Thomas-Ehrman shifts in nuclei around ^{16}O and role of residual nuclear interaction

The asymmetry in the energy spectra between mirror nuclei (the Thomas-Ehrman shifts) around $^{16}$O is investigated from a phenomenological viewpoint. The recent data on proton-rich nuclei indicates that the residual nuclear interaction is reduced for the loosely bound s-orbit by as much as 30%, which originates in the broad radial distribution of the proton single-particle wave function.Comment: to appear in Phys. Lett. B, with 3 eps figure

Reflection equation for the N=3 Cremmer-Gervais R-matrix

We consider the reflection equation of the N=3 Cremmer-Gervais R-matrix. The reflection equation is shown to be equivalent to 38 equations which do not depend on the parameter of the R-matrix, q. Solving those 38 equations. the solution space is found to be the union of two types of spaces, each of which is parametrized by the algebraic variety $\mathbb{P}^1(\mathbb{C}) \times \mathbb{P}^1(\mathbb{C}) \times \mathbb{P}^2(\mathbb{C})$ and $\mathbb{C} \times \mathbb{P}^1(\mathbb{C}) \times \mathbb{P}^2(\mathbb{C})$.Comment: 28 pages, revised versio

Simultaneous disruption of two DNA polymerases, Polη and Polζ, in Avian DT40 cells unmasks the role of Polη in cellular response to various DNA lesions

Replicative DNA polymerases are frequently stalled by DNA lesions. The resulting replication blockage is released by homologous recombination (HR) and translesion DNA synthesis (TLS). TLS employs specialized TLS polymerases to bypass DNA lesions. We provide striking in vivo evidence of the cooperation between DNA polymerase η, which is mutated in the variant form of the cancer predisposition disorder xeroderma pigmentosum (XP-V), and DNA polymerase ζ by generating POLη−/−/POLζ−/− cells from the chicken DT40 cell line. POLζ−/− cells are hypersensitive to a very wide range of DNA damaging agents, whereas XP-V cells exhibit moderate sensitivity to ultraviolet light (UV) only in the presence of caffeine treatment and exhibit no significant sensitivity to any other damaging agents. It is therefore widely believed that Polη plays a very specific role in cellular tolerance to UV-induced DNA damage. The evidence we present challenges this assumption. The phenotypic analysis of POLη−/−/POLζ−/− cells shows that, unexpectedly, the loss of Polη significantly rescued all mutant phenotypes of POLζ−/− cells and results in the restoration of the DNA damage tolerance by a backup pathway including HR. Taken together, Polη contributes to a much wide range of TLS events than had been predicted by the phenotype of XP-V cells

Tuba, a Cdc42 GEF, is required for polarized spindle orientation during epithelial cyst formation

An RNAi screen picks Tuba out of the GTPase exchange factor (GEF) orchestra as a regulator of cell polarity in epithelial morphogenesis. (See also a companion paper from Rodriguez-Fraticelli et al., in this issue.

In Vitro Contraction of Cytokinetic Ring Depends on Myosin II but not on Actin Dynamics

10.1038/ncb2781Nature Cell Biology157853-859NCBI

Anaplastic lymphoma kinase (ALK) inhibitor response in neuroblastoma is highly correlated with ALK mutation status, ALK mRNA and protein levels

Background In pediatric neuroblastoma (NBL), high anaplastic lymphoma kinase (ALK) levels appear to be correlated with an unfavorable prognosis, regardless of ALK mutation status. This suggests a therapeutic role for ALK inhibitors in NBL patients. We examined the correlation between levels of ALK, phosphorylated ALK (pALK) and downstream signaling proteins and response to ALK inhibition in a large panel of both ALK mutated and wild type (WT) NBL cell lines. Methods We measured protein levels by western blot and ALK inhibitor sensitivity (TAE684) by viability assays in 19 NBL cell lines of which 6 had a point mutation and 4 an amplification of the ALK gene. Results ALK 220 kDa (p=0.01) and ALK 140 kDa (p= 0.03) protein levels were higher in ALK mutant than WT cell lines. Response to ALK inhibition was significantly correlated with ALK protein levels (p<0.01). ALK mutant cell lines (n=4) were 14,9 fold (p<0,01) more sensitive to ALK inhibition than eight WT cell lines. Conclusion NBL cell lines often express ALK at high levels and are responsive to ALK inhibitors. Mutated cell lines express ALK at higher levels, which may define their superior response to ALK inhibition

Spt2p Defines a New Transcription-Dependent Gross Chromosomal Rearrangement Pathway

Large numbers of gross chromosomal rearrangements (GCRs) are frequently observed in many cancers. High mobility group 1 (HMG1) protein is a non-histone DNA-binding protein and is highly expressed in different types of tumors. The high expression of HMG1 could alter DNA structure resulting in GCRs. Spt2p is a non-histone DNA binding protein in Saccharomyces cerevisiae and shares homology with mammalian HMG1 protein. We found that Spt2p overexpression enhances GCRs dependent on proteins for transcription elongation and polyadenylation. Excess Spt2p increases the number of cells in S phase and the amount of single-stranded DNA (ssDNA) that might be susceptible to cause DNA damage and GCR. Consistently, RNase H expression, which reduces levels of ssDNA, decreased GCRs in cells expressing high level of Spt2p. Lastly, high transcription in the chromosome V, the location at which GCR is monitored, also enhanced GCR formation. We propose a new pathway for GCR where DNA intermediates formed during transcription can lead to genomic instability