A new interferometric study of four exoplanet host stars : {\theta} Cygni, 14 Andromedae, {\upsilon} Andromedae and 42 Draconis

Studying exoplanet host stars is of the utmost importance to establish the link between the presence of exoplanets around various types of stars and to understand the respective evolution of stars and exoplanets. Using the limb-darkened diameter (LDD) obtained from interferometric data, we determine the fundamental parameters of four exoplanet host stars. We are particularly interested in the F4 main-sequence star, {\theta} Cyg, for which Kepler has recently revealed solar-like oscillations that are unexpected for this type of star. Furthermore, recent photometric and spectroscopic measurements with SOPHIE and ELODIE (OHP) show evidence of a quasi-periodic radial velocity of \sim150 days. Models of this periodic change in radial velocity predict either a complex planetary system orbiting the star, or a new and unidentified stellar pulsation mode. We performed interferometric observations of {\theta} Cyg, 14 Andromedae, {\upsilon} Andromedae and 42 Draconis for two years with VEGA/CHARA (Mount Wilson, California) in several three-telescope configurations. We measured accurate limb darkened diameters and derived their radius, mass and temperature using empirical laws. We obtain new accurate fundamental parameters for stars 14 And, {\upsilon} And and 42 Dra. We also obtained limb darkened diameters with a minimum precision of \sim 1.3%, leading to minimum planet masses of Msini=5.33\pm 0.57, 0.62 \pm 0.09 and 3.79\pm0.29 MJup for 14 And b, {\upsilon} And b and 42 Dra b, respectively. The interferometric measurements of {\theta} Cyg show a significant diameter variability that remains unexplained up to now. We propose that the presence of these discrepancies in the interferometric data is caused by either an intrinsic variation of the star or an unknown close companion orbiting around it.Comment: 10 pages + 2 pages appendix, 16 figures, accepted for publication in A&

Enhanced Halpha activity at periastron in the young and massive spectroscopic binary HD200775

Young close binaries clear central cavities in their surrounding circumbinary disk from which the stars can still accrete material. This process takes place within the very first astronomical units, and is still not well constrained as the observational evidence has been gathered, until now, only by means of spectroscopy. The young object HD200775 (MWC361) is a massive spectroscopic binary (separation of ~15.9mas, ~5.0~AU), with uncertain classification (early/late Be), that shows a strong and variable Halpha emission. We aim to study the mechanisms that produce the Halpha line at the AU-scale. Combining the radial velocity measurements and astrometric data available in the literature, we determined new orbital parameters. With the VEGA instrument on the CHARA array, we spatially and spectrally resolved the Halpha emission of HD200775, at low and medium spectral resolutions (R~1600 and 5000) over a full orbital period (~3.6 years). We observe that the Halpha equivalent width varies with the orbital phase, and increases close to periastron, as expected from theoretical models that predict an increase of the mass transfer from the circumbinary disk to the primary disk. In addition, using spectral visibilities and differential phases, we find marginal variations of the typical extent of the Halpha emission (at 1 to 2-sigma level) and location (at 1 to 5-sigma level). The spatial extent of the Halpha emission, as probed by a Gaussian FWHM, is minimum at the ascending node (0.67+/-0.20 mas, i.e., 0.22+/-0.06 AU), and more than doubles at periastron. In addition, the Gaussian photocenter is slightly displaced in the direction opposite to the secondary, ruling out the scenario in which all or most of the Halpha emission is due to accretion onto the secondary. These findings, together with the wide Halpha line profile, may be due to a non-spherical wind enhanced at periastron.Comment: Accepted by Astronomy & Astrophysic

The 2011 outburst of the recurrent novaT Pyx. Evidence for a face-on bipolar ejection

