Non-Abelian Chern-Simons-Higgs vortices with a quartic potential

We have constructed numerically non-Abelian vortices in an SU(2) Chern-Simons-Higgs theory with a quartic Higgs potential. We have analyzed these solutions in detail by means of improved numerical codes and found some unexpected features we did not find when a sixth-order Higgs potential was used. The generic non-Abelian solutions have been generated by using their corresponding Abelian counterparts as initial guess. Typically, the energy of the non-Abelian solutions is lower than that of the corresponding Abelian one (except in certain regions of the parameter space). Regarding the angular momentum, the Abelian solutions possess the maximal value, although there exist non-Abelian solutions which reach that maximal value too. In order to classify the solutions it is useful to consider the non-Abelian solutions with asymptotically vanishing $A_t$ component of the gauge potential, which may be labelled by an integer number $m$. For vortex number $n=3$ and above, we have found uniqueness violation: two different non-Abelian solutions with all the global charges equal. Finally, we have investigated the limit of infinity Higgs self-coupling parameter and found a piecewise Regge-like relation between the energy and the angular momentum.Comment: 9 pages, 13 figure

Static Einstein-Maxwell Magnetic Solitons and Black Holes in an Odd Dimensional AdS Spacetime

We construct a new class of Einstein-Maxwell static solutions with a magnetic field in D-dimensions (with D >= 5 an odd number), approaching at infinity a globally Anti-de Sitter (AdS) spacetime. In addition to the mass, the new solutions possess an extra-parameter associated with a non-zero magnitude of the magnetic potential at infinity. Some of the black holes possess a non-trivial zero-horizon size limit, which corresponds to a solitonic deformation of the AdS background

Local and Semi-local Vortices in Yang-Mills-Chern-Simons model

We study BPS vortex configurations in three dimensional U(N) Yang-Mills theories with Chern-Simons interaction coupled to scalar fields carrying flavor. We consider two kind of configurations: local vortices (when the number of flavors $N_f=N$), and semi-local vortices (when $N_f>N$). In both cases we carefully analyze the electric and magnetic properties and present explicit numerical solutions.Comment: 10 pages, 2 figure

Harrison transformation and charged black objects in Kaluza-Klein theory

We generate charged black brane solutions in $D-$dimensions in a theory of gravity coupled to a dilaton and an antisymmetric form, by using a Harrison-type transformation. The seed vacuum solutions that we use correspond to uplifted Kaluza-Klein black strings and black holes in $(D-p)$-dimensions. A generalization of the Marolf-Mann quasilocal formalism to the Kaluza-Klein theory is also presented, the global charges of the black objects being computed in this way. We argue that the thermodynamics of the charged solutions can be derived from that of the vacuum configurations. Our results show that all charged Kaluza-Klein solutions constructed by means of Harrison transformations are thermodynamically unstable in a grand canonical ensemble. The general formalism is applied to the case of nonuniform black strings and caged black hole solutions in $D=5, 6$ Einstein-Maxwell-dilaton gravity, whose geometrical properties and thermodynamics are discussed. We argue that the topology changing transition scenario, which was previously proposed in the vacuum case, also holds in this case. Spinning generalizations of the charged black strings are constructed in six dimensions in the slowly rotating limit. We find that the gyromagnetic ratio of these solutions possesses a nontrivial dependence on the nonuniformity parameter.Comment: 42 pages, 12 figure

Dynein light chain 1 functions in somatic cyst cells regulate spermatogonial divisions in Drosophila

Stem cell progeny often undergo transit amplifying divisions before differentiation. In Drosophila, a spermatogonial precursor divides four times within an enclosure formed by two somatic-origin cyst cells, before differentiating into spermatocytes. Although germline and cyst cell-intrinsic factors are known to regulate these divisions, the mechanistic details are unclear. Here, we show that loss of dynein-light-chain-1 (DDLC1/LC8) in the cyst cells eliminates bag-of-marbles (bam) expression in spermatogonia, causing gonial cell hyperplasia in Drosophila testis. The phenotype is dominantly enhanced by Dhc64C (cytoplasmic Dynein) and didum (Myosin V) loss-of-function alleles. Loss of DDLC1 or Myosin V in the cyst cells also affects their differentiation. Furthermore, cyst cell-specific loss of ddlc1 disrupts Armadillo, DE-cadherin and Integrin-βPS localizations in the cyst. Together, these results suggest that Dynein and Myosin V activities, and independent DDLC1 functions in the cyst cells organize the somatic microenvironment that regulates spermatogonial proliferation and differentiation

