A post-merger enhancement only in star-forming Type 2 Seyfert galaxies:the deep learning view

Supermassive black holes require a reservoir of cold gas at the centre of their host galaxy in order to accrete and shine as active galactic nuclei (AGN). Major mergers have the ability to drive gas rapidly inwards, but observations trying to link mergers with AGN have found mixed results due to the difficulty of consistently identifying galaxy mergers in surveys. This study applies deep learning to this problem, using convolutional neural networks trained to identify simulated post-merger galaxies from survey-realistic imaging. This provides a fast and repeatable alternative to human visual inspection. Using this tool, we examine a sample of ~8500 Seyfert 2 galaxies (L[OIII] ~ $10^{38.5 - 42}$ erg/s) at z < 0.3 in the Sloan Digital Sky Survey and find a merger fraction of $2.19_{-0.17}^{+0.21}$% compared with inactive control galaxies, in which we find a merger fraction of $2.96_{-0.20}^{+0.26}$%, indicating an overall lack of mergers among AGN hosts compared with controls. However, matching the controls to the AGN hosts in stellar mass and star formation rate reveals that AGN hosts in the star-forming blue cloud exhibit a ~$2\times$ merger enhancement over controls, while those in the quiescent red sequence have significantly lower relative merger fractions, leading to the observed overall deficit due to the differing $M_{\ast} -$SFR distributions. We conclude that while mergers are not the dominant trigger of all low-luminosity, obscured AGN activity in the nearby Universe, they are more important to AGN fuelling in galaxies with higher cold gas mass fractions as traced through star formation

The ALHAMBRA Survey: Bayesian Photometric Redshifts with 23 bands for 3 squared degrees

The ALHAMBRA (Advance Large Homogeneous Area Medium Band Redshift Astronomical) survey has observed 8 different regions of the sky, including sections of the COSMOS, DEEP2, ELAIS, GOODS-N, SDSS and Groth fields using a new photometric system with 20 contiguous ~ $300\AA$ filters covering the optical range, combining them with deep $JHKs$ imaging. The observations, carried out with the Calar Alto 3.5m telescope using the wide field (0.25 sq. deg FOV) optical camera LAICA and the NIR instrument Omega-2000, correspond to ~700hrs on-target science images. The photometric system was designed to maximize the effective depth of the survey in terms of accurate spectral-type and photo-zs estimation along with the capability of identification of relatively faint emission lines. Here we present multicolor photometry and photo-zs for ~438k galaxies, detected in synthetic F814W images, complete down to I~24.5 AB, taking into account realistic noise estimates, and correcting by PSF and aperture effects with the ColorPro software. The photometric ZP have been calibrated using stellar transformation equations and refined internally, using a new technique based on the highly robust photometric redshifts measured for emission line galaxies. We calculate photometric redshifts with the BPZ2 code, which includes new empirically calibrated templates and priors. Our photo-zs have a precision of $dz/(1+z_s)=1$ for I<22.5 and 1.4% for 22.5<I<24.5. Precisions of less than 0.5% are reached for the brighter spectroscopic sample, showing the potential of medium-band photometric surveys. The global $P(z)$ shows a mean redshift =0.56 for I=0.86 for I<24.5 AB. The data presented here covers an effective area of 2.79 sq. deg, split into 14 strips of 58.5'x15.5' and represents ~32 hrs of on-target.Comment: The catalog data and a full resolution version of this paper is available at https://cloud.iaa.csic.es/alhambra

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1

DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding protein–interacting protein (CtIP) is phosphorylated in G2 by cyclin-dependent kinases to initiate resection and promote HR. CtIP also exerts functions during NHEJ, although the mechanism phosphorylating CtIP in G1 is unknown. In this paper, we identify Plk3 (Polo-like kinase 3) as a novel DSB response factor that phosphorylates CtIP in G1 in a damage-inducible manner and impacts on various cellular processes in G1. First, Plk3 and CtIP enhance the formation of ionizing radiation-induced translocations; second, they promote large-scale genomic deletions from restriction enzyme-induced DSBs; third, they are required for resection and repair of complex DSBs; and finally, they regulate alternative NHEJ processes in Ku−/− mutants. We show that mutating CtIP at S327 or T847 to nonphosphorylatable alanine phenocopies Plk3 or CtIP loss. Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847

N7-methylguanosine methylation of tRNAs regulates survival to stress in cancer

Tumour progression and therapy tolerance are highly regulated and complex processes largely dependent on the plasticity of cancer cells and their capacity to respond to stress. The higher plasticity of cancer cells highlights the need for identifying targetable molecular pathways that challenge cancer cell survival. Here, we show that