We report on near-IR interferometric observations of the outburst of the recurrent nova T Pyx. We obtained near-IR observations of T Pyx at dates ranging from t=2.37d to t=48.2d after the outburst, with the CLASSIC recombiner, located at the CHARA array, and with the PIONIER and AMBER recombiners, located at the VLTI array. These data are supplemented with near-IR photometry and spectra obtained at Mount Abu, India. Slow expansion velocities were measured (<300km/s) before t=20d (assuming D=3.5kpc). From t=28d on, the AMBER and PIONIER continuum visibilities (K and H band, respectively) are best simulated with a two component model consisting of an unresolved source plus an extended source whose expansion velocity onto the sky plane is lower than 700km/s. The expansion of the Brgamma line forming region, as inferred at t=28d and t=35d is slightly larger, implying velocities in the range 500-800km/s, still strikingly lower than the velocities of 1300-1600km/s inferred from the Doppler width of the line. Moreover, a remarkable pattern was observed in the Brgamma differential phases. A semi-quantitative model using a bipolar flow with a contrast of 2 between the pole and equator velocities, an inclination of i=15^{\circ} and a position angle P.A.=110^{\circ} provides a good match to the AMBER observables (spectra, differential visibilities and phases). At t=48d, a PIONIER dataset confirms the two component nature of the H band emission, consisting of an unresolved stellar source and an extended region whose appearance is circular and symmetric within error bars.These observations are most simply interpreted within the frame of a bipolar model, oriented nearly face-on. This finding has profound implications for the interpretation of past, current and future observations of the expanding nebula.Comment: Accepted Astronomy and Astrophysics (2011

N-Glycosylation of ß4 Integrin Controls the Adhesion and Motility of Keratinocytes

α6ß4 integrin is an essential component of hemidesmosomes and modulates cell migration in wound healing and cancer invasion. To elucidate the role of N-glycosylation on ß4 integrin, we investigated keratinocyte adhesion and migration through the re-expression of wild-type or N-glycosylation-defective ß4 integrin (ΔNß4) in ß4 integrin null keratinocytes. N-glycosylation of ß4 integrin was not essential for the heterodimer formation of ß4 integrin with α6 integrin and its expression on a cell surface, but N-glycosylation was required for integrin-mediated cell adhesion and migration. Concomitantly with the reduction of ß4 integrin in the membrane microdomain, the intracellular signals of Akt and ERK activation were decreased in cells expressing ΔNß4 integrin. Forced cross-linking of ß4 integrin rescued the decreased ERK activation in ΔNß4 integrin-expressing cells to a similar extent in wild-type ß4 integrin-expressing cells. Surprisingly, compared with cells expressing wild-type ß4 integrin, an alternation in N-glycan structures expressed on epidermal growth factor receptor (EGFR), and the induction of a stronger association between EGFR and ß4 integrin were observed in ΔNß4 integrin-expressing cells. These results clearly demonstrated that N-glycosylation on ß4 integrin plays an essential role in keratinocyte cellular function by allowing the appropriate complex formation on cell surfaces

Clara cell adhesion and migration to extracellular matrix

<p>Abstract</p> <p>Background</p> <p>Clara cells are the epithelial progenitor cell of the small airways, a location known to be important in many lung disorders. Although migration of alveolar type II and bronchiolar ciliated epithelial cells has been examined, the migratory response of Clara cells has received little attention.</p> <p>Methods</p> <p>Using a modification of existing procedures for Clara cell isolation, we examined mouse Clara cells and a mouse Clara-like cell line (C22) for adhesion to and migration toward matrix substrate gradients, to establish the nature and integrin dependence of migration in Clara cells.</p> <p>Results</p> <p>We observed that Clara cells adhere preferentially to fibronectin (Fn) and type I collagen (Col I) similar to previous reports. Migration of Clara cells can be directed by a fixed gradient of matrix substrates (haptotaxis). Migration of the C22 cell line was similar to the Clara cells so integrin dependence of migration was evaluated with this cell line. As determined by competition with an RGD containing-peptide, migration of C22 cells toward Fn and laminin (Lm) 511 (formerly laminin 10) was significantly RGD integrin dependent, but migration toward Col I was RGD integrin independent, suggesting that Clara cells utilize different receptors for these different matrices.</p> <p>Conclusion</p> <p>Thus, Clara cells resemble alveolar type II and bronchiolar ciliated epithelial cells by showing integrin mediated pro-migratory changes to extracellular matrix components that are present in tissues after injury.</p

