The detection rate of early UV emission from supernovae: A dedicated GALEX/PTF survey and calibrated theoretical estimates

The radius and surface composition of an exploding massive star,as well as the explosion energy per unit mass, can be measured using early UV observations of core collapse supernovae (SNe). We present the first results from a simultaneous GALEX/PTF search for early UV emission from SNe. Six Type II SNe and one Type II superluminous SN (SLSN-II) are clearly detected in the GALEX NUV data. We compare our detection rate with theoretical estimates based on early, shock-cooling UV light curves calculated from models that fit existing Swift and GALEX observations well, combined with volumetric SN rates. We find that our observations are in good agreement with calculated rates assuming that red supergiants (RSGs) explode with fiducial radii of 500 solar, explosion energies of 10^51 erg, and ejecta masses of 10 solar masses. Exploding blue supergiants and Wolf-Rayet stars are poorly constrained. We describe how such observations can be used to derive the progenitor radius, surface composition and explosion energy per unit mass of such SN events, and we demonstrate why UV observations are critical for such measurements. We use the fiducial RSG parameters to estimate the detection rate of SNe during the shock-cooling phase (<1d after explosion) for several ground-based surveys (PTF, ZTF, and LSST). We show that the proposed wide-field UV explorer ULTRASAT mission, is expected to find >100 SNe per year (~0.5 SN per deg^2), independent of host galaxy extinction, down to an NUV detection limit of 21.5 mag AB. Our pilot GALEX/PTF project thus convincingly demonstrates that a dedicated, systematic SN survey at the NUV band is a compelling method to study how massive stars end their life.Comment: See additional information including animations on http://www.weizmann.ac.il/astrophysics/ultrasa

Developing Chemical Genetic Approaches to Explore G Protein-Coupled Receptor Function: Validation of the Use of a Receptor Activated Solely by Synthetic Ligand (RASSL)

Molecular evolution and chemical genetics have been applied to generate functional pairings of mutated G protein-coupled receptors (GPCRs) and nonendogenous ligands. These mutant receptors, referred to as receptors activated solely by synthetic ligands (RASSLs) or designer receptors exclusively activated by designer drugs (DREADDs), have huge potential to define physiological roles of GPCRs and to validate receptors in animal models as therapeutic targets to treat human disease. However, appreciation of ligand bias and functional selectivity of different ligands at the same receptor suggests that RASSLs may signal differently than wild-type receptors activated by endogenous agonists. We assessed this by generating forms of wild-type human M3 muscarinic receptor and a RASSL variant that responds selectively to clozapine N-oxide. Although the RASSL receptor had reduced affinity for muscarinic antagonists, including atropine, stimulation with clozapine N-oxide produced effects very similar to those generated by acetylcholine at the wild-type M3-receptor. Such effects included the relative movement of the third intracellular loop and C-terminal tail of intramolecular fluorescence resonance energy transfer sensors and the ability of the wild type and evolved mutant to regulate extracellular signal-regulated kinase 1/2 phosphorylation. Each form interacted similarly with β-arrestin 2 and was internalized from the cell surface in response to the appropriate ligand. Furthermore, the pattern of phosphorylation of specific serine residues within the evolved receptor in response to clozapine N-oxide was very similar to that produced by acetylcholine at the wild type. Such results provide confidence that, at least for the M3 muscarinic receptor, results obtained after transgenic expression of this RASSL are likely to mirror the actions of acetylcholine at the wild type receptor