Neutrino masses in R-parity violating supersymmetric models

We study neutrino masses and mixing in R-parity violating supersymmetric models with generic soft supersymmetry breaking terms. Neutrinos acquire masses from various sources: Tree level neutrino--neutralino mixing and loop effects proportional to bilinear and/or trilinear R-parity violating parameters. Each of these contributions is controlled by different parameters and have different suppression or enhancement factors which we identified. Within an Abelian horizontal symmetry framework these factors are related and specific predictions can be made. We found that the main contributions to the neutrino masses are from the tree level and the bilinear loops and that the observed neutrino data can be accommodated once mild fine-tuning is allowed.Comment: 18 pages; minor typos corrected. To be published in Physical Review

Solar Neutrino Masses and Mixing from Bilinear R-Parity Broken Supersymmetry: Analytical versus Numerical Results

We give an analytical calculation of solar neutrino masses and mixing at one-loop order within bilinear R-parity breaking supersymmetry, and compare our results to the exact numerical calculation. Our method is based on a systematic perturbative expansion of R-parity violating vertices to leading order. We find in general quite good agreement between approximate and full numerical calculation, but the approximate expressions are much simpler to implement. Our formalism works especially well for the case of the large mixing angle MSW solution (LMA-MSW), now strongly favoured by the recent KamLAND reactor neutrino data.Comment: 34 pages, 14 ps figs, some clarifying comments adde

Crk Adapter Proteins Promote an Epithelial–Mesenchymal-like Transition and Are Required for HGF-mediated Cell Spreading and Breakdown of Epithelial Adherens Junctions

Activation of the Met receptor tyrosine kinase through its ligand, hepatocyte growth factor (HGF), promotes an epithelial–mesenchymal transition and cell dispersal. However, little is known about the HGF-dependent signals that regulate these events. HGF stimulation of epithelial cell colonies leads to the enhanced recruitment of the CrkII and CrkL adapter proteins to Met-dependent signaling complexes. We provide evidence that signals involving CrkII and CrkL are required for the breakdown of adherens junctions, the spreading of epithelial colonies, and the formation of lamellipodia in response to HGF. The overexpression of a CrkI SH3 domain mutant blocks these HGF-dependent events. In addition, the overexpression of CrkII or CrkL promotes lamellipodia formation, loss of adherens junctions, cell spreading, and dispersal of colonies of breast cancer epithelial cells in the absence of HGF. Stable lines of epithelial cells overexpressing CrkII show enhanced activation of Rac1 and Rap1. The Crk-dependent breakdown of adherens junctions and cell spreading is inhibited by the expression of a dominant negative mutant of Rac1 but not Rap1. These findings provide evidence that Crk adapter proteins play a critical role in the breakdown of adherens junctions and the spreading of sheets of epithelial cells