Effects of the Final-State Electron-ion Interactions on the Fully Differential Cross Sections for Heavy-Particle-Impact Ionization of Helium

Three-dimensional fully differential cross sections for heavy-particle-impact ionization of helium are examined. Previously, the three-body distorted-wave (3DW) model has achieved good agreement with experiment in the scattering plane for small momentum transfers, but poor agreement for large momentum transfers. Poor agreement was also observed outside the scattering plane for all momentum transfers. In particular, the 3DW calculations predicted cross sections that were too small both perpendicular to the scattering plane and for large momentum transfers. The important unanswered question concerns the physical effects that cause the significant disagreement between experiment and theory. In previous works, the role of the projectile-ion interaction has been examined. Although the importance of exchange between the ejected electron and the residual bound electrons has been well established, and frequently studied, for electron-impact ionization, the importance of this effect has not been examined for heavy-particle scattering. In this paper we examine the role of this effect for heavy-particle scattering

Ionization and ionization-excitation of helium to the n=1–4 states of He+ by electron impact

We present experimental and theoretical results for the electron-impact-induced ionization of ground-state helium atoms. Using a high-sensitivity toroidal electron spectrometer, we measured cross-section ratios for transitions leading to the first three excited states of the residual helium ion relative to the transition leaving the ion in the ground state. Measurements were performed for both symmetric- and asymmetric-energy-sharing kinematics. By presenting results as a ratio, a direct comparison can be made between theoretical and experimental predictions without recourse to normalization. The experimental data are compared to theoretical predictions employing various first-order models and a second-order hybrid distorted-wave + convergent R matrix with pseudostates close-coupling approach. All the first-order models fail in predicting even the approximate size of the cross-section ratios. The second-order calculations are found to describe the experimental data for asymmetric-energy-sharing with reasonable fidelity, although significant disparities are evident for the symmetric-energy-sharing cases. These comparisons demonstrate the need for further theoretical developments, in which all four charged particles are treated on an equal footing.S. Bellm, J. Lower, K. Bartschat, X. Guan, D. Weflen, M. Foster, A. L. Harris, and D. H. Madiso

A New Role for Translation Initiation Factor 2 in Maintaining Genome Integrity

Escherichia coli translation initiation factor 2 (IF2) performs the unexpected function of promoting transition from recombination to replication during bacteriophage Mu transposition in vitro, leading to initiation by replication restart proteins. This function has suggested a role of IF2 in engaging cellular restart mechanisms and regulating the maintenance of genome integrity. To examine the potential effect of IF2 on restart mechanisms, we characterized its influence on cellular recovery following DNA damage by methyl methanesulfonate (MMS) and UV damage. Mutations that prevent expression of full-length IF2-1 or truncated IF2-2 and IF2-3 isoforms affected cellular growth or recovery following DNA damage differently, influencing different restart mechanisms. A deletion mutant (del1) expressing only IF2-2/3 was severely sensitive to growth in the presence of DNA-damaging agent MMS. Proficient as wild type in repairing DNA lesions and promoting replication restart upon removal of MMS, this mutant was nevertheless unable to sustain cell growth in the presence of MMS; however, growth in MMS could be partly restored by disruption of sulA, which encodes a cell division inhibitor induced during replication fork arrest. Moreover, such characteristics of del1 MMS sensitivity were shared by restart mutant priA300, which encodes a helicase-deficient restart protein. Epistasis analysis indicated that del1 in combination with priA300 had no further effects on cellular recovery from MMS and UV treatment; however, the del2/3 mutation, which allows expression of only IF2-1, synergistically increased UV sensitivity in combination with priA300. The results indicate that full-length IF2, in a function distinct from truncated forms, influences the engagement or activity of restart functions dependent on PriA helicase, allowing cellular growth when a DNA–damaging agent is present

Nonlinearity and Topology

The interplay of nonlinearity and topology results in many novel and emergent properties across a number of physical systems such as chiral magnets, nematic liquid crystals, Bose-Einstein condensates, photonics, high energy physics, etc. It also results in a wide variety of topological defects such as solitons, vortices, skyrmions, merons, hopfions, monopoles to name just a few. Interaction among and collision of these nontrivial defects itself is a topic of great interest. Curvature and underlying geometry also affect the shape, interaction and behavior of these defects. Such properties can be studied using techniques such as, e.g. the Bogomolnyi decomposition. Some applications of this interplay, e.g. in nonreciprocal photonics as well as topological materials such as Dirac and Weyl semimetals, are also elucidated

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Effects of the final-state electron-ion interactions on the fully differential cross sections for heavy-particle-impact ionization of helium

Three-dimensional fully differential cross sections for heavy-particle-impact ionization of helium are examined. Previously, the three-body distorted-wave (3DW) model has achieved good agreement with experiment in the scattering plane for small momentum transfers, but poor agreement for large momentum transfers. Poor agreement was also observed outside the scattering plane for all momentum transfers. In particular, the 3DW calculations predicted cross sections that were too small both perpendicular to the scattering plane and for large momentum transfers. The important unanswered question concerns the physical effects that cause the significant disagreement between experiment and theory. In previous works, the role of the projectile-ion interaction has been examined. Although the importance of exchange between the ejected electron and the residual bound electrons has been well established, and frequently studied, for electron-impact ionization, the importance of this effect has not been examined for heavy-particle scattering. In this paper we examine the role of this effect for heavy-particle scattering

Role of IF2 isoforms in the major replication restart pathways.