Conserved Genes Act as Modifiers of Invertebrate SMN Loss of Function Defects

Spinal Muscular Atrophy (SMA) is caused by diminished function of the Survival of Motor Neuron (SMN) protein, but the molecular pathways critical for SMA pathology remain elusive. We have used genetic approaches in invertebrate models to identify conserved SMN loss of function modifier genes. Drosophila melanogaster and Caenorhabditis elegans each have a single gene encoding a protein orthologous to human SMN; diminished function of these invertebrate genes causes lethality and neuromuscular defects. To find genes that modulate SMN function defects across species, two approaches were used. First, a genome-wide RNAi screen for C. elegans SMN modifier genes was undertaken, yielding four genes. Second, we tested the conservation of modifier gene function across species; genes identified in one invertebrate model were tested for function in the other invertebrate model. Drosophila orthologs of two genes, which were identified originally in C. elegans, modified Drosophila SMN loss of function defects. C. elegans orthologs of twelve genes, which were originally identified in a previous Drosophila screen, modified C. elegans SMN loss of function defects. Bioinformatic analysis of the conserved, cross-species, modifier genes suggests that conserved cellular pathways, specifically endocytosis and mRNA regulation, act as critical genetic modifiers of SMN loss of function defects across species

Protein kinase D interacts with neuronal nitric oxide synthase and phosphorylates the activatory residue serine1412

Neuronal Nitric Oxide Synthase (nNOS) is the biosynthetic enzyme responsible for nitric oxide (·NO) production in muscles and in the nervous system. This constitutive enzyme, unlike its endothelial and inducible counterparts, presents an N-terminal PDZ domain known to display a preference for PDZ-binding motifs bearing acidic residues at -2 position. In a previous work, we discovered that the C-terminal end of two members of protein kinase D family (PKD1 and PKD2) constitutes a PDZ-ligand. PKD1 has been shown to regulate multiple cellular processes and, when activated, becomes autophosphorylated at Ser 916, a residue located at -2 position of its PDZ-binding motif. Since nNOS and PKD are spatially enriched in postsynaptic densities and dendrites, the main objective of our study was to determine whether PKD1 activation could result in a direct interaction with nNOS through their respective PDZ-ligand and PDZ domain, and to analyze the functional consequences of this interaction. Herein we demonstrate that PKD1 associates with nNOS in neurons and in transfected cells, and that kinase activation enhances PKD1-nNOS co-immunoprecipitation and subcellular colocalization. However, transfection of mammalian cells with PKD1 mutants and yeast two hybrid assays showed that the association of these two enzymes does not depend on PKD1 PDZ-ligand but its pleckstrin homology domain. Furthermore, this domain was able to pull-down nNOS from brain extracts and bind to purified nNOS, indicating that it mediates a direct PKD1-nNOS interaction. In addition, using mass spectrometry we demonstrate that PKD1 specifically phosphorylates nNOS in the activatory residue Ser 1412, and that this phosphorylation increases nNOS activity and ·NO production in living cells. In conclusion, these novel findings reveal a crucial role of PKD1 in the regulation of nNOS activation and synthesis of ·NO, a mediator involved in physiological neuronal signaling or neurotoxicity under pathological conditions such as ischemic stroke or neurodegeneration.This work was supported by the Ministerio de Economía y Competitividad [SAF2011-26233 to T.I., BFU2009-10442 and BFU2012-37934 to I.R-C.]; Comunidad de Madrid [S2010/BMD-2331-Neurodegmodels-CM to T.I.]; and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas – CIBERNED, Instituto de Salud Carlos III, to T.I. Postdoctoral fellows L.S-R. and L.G-G. have been funded by research contracts from CIBERNED; Clara Aicart-Ramos is a recipient of a FPU predoctoral fellowship from Ministerio de Economía y Competitividad.Peer Reviewe