BEER analysis of Kepler and CoRoT light curves: I. Discovery of Kepler-76b: A hot Jupiter with evidence for superrotation

We present the first case in which the BEER algorithm identified a hot Jupiter in the Kepler light curve, and its reality was confirmed by orbital solutions based on follow-up spectroscopy. The companion Kepler-76b was identified by the BEER algorithm, which detected the BEaming (sometimes called Doppler boosting) effect together with the Ellipsoidal and Reflection/emission modulations (BEER), at an orbital period of 1.54 days, suggesting a planetary companion orbiting the 13.3 mag F star. Further investigation revealed that this star appeared in the Kepler eclipsing binary catalog with estimated primary and secondary eclipse depths of 5e-3 and 1e-4 respectively. Spectroscopic radial-velocity follow-up observations with TRES and SOPHIE confirmed Kepler-76b as a transiting 2.0+/-0.26 Mjup hot Jupiter. The mass of a transiting planet can be estimated from either the beaming or the ellipsoidal amplitude. The ellipsoidal-based mass estimate of Kepler-76b is consistent with the spectroscopically measured mass while the beaming-based estimate is significantly inflated. We explain this apparent discrepancy as evidence for the superrotation phenomenon, which involves eastward displacement of the hottest atmospheric spot of a tidally-locked planet by an equatorial super-rotating jet stream. This phenomenon was previously observed only for HD 189733b in the infrared. We show that a phase shift of 10.3+/-2.0 degrees of the planet reflection/emission modulation, due to superrotation, explains the apparently inflated beaming modulation, resolving the ellipsoidal/beaming amplitude discrepancy. Kepler-76b is one of very few confirmed planets in the Kepler light curves that show BEER modulations and the first to show superrotation evidence in the Kepler band. Its discovery illustrates for the first time the ability of the BEER algorithm to detect short-period planets and brown dwarfs.Comment: 28 pages, 6 tables and 7 figures. Planet name changed to Kepler-76b. Accepted for publication in the Astrophysical Journa

A red giant orbiting a black hole

We report spectroscopic and photometric follow-up of a dormant black hole (BH) candidate from Gaia DR3. We show that the system, which we call Gaia BH2, contains a $\sim 1M_{\odot}$ red giant and a dark companion with mass $M_2 = 8.9\pm 0.3\,M_{\odot}$ that is very likely a BH. The orbital period, $P_{\rm orb} = 1277$ days, is much longer than that of any previously studied BH binary. Our radial velocity (RV) follow-up over a 6-month period spans most of the orbit's dynamic range in RV and is in excellent agreement with predictions of the Gaia solution. UV imaging and high-resolution optical spectra rule out all plausible luminous companions that could explain the orbit. The star is a bright ($G=12.3$), slightly metal-poor ($\rm [Fe/H]=-0.22$) low-luminosity giant ($T_{\rm eff}=4600\,\rm K$; $R = 7.9\,R_{\odot}$; $\log\left[g/\left({\rm cm\,s^{-2}}\right)\right] = 2.6$). The binary's orbit is moderately eccentric ($e=0.52$). The giant is strongly enhanced in $\alpha-$elements, with $\rm [\alpha/Fe] = +0.26$, but the system's Galactocentric orbit is typical of the thin disk. We obtained X-ray and radio nondetections of the source near periastron, which support BH accretion models in which the net accretion rate at the horizon is much lower than the Bondi-Hoyle-Lyttleton rate. At a distance of 1.16 kpc, Gaia BH2 is the second-nearest known BH, after Gaia BH1. Its orbit -- like that of Gaia BH1 -- seems too wide to have formed through common envelope evolution. Gaia BH1 and BH2 have orbital periods at opposite edges of the Gaia DR3 sensitivity curve, perhaps hinting at a bimodal intrinsic period distribution for wide BH binaries. Dormant BH binaries like Gaia BH1 and Gaia BH2 likely significantly outnumber their close, X-ray bright cousins, but their formation pathways remain uncertain.Comment: 22 pages, 15 figures. Submitted to MNRA

To which world regions does the valence–dominance model of social perception apply?