Regulator of G-Protein Signaling 14 (RGS14) Is a Selective H-Ras Effector

Background: Regulator of G-protein signaling (RGS) proteins have been well-described as accelerators of Ga-mediated GTP hydrolysis (‘‘GTPase-accelerating proteins’’ or GAPs). However, RGS proteins with complex domain architectures are now known to regulate much more than Ga GTPase activity. RGS14 contains tandem Ras-binding domains that have been reported to bind to Rap- but not Ras GTPases in vitro, leading to the suggestion that RGS14 is a Rap-specific effector. However, more recent data from mammals and Drosophila imply that, in vivo, RGS14 may instead be an effector of Ras.Methodology/Principal Findings: Full-length and truncated forms of purified RGS14 protein were found to bind indiscriminately in vitro to both Rap- and Ras-family GTPases, consistent with prior literature reports. In stark contrast, however, we found that in a cellular context RGS14 selectively binds to activated H-Ras and not to Rap isoforms. Co- transfection / co-immunoprecipitation experiments demonstrated the ability of full-length RGS14 to assemble a multiprotein complex with components of the ERK MAPK pathway in a manner dependent on activated H-Ras. Small interfering RNA-mediated knockdown of RGS14 inhibited both nerve growth factor- and basic fibrobast growth factor- mediated neuronal differentiation of PC12 cells, a process which is known to be dependent on Ras-ERK signaling.Conclusions/Significance: In cells, RGS14 facilitates the formation of a selective Ras?GTP-Raf-MEK-ERK multiprotein complex to promote sustained ERK activation and regulate H-Ras-dependent neuritogenesis. This cellular function for RGS14 is similar but distinct from that recently described for its closely-related paralogue, RGS12, which shares the tandem Ras- binding domain architecture with RGS14

R-Ras Regulates Migration through an Interaction with Filamin A in Melanoma Cells

Changes in cell adhesion and migration in the tumor microenvironment are key in the initiation and progression of metastasis. R-Ras is one of several small GTPases that regulate cell adhesion and migration on the extracellular matrix, however the mechanism has not been completely elucidated. Using a yeast two-hybrid approach we sought to identify novel R-Ras binding proteins that might mediate its effects on integrins.We identified Filamin A (FLNa) as a candidate interacting protein. FLNa is an actin-binding scaffold protein that also binds to integrin β1, β2 and β7 tails and is associated with diverse cell processes including cell migration. Indeed, M2 melanoma cells require FLNa for motility. We further show that R-Ras and FLNa interact in co-immunoprecipitations and pull-down assays. Deletion of FLNa repeat 3 (FLNaΔ3) abrogated this interaction. In M2 melanoma cells active R-Ras co-localized with FLNa but did not co-localize with FLNa lacking repeat 3. Thus, activated R-Ras binds repeat 3 of FLNa. The functional consequence of this interaction was that active R-Ras and FLNa coordinately increased cell migration. In contrast, co-expression of R-Ras and FLNaΔ3 had a significantly reduced effect on migration. While there was enhancement of integrin activation and fibronectin matrix assembly, cell adhesion was not altered. Finally, siRNA knockdown of endogenous R-Ras impaired FLNa-dependent fibronectin matrix assembly.These data support a model in which R-Ras functionally associates with FLNa and thereby regulates integrin-dependent migration. Thus in melanoma cells R-Ras and FLNa may cooperatively promote metastasis by enhancing cell migration

Structure of a double ubiquitin-like domain in the talin head: a role in integrin activation

