Supersymmetric Grand Unification and Lepton Universality in K-> l \nu Decays

Motivated by the prospects for an improved test of lepton universality in K -> l \nu decays by the NA62 experiment at CERN, we study predictions for the possible lepton non-universality in K -> l \nu decays in supersymmetric models. Violations of \mu-e universality in this process may originate from mixing effects in the right-handed slepton sector, providing a unique window into this aspect of supersymmetric flavour physics in the large-\tan\beta region. Minimal unification scenarios with universal soft supersymmetry-breaking terms at the GUT scale would predict negligible violation of lepton universality. However, lepton non-universality may be observable in non-minimal grand unified models with higher-dimensional terms contributing to fermion masses, in which case renormalization effects above the GUT scale may enhance the mixing among the right-handed sleptons. This could leads to observable lepton non-universality in K -> l \nu decays in specific regions of the parameter space with high \tan \beta, large A terms and small charged Higgs boson mass. Observable non-universality in K -> l \nu decays would be correlated with a large value of BR(\tau -> e \gamma). The experimental upper limit on the electric dipole moment of the electron could be reconciled with leptogenesis, if the latter occurs at a relatively low scale, which would also alleviate the cosmological gravitino problem. Even if lepton non-universality is not seen in the near future, one may nevertheless obtain significant constraints on the model parameters and unknown aspects of right-handed fermion and sfermion mixing.Comment: 19 pages, 3 figure

MSSM Higgs sector CP violation at photon colliders: Revisited

We present a comprehensive analysis on the MSSM Higgs sector CP violation at photon colliders including the chargino contributions as well as the contributions of other charged particles. The chargino loop contributions can be important for the would-be CP odd Higgs production at photon colliders. Polarization asymmetries are indispensable in determining the CP properties of neutral Higgs bosons.Comment: 24 pages, 40 figure

Long-lived neutral-kaon flux measurement for the KOTO experiment

The KOTO ($K^0$ at Tokai) experiment aims to observe the CP-violating rare decay $K_L \rightarrow \pi^0 \nu \bar{\nu}$ by using a long-lived neutral-kaon beam produced by the 30 GeV proton beam at the Japan Proton Accelerator Research Complex. The $K_L$ flux is an essential parameter for the measurement of the branching fraction. Three $K_L$ neutral decay modes, $K_L \rightarrow 3\pi^0$, $K_L \rightarrow 2\pi^0$, and $K_L \rightarrow 2\gamma$ were used to measure the $K_L$ flux in the beam line in the 2013 KOTO engineering run. A Monte Carlo simulation was used to estimate the detector acceptance for these decays. Agreement was found between the simulation model and the experimental data, and the remaining systematic uncertainty was estimated at the 1.4\% level. The $K_L$ flux was measured as $(4.183 \pm 0.017_{\mathrm{stat.}} \pm 0.059_{\mathrm{sys.}}) \times 10^7$ $K_L$ per $2\times 10^{14}$ protons on a 66-mm-long Au target.Comment: 27 pages, 16 figures. To be appeared in Progress of Theoretical and Experimental Physic

Searching for realistic 4d string models with a Pati-Salam symmetry -- Orbifold grand unified theories from heterotic string compactification on a Z6 orbifold

