mutable to cause genome instability than the others. These observations inform our understanding of recurring CIN mutations in human cancers where presumably random mutations are responsible for initiating the frequently observed CIN phenotype of tumors
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