Towards testing a two-Higgs-doublet model with maximal CP symmetry at the LHC: construction of a Monte Carlo event generator

A Monte Carlo event generator is constructed for a two-Higgs-doublet model with maximal CP symmetry, the MCPM. The model contains five physical Higgs bosons; the $\rho'$, behaving similarly to the standard-model Higgs boson, two extra neutral bosons $h'$ and $h"$, and a charged pair $H^\pm$. The special feature of the MCPM is that, concerning the Yukawa couplings, the bosons $h'$, $h"$ and $H^\pm$ couple directly only to the second generation fermions but with strengths given by the third-generation-fermion masses. Our event generator allows the simulation of the Drell-Yan-type production processes of $h'$, $h"$ and $H^\pm$ in proton-proton collisions at LHC energies. Also the subsequent leptonic decays of these bosons into the $\mu^+ \mu^-$, $\mu^+ \nu_\mu$ and $\mu^- \bar \nu_\mu$ channels are studied as well as the dominant background processes. We estimate the integrated luminosities needed in $p p$ collisions at center-of-mass energies of 8 TeV and 14 TeV for significant observations of the Higgs bosons $h'$, $h"$ and $H^\pm$ in these muonic channels

Minimizing Higgs Potentials via Numerical Polynomial Homotopy Continuation

The study of models with extended Higgs sectors requires to minimize the corresponding Higgs potentials, which is in general very difficult. Here, we apply a recently developed method, called numerical polynomial homotopy continuation (NPHC), which guarantees to find all the stationary points of the Higgs potentials with polynomial-like nonlinearity. The detection of all stationary points reveals the structure of the potential with maxima, metastable minima, saddle points besides the global minimum. We apply the NPHC method to the most general Higgs potential having two complex Higgs-boson doublets and up to five real Higgs-boson singlets. Moreover the method is applicable to even more involved potentials. Hence the NPHC method allows to go far beyond the limits of the Gr\"obner basis approach.Comment: 9 pages, 4 figure

A new type of CP symmetry, family replication and fermion mass hierarchies

We study a two-Higgs-doublet model with four generalised CP symmetries in the scalar sector. Electroweak symmetry breaking leads automatically to spontaneous breaking of two of them. We require that these four CP symmetries can be extended from the scalar sector to the full Lagrangian and call this requirement the principle of maximal CP invariance. The Yukawa interactions of the fermions are severely restricted by this requirement. In particular, a single fermion family cannot be coupled to the Higgs fields. For two fermion families, however, this is possible. Enforcing the absence of flavour-changing neutral currents, we find degenerate masses in both families or one family massless and one massive. In the latter case the Lagrangian is highly symmetric, with the mass hierarchy being generated by electroweak symmetry breaking. Adding a third family uncoupled to the Higgs fields and thus keeping it massless we get a model which gives a rough approximation of some features of the fermions observed in Nature. We discuss a number of predictions of the model which may be checked in future experiments at the LHC.Comment: 24 pages. Version published in EPJC. Minor changes as suggested by the refere

CP properties of symmetry-constrained two-Higgs-doublet models

The two-Higgs-doublet model can be constrained by imposing Higgs-family symmetries and/or generalized CP symmetries. It is known that there are only six independent classes of such symmetry-constrained models. We study the CP properties of all cases in the bilinear formalism. An exact symmetry implies CP conservation. We show that soft breaking of the symmetry can lead to spontaneous CP violation (CPV) in three of the classes.Comment: 14 pages, 2 tables, revised version adapted to the journal publicatio

The Exocyst Subunit Sec6 Interacts with Assembled Exocytic SNARE Complexes

In eukaryotic cells, membrane-bound vesicles carry cargo between intracellular compartments, to and from the cell surface, and into the extracellular environment. Many conserved families of proteins are required for properly localized vesicle fusion, including the multisubunit tethering complexes and the SNARE complexes. These protein complexes work together to promote proper vesicle fusion in intracellular trafficking pathways. However, the mechanism by which the exocyst, the exocytosis-specific multisubunit tethering complex, interacts with the exocytic SNAREs to mediate vesicle targeting and fusion is currently unknown. We have demonstrated previously that the Saccharomyces cerevisiae exocyst subunit Sec6 directly bound the plasma membrane SNARE protein Sec9 in vitro and that Sec6 inhibited the assembly of the binary Sso1-Sec9 SNARE complex. Therefore, we hypothesized that the interaction between Sec6 and Sec9 prevented the assembly of premature SNARE complexes at sites of exocytosis. To map the determinants of this interaction, we used cross-linking and mass spectrometry analyses to identify residues required for binding. Mutation of residues identified by this approach resulted in a growth defect when introduced into yeast. Contrary to our previous hypothesis, we discovered that Sec6 does not change the rate of SNARE assembly but, rather, binds both the binary Sec9-Sso1 and ternary Sec9-Sso1-Snc2 SNARE complexes. Together, these results suggest a new model in which Sec6 promotes SNARE complex assembly, similar to the role proposed for other tether subunit-SNARE interactions

