Dynamical generation of dark solitons in spin-orbit-coupled Bose-Einstein condensates

We numerically investigate the ground state, the Raman-driving dynamics and the nonlinear excitations of a realized spin-orbit-coupled Bose-Einstein condensate in a one-dimensional harmonic trap. Depending on the Raman coupling and the interatomic interactions, three ground-state phases are identified: stripe, plane wave and zero-momentum phases. A narrow parameter regime with coexistence of stripe and zero-momentum or plane wave phases in real space is found. Several sweep progresses across different phases by driving the Raman coupling linearly in time is simulated and the non-equilibrium dynamics of the system in these sweeps are studied. We find kinds of nonlinear excitations, with the particular dark solitons excited in the sweep from the stripe phase to the plane wave or zero-momentum phase within the trap. Moreover, the number and the stability of the dark solitons can be controlled in the driving, which provide a direct and easy way to generate dark solitons and study their dynamics and interaction properties.Comment: 10 pages, 9 figur

Uncovering new signaling proteins and potential drug targets through the interactome analysis of Mycobacterium tuberculosis

<p>Abstract</p> <p>Background</p> <p>Analysis of the pathogen interactome is a powerful approach for dissecting potential signal transduction and virulence pathways. It also offers opportunities for exploring new drug targets.</p> <p>Results</p> <p>In this study, a protein-protein interaction (PPI) network of <it>Mycobacterium tuberculosis </it>H37Rv was constructed using a homogenous protein mapping method, which has shown molecular chaperones, ribosomal proteins and ABC transporters to be highly interconnected proteins. A further analysis of this network unraveled the function of hypothetical proteins as well as a potential signaling pathway. A hypothetical protein, Rv2752c, which was linked to a metal cation-transporting ATPase, was characterized as a metal-beta-lactamase, through domain analysis in combination with an <it>in vitro </it>activity experiment. A second hypothetical protein, Rv1354c, and an unknown protein kinase, PknK, interacted with a similar group of inner membrane-associated ABC transporters in the PPI network. The interactions of Rv1354 with these proteins were also confirmed by a further bacterial two-hybrid analysis. According to protein domain structures, the unique <it>M. tuberculosis </it>Rv1354c gene was proposed, for the first time, to be responsible for the turnover of cyclic-di-GMP, a second messenger molecule in this bacterium. A further structure-based inhibitors screening for Rv1354c was also performed <it>in silicon</it>.</p> <p>Conclusion</p> <p>We constructed a comprehensive protein-protein interaction network for <it>M. tuberculosis </it>consisting of 738 proteins and 5639 interaction pairs. Our analysis unraveled the function of hypothetical proteins as well as a potential signaling pathway. The group of ABC transporters, PknK, and Rv1354c were proposed to constitute a potential membrane-associated signaling pathway that cooperatively responds to environmental stresses in <it>M. tuberculosis</it>. The study therefore provides valuable clues in exploring new signaling proteins, virulence pathways, and drug targets.</p

Exdpf Is a Key Regulator of Exocrine Pancreas Development Controlled by Retinoic Acid and ptf1a in Zebrafish

Both endocrine and exocrine pancreatic cells arise from pancreatic-duodenal homeobox 1 (pdx1)-positive progenitors. The molecular mechanisms controlling cell fate determination and subsequent proliferation, however, are poorly understood. Unlike endocrine cells, less is known about exocrine cell specification. We report here the identification and characterization of a novel exocrine cell determinant gene, exocrine differentiation and proliferation factor (exdpf), which is highly expressed in the exocrine cell progenitors and differentiated cells of the developing pancreas in zebrafish. Knockdown of exdpf by antisense morpholino caused loss or significant reduction of exocrine cells due to lineage-specific cell cycle arrest but not apoptosis, whereas the endocrine cell mass appeared normal. Real-time PCR results demonstrated that the cell cycle arrest is mediated by up-regulation of cell cycle inhibitor genes p21Cip, p27Kip, and cyclin G1 in the exdpf morphants. Conversely, overexpression of exdpf resulted in an overgrowth of the exocrine pancreas and a severe reduction of the endocrine cell mass, suggesting an inhibitory role for exdpf in endocrine cell progenitors. We show that exdpf is a direct target gene of pancreas-specific transcription factor 1a (Ptf1a), a transcription factor critical for exocrine formation. Three consensus Ptf1a binding sites have been identified in the exdpf promoter region. Luciferase assay demonstrated that Ptf1a promotes transcription of the exdpf promoter. Furthermore, exdpf expression in the exocrine pancreas was lost in ptf1a morphants, and overexpression of exdpf successfully rescued exocrine formation in ptf1a-deficient embryos. Genetic evidence places expdf downstream of retinoic acid (RA), an instructive signal for pancreas development. Knocking down exdpf by morpholino abolished ectopic carboxypeptidase A (cpa) expression induced by RA. On the other hand, exdpf mRNA injection rescued endogenous cpa expression in embryos treated with diethylaminobenzaldehyde, an inhibitor of RA signaling. Moreover, exogenous RA treatment induced anterior ectopic expression of exdpf and trypsin in a similar pattern. Our study provides a new understanding of the molecular mechanisms controlling exocrine cell specification and proliferation by a novel gene, exdpf. Highly conserved in mammals, the expression level of exdpf appears elevated in several human tumors, suggesting a possible role in tumor pathogenesis