<p>A) The major restart pathways and the influence of IF2 isoforms. Genetic analysis indicates that IF2-1 influences the restart pathways dependent on PriA helicase, including not only PriA-PriC pathway but also part of the PriA-PriB pathway. IF2-2/3 may play a prominent role in the pathways that do not require PriA helicase. The diagram should not be interpreted to indicate that IF2-2/3 cannot participate in reactions involving PriA helicase or that IF2-1 cannot participate in reactions where PriA's helicase is inactive. However, under these circumstances restart pathways do not function optimally to maintain maximal cell viability. The minor, less robust pathways such as the Rep-PriC pathway are not shown here. These PriA-independent pathways require suppressor mutations in <i>dnaC</i> to support a significant level of cell viability <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002648#pgen.1002648-Sandler1" target="_blank">[18]</a>, <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002648#pgen.1002648-Sandler3" target="_blank">[38]</a>, <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002648#pgen.1002648-Sandler4" target="_blank">[39]</a>. B) Model for the IF2-2/PriA helicase pathway. i) The starting point is a stalled replication fork with bound IF2-1. ii) Binding of restart proteins. The key protein to bind at this stage is PriA, which is poised to displace IF2-1 upon activation of its helicase activity. iii) Replisome assembly. PriA helicase action disassembles IF2-1 from the template, making way for initiation of DNA replication. It is hypothesized that removal of IF2-1 by PriA helicase can be regulated, extensive damage to the DNA template being able to inhibit this process and prevent replication restart. Removal of IF2-2/3 by PriA helicase bypasses this regulation, and IF2-2/3 may also be removed from the DNA by other mechanisms.</p

Epistasis analysis of <i>infB</i> alleles with <i>del(priB)302</i> and <i>priA300</i>.

<p>A) UV sensitivity of GTN1117 expressing <i>priB</i> or <i>priC</i> from pBAD24. GTN1117, which is <i>del(priB)302 </i>, bearing plasmid pBAD24-<i>priB</i> or pBAD24-<i>priC</i> were grown up in LB medium containing 100 µg/ml ampicillin and 0.02% L-arabinose or 0.2% D-glucose as indicated. After UV irradiation, cells were plated on 0.02% arabinose/LB and plain LB plates for viability, both of which produced identical results. B) Interaction of <i>infB</i> alleles with <i>priA300</i>. Survival of <i>priA300</i> strains with the <i></i> (GTN1298), <i></i> (GTN1323), and <i></i> (GTN1297) after UV irradiation was measured.</p

Binding of S-IF2 to Mu ends upon induction of phage replication by transposition.

<p>Mu development in GTN373 (<i>his::</i>Mu<i>cts62 priA300 del(gpt-lac)5</i>) and GTN622 (<i>his::</i>Mu<i>cts62 priA300 clpX::kan del(gpt-lac)5</i>) transformed with pBAD24-S-IF2-1, pBAD24-S-IF2-2, or pBAD24-IF2-2 were induced by incubation at 42°C, and immunoprecipitation with anti-S-tag monoclonal antibody was conducted with samples from 0 and 35 min postinduction. The presence of host and Mu DNA sequences in immunocomplexes were detected by amplifying 200–400 bp segments of template DNA (2 µl of indicated DNA dilutions in 10-µl reactions) in a 26-cycle PCR, using primers for amplifying <i>thrA</i>, <i>pyrD</i>, <i>serA</i>, Mu left end (L), Mu center (C), and Mu right end (R). A) Pull-down of Mu sequences by anti-S-tag antibody during Mu development. 1:20 dilutions of the immunoprecipitation (IP) and the no antibody control and 1∶2500 dilutions of total DNA were used. B) Comparison of IP with S-tagged and untagged IF2-2. GTN373 transformed with the indicated plasmids were used. C) Binding of S-IF2-2 concentrated at or near Mu ends. Analysis was conducted with induced pBAD24-S-IF2-2/GTN373, using one-fifth the standard amount of antibody.</p

Characteristics of MMS sensitivity exhibited by <i></i> mutants and similarity to <i>priA300</i>.

<p>A) Sensitivity of <i></i> and <i>priA300</i> mutants for growth in MMS and suppression by a <i>sulA</i> mutation. The indicated strains are the same as those listed in the legend to <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002648#pgen-1002648-g004" target="_blank">Figure 4C</a>. In addition, the <i>sulA::</i>Mu<i>d(lac,Ap,B::Tn9)</i> allele is present in GTN1387 (<i></i> SulA<b>⁻</b>) and GTN1384 (<i>priA300</i> SulA<b>⁻</b>), and the Mu<i>d(lac,Ap,B::Tn9)</i> is integrated in a site other than <i>sulA</i> in GTN1399 (<i>infB(del1</i>) SulA<b>⁺</b>) and GTN1396 (<i>priA300</i> SulA<b>⁺</b>). Viability of GTN1376 (<i>recA938</i>) on MMS plates was less than 10<b>⁻</b>⁵%. Results are the average of at least 3 independent determinations. B) SOS induction monitored using the <i>sulA::lacZ</i> reporter. GTN1385 (<i>infB(wt)</i> PriA⁺), GTN1384 (<i>priA300</i>), and GTN1387 (<i> PriA⁺) were grown in LB to OD₆₀₀ of 0.3. To 2-ml portions of each culture, MMS was added to 18 mM final concentration. β-galactosidase activity in MMS-treated (+) and untreated (−) cultures was measured. β-galactosidase activity of untreated GTN1639 (GTN1385 <i>priA2::kan</i>) is shown for comparison.</i></p