Talin is a 270-kDa protein that activates integrins and couples them to cytoskeletal actin. Talin contains an N-terminal FERM domain comprised of F1, F2 and F3 domains, but it is atypical in that F1 contains a large insert and is preceded by an extra domain F0. Although F3 contains the binding site for β-integrin tails, F0 and F1 are also required for activation of β1-integrins. Here, we report the solution structures of F0, F1 and of the F0F1 double domain. Both F0 and F1 have ubiquitin-like folds joined in a novel fixed orientation by an extensive charged interface. The F1 insert forms a loop with helical propensity, and basic residues predicted to reside on one surface of the helix are required for binding to acidic phospholipids and for talin-mediated activation of β1-integrins. This and the fact that basic residues on F2 and F3 are also essential for integrin activation suggest that extensive interactions between the talin FERM domain and acidic membrane phospholipids are required to orientate the FERM domain such that it can activate integrins

PDE8 Regulates Rapid Teff Cell Adhesion and Proliferation Independent of ICER

BACKGROUND: Abolishing the inhibitory signal of intracellular cAMP by phosphodiesterases (PDEs) is a prerequisite for effector T (Teff) cell function. While PDE4 plays a prominent role, its control of cAMP levels in Teff cells is not exclusive. T cell activation has been shown to induce PDE8, a PDE isoform with 40- to 100-fold greater affinity for cAMP than PDE4. Thus, we postulated that PDE8 is an important regulator of Teff cell functions. METHODOLOGY/PRINCIPAL FINDINGS: We found that Teff cells express PDE8 in vivo. Inhibition of PDE8 by the PDE inhibitor dipyridamole (DP) activates cAMP signaling and suppresses two major integrins involved in Teff cell adhesion. Accordingly, DP as well as the novel PDE8-selective inhibitor PF-4957325-00 suppress firm attachment of Teff cells to endothelial cells. Analysis of downstream signaling shows that DP suppresses proliferation and cytokine expression of Teff cells from Crem-/- mice lacking the inducible cAMP early repressor (ICER). Importantly, endothelial cells also express PDE8. DP treatment decreases vascular adhesion molecule and chemokine expression, while upregulating the tight junction molecule claudin-5. In vivo, DP reduces CXCL12 gene expression as determined by in situ probing of the mouse microvasculature by cell-selective laser-capture microdissection. CONCLUSION/SIGNIFICANCE: Collectively, our data identify PDE8 as a novel target for suppression of Teff cell functions, including adhesion to endothelial cells

Gene Expression Profiles of the NCI-60 Human Tumor Cell Lines Define Molecular Interaction Networks Governing Cell Migration Processes

Although there is extensive information on gene expression and molecular interactions in various cell types, integrating those data in a functionally coherent manner remains challenging. This study explores the premise that genes whose expression at the mRNA level is correlated over diverse cell lines are likely to function together in a network of molecular interactions. We previously derived expression-correlated gene clusters from the database of the NCI-60 human tumor cell lines and associated each cluster with function categories of the Gene Ontology (GO) database. From a cluster rich in genes associated with GO categories related to cell migration, we extracted 15 genes that were highly cross-correlated; prominent among them were RRAS, AXL, ADAM9, FN14, and integrin-beta1. We then used those 15 genes as bait to identify other correlated genes in the NCI-60 database. A survey of current literature disclosed, not only that many of the expression-correlated genes engaged in molecular interactions related to migration, invasion, and metastasis, but that highly cross-correlated subsets of those genes engaged in specific cell migration processes. We assembled this information in molecular interaction maps (MIMs) that depict networks governing 3 cell migration processes: degradation of extracellular matrix, production of transient focal complexes at the leading edge of the cell, and retraction of the rear part of the cell. Also depicted are interactions controlling the release and effects of calcium ions, which may regulate migration in a spaciotemporal manner in the cell. The MIMs and associated text comprise a detailed and integrated summary of what is currently known or surmised about the role of the expression cross-correlated genes in molecular networks governing those processes