Distinguishing charged Higgs bosons from different representations at the LHC

Extending the Standard Model (SM) scalar sector via one or multiple Higgs field(s) in higher representation brings one or more charged Higgs bosons in the spectrum. Some of these gauge representations with appropriate hypercharge can bring up doubly charged Higgs boson and can be easily distinguished from the existing models with only singly charged Higgs boson. In this study we focus on distinguishing the singly charged Higgs bosons from different representations, viz. doublets and triplets of $SU(2)_L$ gauge group. We consider a supersymmetric extension of SM with a gauge singlet and $SU(2)_L$ triplet with $Y=0$ as a benchmark scenario with the possibility of rich phenomenology due to existence of light pseudoscalar for $Z_3$ symmetric superpotential. A detailed collider simulation considering all the SM backgrounds has been carried out in order to classify the final states which are favourable to charged Higgs boson from one particular representation than others. We show that such different representations can be probed an distinguished via looking at single charged Higgs boson phenomenology at the LHC with 14 TeV center of mass energy within $\sim 50$ fb$^{-1}$ of integrated luminosity.Comment: 28 pages, 14 figures, 14 tables. updated version with references reordere

Short Term Topological Changes of Coronal Holes Associated with Prominence Eruptions and Subsequent CMEs

We study the short--term topological changes of equatorial and polar coronal hole (CH) boundaries, such as a variation of their area and disintegration, associated to reconnection with nearby (within 15$^\circ$ distance) quiescent prominence magnetic fields leading to eruptions and subsequent Coronal Mass Ejections (CMEs). The examples presented here correspond to the recent solar minimum years 2008 and 2009. We consider a temporal window of one day between the CH topological changes and the start and end times of prominence eruptions and onset of CMEs. To establish this association we took into account observational conditions related to the instability of prominence/filaments, the occurrence of a CME, as well as the subsequent evolution after the CME. We found an association between short--term local topological changes in CH boundaries and the formation/disappearance of bright points near them, as well as, between short--term topological changes within the whole CH and eruptions of nearby quiescent prominences followed by the appearance of one or more CMEs.Comment: 15 pages, 11 figures; Journal Advances Space Research (2012

The alternate GNB3 splice variant, Gβ3s, exhibits an altered signalling response to EGF stimulation, which leads to enhanced cell migration

It has recently been reported that the duplication of the GNB3 gene has been shown to be directly linked to an obesity phenotype, both in humans and also in a humanised mouse model. Moreover, the common human GNB3 c.825C>T polymorphism (rs5443) causes this ubiquitously expressed gene to be aberrantly spliced approximately 50% of the time leading to the production of both a normal Gβ3 protein and a truncated, possibly less stable subunit, known as Gβ3s. The presence of the GNB3 825T allele has previously been shown to be associated with predisposition to hypertension, obesity, various cancers, Alzheimers, age related cognitive function, erectile dysfunction as well as a marker for pharmacogenetic drug action. Great controversy, however, currently exists as to whether these phenotypes associated with the 825T allele are a) mainly due to the presence of the smaller, possibly more active, Gβ3s subunit or b) merely down to the haploinsufficiency of the normal GNB3 transcript, due to its frequent aberrant splicing. In order to try and address these two conflicting hypothesis, we report on the identification and characterisation of signalling alterations unique to the presence of Gβ3s protein subunit. Moreover we also show the physiological consequences associated with altered signalling, directly induced by the Gβ3s subunit. For this, we used both an EBV transformed lymphoblast cell line homozygote for GNB3 825T/825T (TT) and a stable Gβ3s expressing recombinant COS-7 clone. In both of these cell lines that express the Gβ3s subunit, we found enhanced cytosolic calcium influx upon stimulation with EGF, TGFα and VEGF ligands, as compared to “normal” GNB3 controls with the 825C/825C (CC) genotype. This aberrant calcium influx also led to an increase in ERK, but not AKT1, phosphorylation. Despite the lack of AKT1 activation, we paradoxically observed a significant increase in phosphorylation of its downstream substrates, namely mTOR and p70S6k (KS6B2). Moreover we observed a decrease in phospho FoxO3a only in Gβ3s expressing cells, but not in the “normal” GNB3 (CC) control cell line. The presence of the Gβ3s subunit also appeared to alter the distinct localisation patterns of both Foxo3a and AKT1, while also increasing the colocalisation of mTOR and p70S6K. Subsequent growth factor stimulation studies revealed that EGF treatment, of Gβ3s expressing cells, appeared to cause a significant decrease in cAMP levels, which, in turn resulted in both enhanced caveolin-1a phosphorylation, and an increase in actin stress fibre formation. The identification of these distinct Gβ3s specific signalling alterations were indicative of a more aggressive migratory phenotype. This led us to further investigate and confirm that the presence of the Gβ3s subunit also appears to cause significantly enhanced migration and robust scratch wound healing kinetics, as compared to cells harbouring only the normal copy of the gene. These data therefore present convincing evidence that the Gβ3s subunit is stable, functional and its presence can significantly alter signalling pathways, in different cell types

Mammalian EAK-7 activates alternative mTOR signaling to regulate cell proliferation and migration.

Nematode EAK-7 (enhancer-of-akt-1-7) regulates dauer formation and controls life span; however, the function of the human ortholog mammalian EAK-7 (mEAK-7) is unknown. We report that mEAK-7 activates an alternative mechanistic/mammalian target of rapamycin (mTOR) signaling pathway in human cells, in which mEAK-7 interacts with mTOR at the lysosome to facilitate S6K2 activation and 4E-BP1 repression. Despite interacting with mTOR and mammalian lethal with SEC13 protein 8 (mLST8), mEAK-7 does not interact with other mTOR complex 1 (mTORC1) or mTOR complex 2 (mTORC2) components; however, it is essential for mTOR signaling at the lysosome. This phenomenon is distinguished by S6 and 4E-BP1 activity in response to nutrient stimulation. Conventional S6K1 phosphorylation is uncoupled from S6 phosphorylation in response to mEAK-7 knockdown. mEAK-7 recruits mTOR to the lysosome, a crucial compartment for mTOR activation. Loss of mEAK-7 results in a marked decrease in lysosomal localization of mTOR, whereas overexpression of mEAK-7 results in enhanced lysosomal localization of mTOR. Deletion of the carboxyl terminus of mEAK-7 significantly decreases mTOR interaction. mEAK-7 knockdown decreases cell proliferation and migration, whereas overexpression of mEAK-7 enhances these cellular effects. Constitutively activated S6K rescues mTOR signaling in mEAK-7-knocked down cells. Thus, mEAK-7 activates an alternative mTOR signaling pathway through S6K2 and 4E-BP1 to regulate cell proliferation and migration