Writing, Reading, and Translating the Clustered Protocadherin Cell Surface Recognition Code for Neural Circuit Assembly

The ability of neurites of individual neurons to distinguish between themselves and neurites from other neurons and to avoid self (self-avoidance) plays a key role in neural circuit assembly in both invertebrates and vertebrates. Similarly, when individual neurons of the same type project into receptive fields of the brain, they must avoid each other to maximize target coverage (tiling). Counterintuitively, these processes are driven by highly specific homophilic interactions between cell surface proteins that lead to neurite repulsion rather than adhesion. Among these proteins in vertebrates are the clustered protocadherins (Pcdhs), and key to their function is the generation of enormous cell surface structural diversity. Here we review recent advances in understanding how a Pcdh cell surface code is generated by stochastic promoter choice; how this code is amplified and read by homophilic interactions between Pcdh complexes at the surface of neurons; and, finally, how the Pcdh code is translated to cellular function, which mediates self-avoidance and tiling and thus plays a central role in the development of complex neural circuits. Not surprisingly, Pcdh mutations that diminish homophilic interactions lead to wiring defects and abnormal behavior in mice, and sequence variants in the Pcdh gene cluster are associated with autism spectrum disorders in family-based genetic studies in humans

Baryogenesis in the Two-Higgs Doublet Model

We consider the generation of the baryon asymmetry in the two-Higgs doublet model. Investigating the thermal potential in the presence of CP violation, as relevant for baryogenesis, we find a strong first-order phase transition if the extra Higgs states are heavier than about 300 GeV. The mass of the lightest Higgs can be as large as about 200 GeV. We compute the bubble wall properties, including the profile of the relative complex phase between the two Higgs vevs. The baryon asymmetry is generated by top transport, which we treat in the WKB approximation. We find a baryon asymmetry consistent with observations. The neutron electric dipole moment is predicted to be larger than about 10^{-27}ecm and can reach the current experimental bound. Low values of tan\beta are favored.Comment: 25 pages, 7 figure

Protocadherins Mediate Dendritic Self-Avoidance in the Mammalian Nervous System

Dendritic arbors of many neurons are patterned by a process called self-avoidance, in which branches arising from a single neuron repel each other. By minimizing gaps and overlaps within the arbor, self-avoidance facilitates complete coverage of a neuron’s territory by its neurites. Remarkably, some neurons that display self-avoidance interact freely with other neurons of the same subtype, implying that they discriminate self from non-self. Here, we demonstrate roles for the clustered protocadherins (Pcdhs) in dendritic self-avoidance and self/non-self discrimination. The Pcdh locus encodes ~60 related cadherin-like transmembrane proteins, at least some of which exhibit isoform-specific homophilic adhesion in heterologous cells and are expressed stochastically and combinatorially in single neurons. Deletion of all 22 Pcdhs in the mouse gamma subcluster (Pcdhgs) disrupts self-avoidance of dendrites in retinal starburst amacrine cells (SACs) and cerebellar Purkinje cells. Further genetic analysis of SACs showed that Pcdhgs act cell-autonomously during development, and that replacement of the 22 Pcdhgs with a single isoform restores self-avoidance. Moreover, expression of the same single isoform in all SACs decreases interactions among dendrites of neighboring SACs (heteroneuronal interactions). These results suggest that homophilic Pcdhg interactions between sibling neurites (isoneuronal interactions) generate a repulsive signal that leads to self-avoidance. In this model, heteroneuronal interactions are normally permitted because dendrites seldom encounter a matched set of Pcdhgs unless they emanate from the same soma. In many respects, our results mirror those reported for Dscam1 in Drosophila: this complex gene encodes thousands of recognition molecules that exhibit stochastic expression and isoform-specific interactions, and mediate both self-avoidance and self/non-self discrimination. Thus, although insect Dscams and vertebrate Pcdhs share no sequence homology, they appear to underlie similar strategies for endowing neurons with distinct molecular identities and patterning their arbors.Molecular and Cellular Biolog