Total Nuclear Reaction Cross Section Induced by Halo Nuclei and Stable Nuclei

We develop the method for the calculation of the total reaction cross sections induced by the halo nuclei and stable nuclei. This approach is based on the Glauber theory, which is valid for nuclear reactions at high energy. It is extended for nuclear reactions at low energy and intermediate energy by including both the quantum correction and Coulomb correction under the assumption of the effective nuclear density distribution. The calculated results of the total reaction cross section induced by stable nuclei agree well with the 30 experimental data within 10 percent accuracy.The comparison between the numerical results and the 20 experimental data for the total nuclear reaction cross section induced by the neutron halo nuclei and the proton halo nuclei indicates a satisfactory agreement after considering the halo structure of these nuclei, which implies the quite different mean fields for the nuclear reactions induced by halo nuclei and stable nuclei. The halo nucleon distributions and the root mean square radii of these nuclei can be extracted from above comparison based on the improved Glauber model, which indicate clearly the halo structures of these nuclei. Especially, it is clear to see that the medium correction of the nucleon-nucleon collision has little effect on the total reaction cross sections induced by the halo nuclei due to the very weak binding and the very extended density distribution.Comment: 15 pages,2 figures. Communucations in Theoretical Physics, (2003) in pres

Transcriptional regulator-mediated activation of adaptation genes triggers CRISPR <i>de novo</i> spacer acquisition

Acquisition of de novo spacer sequences confers CRISPR-Cas with a memory to defend against invading genetic elements. However, the mechanism of regulation of CRISPR spacer acquisition remains unknown. Here we examine the transcriptional regulation of the conserved spacer acquisition genes in Type I-A of Sulfolobus islandicus REY15A. Csa3a, a MarR-like transcription factor encoded by the gene located adjacent to csa1, cas1, cas2 and cas4 cluster, but on the reverse strand, was demonstrated to specifically bind to the csa1 and cas1 promoters with the imperfect palindromic sequence. Importantly, it was demonstrated that the transcription level of csa1, cas1, cas2 and cas4 was significantly enhanced in a csa3a-overexpression strain and, moreover, the Csa1 and Cas1 protein levels were increased in this strain. Furthermore, we demonstrated the hyperactive uptake of unique spacers within both CRISPR loci in the presence of the csa3a overexpression vector. The spacer acquisition process is dependent on the CCN PAM sequence and protospacer selection is random and non-directional. These results suggested a regulation mechanism of CRISPR spacer acquisition where a single transcriptional regulator senses the presence of an invading element and then activates spacer acquisition gene expression which leads to de novo spacer uptake from the invading element