Motivated by orbifold grand unified theories, we construct a class of three-family Pati-Salam models in a Z6 abelian symmetric orbifold with two discrete Wilson lines. These models have marked differences from previously-constructed three-family models in prime-order orbifolds. In the limit where one of the six compactified dimensions (which lies in a Z2 sub-orbifold) is large compared to the string length scale, our models reproduce the supersymmetry and gauge symmetry breaking pattern of 5d orbifold grand unified theories on an S1/Z2 orbicircle. We find a horizontal 2+1 splitting in the chiral matter spectra -- 2 families of matter are localized on the Z2 orbifold fixed points, and 1 family propagates in the 5d bulk -- and identify them as the first-two and third families. Remarkably, the first two families enjoy a non-abelian dihedral D4 family symmetry, due to the geometric setup of the compactified space. In all our models there are always some color triplets, i.e. (6,1,1) representations of the Pati-Salam group, survive orbifold projections. They could be utilized to spontaneously break the Pati-Salam symmetry to that of the Standard Model. One model, with a 5d E6 symmetry, may give rise to interesting low energy phenomenology. We study gauge coupling unification, allowed Yukawa couplings and some of their phenomenological consequences. The E6 model has a renormalizable Yukawa coupling only for the third family. It predicts a gauge-Yukawa unification relation at the 5d compactification scale, and is capable of generating reasonable quark/lepton masses and mixings. Potential problems are also addressed, they may point to the direction for refining our models.Comment: 58 pages, 5 figures, 4 tables, revtex4 with ams fonts. Version to appear in NP

Study of non-minimal SUSY SU(5) model with realistic fermion sectors

We study a supersymmetric SU(5) model with the extra Higgs multiplets of 45+\bar 45. The unification of the gauge couplings, the fermion masses and the proton lifetime are discussed in details. The dimension-five operators mediated by different colored Higgs sector can be destructive with each other. This effect serves a way of solving the longevity of proton. We analytically analyze this destructive effect in a special limit where the mixing between the 5- and 45-plets is small. Although the theory does not hold in this special limit, it is a revelatory starting point. We can relax this limit and retain the destructive effect. In a generalized parameter space, this model is in accord with experimental results

SUSY GUT Model Building

I discuss an evolution of SUSY GUT model building, starting with the construction of 4d GUTs, to orbifold GUTs and finally to orbifold GUTs within the heterotic string. This evolution is an attempt to obtain realistic string models, perhaps relevant for the LHC. This review is in memory of the sudden loss of Julius Wess, a leader in the field, who will be sorely missed.Comment: 24 pages, 14 figures, lectures given at PiTP 2008, Institute for Advanced Study, Princeton, to be published in the European Physical Journal

Presenilin/γ-Secretase Regulates Neurexin Processing at Synapses

Neurexins are a large family of neuronal plasma membrane proteins, which function as trans-synaptic receptors during synaptic differentiation. The binding of presynaptic neurexins to postsynaptic partners, such as neuroligins, has been proposed to participate in a signaling pathway that regulates synapse formation/stabilization. The identification of mutations in neurexin genes associated with autism and mental retardation suggests that dysfunction of neurexins may underlie synaptic defects associated with brain disorders. However, the mechanisms that regulate neurexin function at synapses are still unclear. Here, we show that neurexins are proteolytically processed by presenilins (PS), the catalytic components of the γ-secretase complex that mediates the intramembraneous cleavage of several type I membrane proteins. Inhibition of PS/γ-secretase by using pharmacological and genetic approaches induces a drastic accumulation of neurexin C-terminal fragments (CTFs) in cultured rat hippocampal neurons and mouse brain. Neurexin-CTFs accumulate mainly at the presynaptic terminals of PS conditional double knockout (PS cDKO) mice lacking both PS genes in glutamatergic neurons of the forebrain. The fact that loss of PS function enhances neurexin accumulation at glutamatergic terminals mediated by neuroligin-1 suggests that PS regulate the processing of neurexins at glutamatergic synapses. Interestingly, presenilin 1 (PS1) is recruited to glutamatergic terminals mediated by neuroligin-1, thus concentrating PS1 at terminals containing β-neurexins. Furthermore, familial Alzheimer's disease (FAD)-linked PS1 mutations differentially affect β-neurexin-1 processing. Expression of PS1 M146L and PS1 H163R mutants in PS−/− cells rescues the processing of β-neurexin-1, whereas PS1 C410Y and PS1 ΔE9 fail to rescue the processing defect. These results suggest that PS regulate the synaptic function and processing of neurexins at glutamatergic synapses, and that impaired neurexin processing by PS may play a role in FAD