The Outskirts of Abell 1795: Probing Gas Clumping in the Intra-Cluster Medium

The outskirts of galaxy clusters host complex interactions between the intra-cluster and circumcluster media. During cluster evolution, ram-pressure stripped gas clumps from infalling substructures break the uniformity of the gas distribution, which may lead to observational biases at large radii. Assessing the contribution of gas clumping, however, poses observational challenges, and requires robust X-ray measurements in the background-dominated regime of cluster outskirts. The aims of this work are isolating faint gas clumps from field sources and from the diffuse emission in the Abell 1795 galaxy cluster, then probing their impact on the observed surface brightness and thermodynamic profiles. We performed imaging analysis on deep Chandra ACIS-I observations of the outskirts of Abell 1795, extending to $\sim1.5r_{200}$ with full azimuthal coverage. We built the $0.7-2.0$ keV surface brightness distribution from the adaptively binned image of the diffuse emission and looked for clumps as $>2\sigma$ outliers. Classification of the clump candidates was based on Chandra and SDSS data. Benefiting from the Chandra point source list, we extracted the thermodynamic profiles of the intra-cluster medium from the associated Suzaku XIS data out to $r_{200}$ using multiple point source and clump candidate removal approaches. We identified 24 clump candidates in the Abell 1795 field, most of which are likely associated with background objects, including AGN, galaxies, and clusters or groups of galaxies, as opposed to intrinsic gas clumps. These sources had minimal impact on the surface brightness and thermodynamic profiles of the cluster emission. After correcting for clump candidates, the measured entropy profile still deviates from a pure gravitational collapse, suggesting complex physics at play in the outskirts, including potential electron-ion non-equilibrium and non-thermal pressure support.Comment: 22 pages, 14 figures, submitted to Astronomy & Astrophysic

A Candidate Supermassive Black Hole in a Gravitationally Lensed Galaxy at Z ≈ 10

While supermassive black holes (SMBHs) are widely observed in the nearby and distant Universe, their origin remains debated with two viable formation scenarios with light and heavy seeds. In the light seeding model, the seed of the first SMBHs form from the collapse of massive stars with masses of 10–100 M _⊙ , while the heavy seeding model posits the formation of 10 ^4–5 M _⊙ seeds from direct collapse. The detection of SMBHs at redshifts z ≳ 10, edging closer to their formation epoch, provides critical observational discrimination between these scenarios. Here, we focus on the JWST-detected galaxy, GHZ 9, at z ≈ 10 that is lensed by the foreground cluster, A2744. Based on 2.1 Ms deep Chandra observations, we detect a candidate X-ray active galactic nucleus (AGN), which is spatially coincident with the high-redshift galaxy, GHZ 9. The SMBH candidate is inferred to have a bolometric luminosity of $({1.0}_{-0.4}^{+0.5})\times {10}^{46}\ \mathrm{erg}\,{{\rm{s}}}^{-1}$ , which corresponds to a black hole (BH) mass of $({8.0}_{-3.2}^{+3.7})\times {10}^{7}\ {M}_{\odot }$ assuming Eddington-limited accretion. This extreme mass at such an early cosmic epoch suggests the heavy seed origin for this BH candidate. Based on the Chandra and JWST discoveries of extremely high-redshift quasars, we have constructed the first simple AGN luminosity function extending to z ≈ 10. Comparison of this luminosity function with theoretical models indicates an overabundant z ≈ 10 SMBH population, consistent with a higher-than-expected seed formation efficiency

Discovery of EMRE in fungi resolves the true evolutionary history of the mitochondrial calcium uniporter

Calcium (Ca2+) influx into mitochondria occurs through a Ca2+-selective uniporter channel, which regulates essential cellular processes in eukaryotic organisms. Previous evolutionary analyses of its pore-forming subunits MCU and EMRE, and gatekeeper MICU1, pinpointed an evolutionary paradox: the presence of MCU homologs in fungal species devoid of any other uniporter components and of mt-Ca2+ uptake. Here, we trace the mt-Ca2+ uniporter evolution across 1,156 fully-sequenced eukaryotes and show that animal and fungal MCUs represent two distinct paralogous subfamilies originating from an ancestral duplication. Accordingly, we find EMRE orthologs outside Holoza and uncover the existence of an animal-like uniporter within chytrid fungi, which enables mt-Ca2+ uptake when reconstituted in vivo in the yeast Saccharomyces cerevisiae. Our study represents the most comprehensive phylogenomic analysis of the mt-Ca2+ uptake system and demonstrates that MCU, EMRE, and MICU formed the core of the ancestral opisthokont uniporter, with major implications for comparative structural and functional studies.T.G. group acknowledges support from the Spanish Ministry of Economy, Industry, and Competitiveness (MEIC) for the EMBL partnership, and grants “Centro de Excelencia Severo Ochoa 2013-2017” SEV-2012-0208 and BFU2015-67107 co-founded by European Regional Development Fund (ERDF); from the CERCA Programme/Generalitat de Catalunya; from the Catalan Research Agency (AGAUR) SGR857; and grants from the European Union’s Horizon 2020 research and innovation programme under the grant agreement ERC-2016-724173. T.G. also receives support from an INB Grant (PT17/0009/0023–ISCIII-SGEFI/ERDF). F.P. group was supported by the Munich Center for Systems Neurology (SyNergy EXC 2145/ID 390857198) and ExNet-0041-Phase2-3 (“SyNergy-HMGU”) through the Initiative and Network Fund of the Helmholtz Association to F.P.; The Bert L & N Kuggie Vallee Foundation (to F.P. and J.W.); the Juniorverbund in der Systemmedizin “mitOmics” (FKZ 01ZX1405B to V.G.). A.A.P. was supported by a postdoctoral research fellowship from EMBO (118-2017) while writing this article. A.C.S. was partially supported by the Aging and Metabolic Programming project (AMPro)

MICU3 is a tissue-specific enhancer of mitochondrial calcium uptake

The versatility and universality of Ca2+ as intracellular messenger is guaranteed by the compartmentalization of changes in [Ca2+]. In this context, mitochondrial Ca2+ plays a central role, by regulating both specific organelle functions and global cellular events. This versatility is also guaranteed by a cell type-specific Ca2+ signaling toolkit controlling specific cellular functions. Accordingly, mitochondrial Ca2+ uptake is mediated by a multimolecular structure, the MCU complex, which differs among various tissues. Its activity is indeed controlled by different components that cooperate to modulate specific channeling properties. We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function