Over the past 10 years, Oosterhof and Todorov’s valence–dominance model has emerged as the most prominent account of how people evaluate faces on social dimensions. In this model, two dimensions (valence and dominance) underpin social judgements of faces. Because this model has primarily been developed and tested in Western regions, it is unclear whether these findings apply to other regions. We addressed this question by replicating Oosterhof and Todorov’s methodology across 11 world regions, 41 countries and 11,570 participants. When we used Oosterhof and Todorov’s original analysis strategy, the valence–dominance model generalized across regions. When we used an alternative methodology to allow for correlated dimensions, we observed much less generalization. Collectively, these results suggest that, while the valence–dominance model generalizes very well across regions when dimensions are forced to be orthogonal, regional differences are revealed when we use different extraction methods and correlate and rotate the dimension reduction solution.C.L. was supported by the Vienna Science and Technology Fund (WWTF VRG13-007); L.M.D. was supported by ERC 647910 (KINSHIP); D.I.B. and N.I. received funding from CONICET, Argentina; L.K., F.K. and Á. Putz were supported by the European Social Fund (EFOP-3.6.1.-16-2016-00004; ‘Comprehensive Development for Implementing Smart Specialization Strategies at the University of Pécs’). K.U. and E. Vergauwe were supported by a grant from the Swiss National Science Foundation (PZ00P1_154911 to E. Vergauwe). T.G. is supported by the Social Sciences and Humanities Research Council of Canada (SSHRC). M.A.V. was supported by grants 2016-T1/SOC-1395 (Comunidad de Madrid) and PSI2017-85159-P (AEI/FEDER UE). K.B. was supported by a grant from the National Science Centre, Poland (number 2015/19/D/HS6/00641). J. Bonick and J.W.L. were supported by the Joep Lange Institute. G.B. was supported by the Slovak Research and Development Agency (APVV-17-0418). H.I.J. and E.S. were supported by a French National Research Agency ‘Investissements d’Avenir’ programme grant (ANR-15-IDEX-02). T.D.G. was supported by an Australian Government Research Training Program Scholarship. The Raipur Group is thankful to: (1) the University Grants Commission, New Delhi, India for the research grants received through its SAP-DRS (Phase-III) scheme sanctioned to the School of Studies in Life Science; and (2) the Center for Translational Chronobiology at the School of Studies in Life Science, PRSU, Raipur, India for providing logistical support. K. Ask was supported by a small grant from the Department of Psychology, University of Gothenburg. Y.Q. was supported by grants from the Beijing Natural Science Foundation (5184035) and CAS Key Laboratory of Behavioral Science, Institute of Psychology. N.A.C. was supported by the National Science Foundation Graduate Research Fellowship (R010138018). We acknowledge the following research assistants: J. Muriithi and J. Ngugi (United States International University Africa); E. Adamo, D. Cafaro, V. Ciambrone, F. Dolce and E. Tolomeo (Magna Græcia University of Catanzaro); E. De Stefano (University of Padova); S. A. Escobar Abadia (University of Lincoln); L. E. Grimstad (Norwegian School of Economics (NHH)); L. C. Zamora (Franklin and Marshall College); R. E. Liang and R. C. Lo (Universiti Tunku Abdul Rahman); A. Short and L. Allen (Massey University, New Zealand), A. Ateş, E. Güneş and S. Can Özdemir (Boğaziçi University); I. Pedersen and T. Roos (Åbo Akademi University); N. Paetz (Escuela de Comunicación Mónica Herrera); J. Green (University of Gothenburg); M. Krainz (University of Vienna, Austria); and B. Todorova (University of Vienna, Austria). The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.https://www.nature.com/nathumbehav/am2023BiochemistryGeneticsMicrobiology and Plant Patholog

Self-association of the SET domains of human ALL-1 and of Drosophila TRITHORAX and ASH1 proteins

The human ALL-1 gene is involved in acute leukemia through gene fusions, partial tandem duplications or a specific deletion. Several sequence motifs within the ALL-1 protein, such as the SET domain, PHD fingers and the region with homology to DNA methyl transferase are shared with other proteins involved in transcription regulation through chromatin alterations. However, the function of these motifs is still not clear. Studying ALL-1 presents an additional challenge because the gene is the human homologue of Drosophila trithorax. The latter is a member of the trithorax-Polycornb gene family which acts to determine the body pattern of Drosophila by maintaining expression or repression of the Antennapedia-bithorax homeotic gene complex. Here we apply yeast two hybrid methodology, in vivo immunoprecipitation and in vitro 'pull down' techniques to show self association of the SET motifs of ALL-1, TRITHORAX and ASH1 proteins (Drosophila ASH1 is encoded by a trithorax-group gene). Point mutations in evolutionary conserved residues of TRITHORAX SET, abolish the interaction. SET-SET interactions might act in integrating the activity of ALL-1 (TRX and ASH1) protein molecules, simultaneously positioned at different maintenance elements and directing expression of the same or different target genes

Trithorax and ASH1 interact directly and associate with the trithorax group-responsive bxd region of the Ultrabithorax promoter

Trithorax (TRX) and ASH1 belong to the trithorax group (trxG) of transcriptional activator proteins, which maintains homeotic gene expression during Drosophila development. TRX and ASH1 are localized on chromosomes and share several homologous domains with other chromatin-associated proteins, including a highly conserved SET domain and PHD fingers. Based on genetic interactions between trx and ash1 and our previous observation that association of the TRX protein with polytene chromosomes is ash1 dependent, we investigated the possibility of a physical linkage between the two proteins. We found that the endogenous TRX and ASH1 proteins coimmunoprecipitate from embryonic extracts and colocalize on salivary gland polytene chromosomes. Furthermore, we demonstrated that TRX and ASH1 bind in vivo to a relatively small (4 kb) bxd subregion of the homeotic gene Ultrabithorax (Ubx), which contains several trx response elements. Analysis of the effects of ash1 mutations on the activity of this regulatory region indicates that it also contains ash1 response element(s). This suggests that ASH1 and TRX act on Ubx in relatively close proximity to each other. Finally, TRX and ASH1 appear to interact directly through their conserved SET domains, based on binding assays in vitro and in yeast and on coimmunoprecipitation assays with embryo extracts. Collectively, these results suggest that TRX and ASH1 are components that interact either within trxG protein complexes or between complexes that act in close proximity on regulatory DNA to maintain Ubx transcription