The SAMI–Fornax Dwarfs Survey – III. Evolution of [α/Fe] in dwarfs, from Galaxy Clusters to the Local Group

Using very deep, high spectral resolution data from the SAMI Integral Field Spectrograph, we study the stellar population properties of a sample of dwarf galaxies in the Fornax Cluster, down to a stellar mass of 107 M☉, which has never been done outside the Local Group. We use full spectral fitting to obtain stellar population parameters. Adding massive galaxies from the ATLAS3D project, which we re-analysed, and the satellite galaxies of the Milky Way, we obtained a galaxy sample that covers the stellar mass range 104–1012 M☉. Using this large range, we find that the mass–metallicity relation is not linear. We also find that the [α/Fe]-stellar mass relation of the full sample shows a U-shape, with a minimum in [α/Fe] for masses between 109 and 1010 M☉. The relation between [α/Fe] and stellar mass can be understood in the following way: when the faintest galaxies enter the cluster environment, a rapid burst of star formation is induced, after which the gas content is blown away by various quenching mechanisms. This fast star formation causes high [α/Fe] values, like in the Galactic halo. More massive galaxies will manage to keep their gas longer and form several bursts of star formation, with lower [α/Fe] as a result. For massive galaxies, stellar populations are regulated by internal processes, leading to [α/Fe] increasing with mass. We confirm this model by showing that [α/Fe] correlates with clustercentric distance in three nearby clusters and also in the halo of the Milky Way.</p

Perspectives of drug-based neuroprotection targeting mitochondria

Mitochondrial dysfunction has been reported in most neurodegenerative diseases. These anomalies include bioenergetic defect, respiratory chain-induced oxidative stress, defects of mitochondrial dynamics, increase sensitivity to apoptosis, and accumulation of damaged mitochondria with instable mitochondrial DNA. Significant progress has been made in our understanding of the pathophysiology of inherited mitochondrial disorders but most have no effective therapies. The development of new metabolic treatments will be useful not only for rare mitochondrial disorders but also for the wide spectrum of common age-related neurodegenerative diseases shown to be associated with mitochondrial dysfunction. A better understanding of the mitochondrial regulating pathways raised several promising perspectives of neuroprotection. This review focuses on the pharmacological approaches to modulate mitochondrial biogenesis, the removal of damaged mitochondria through mitophagy, scavenging free radicals and also dietary measures such as ketogenic diet

The Fornax Deep Survey (FDS) with the VST. XI. The search for signs of preprocessing between the Fornax main cluster and Fornax A group

Context. Galaxies either live in a cluster, a group, or in a field environment. In the hierarchical framework, the group environment bridges the field to the cluster environment, as field galaxies form groups before aggregating into clusters. In principle, environmental mechanisms, such as galaxy-galaxy interactions, can be more efficient in groups than in clusters due to lower velocity dispersion, which lead to changes in the properties of galaxies. This change in properties for group galaxies before entering the cluster environment is known as preprocessing. Whilst cluster and field galaxies are well studied, the extent to which galaxies become preprocessed in the group environment is unclear. Aims: We investigate the structural properties of cluster and group galaxies by studying the Fornax main cluster and the infalling Fornax A group, exploring the effects of galaxy preprocessing in this showcase example. Additionally, we compare the structural complexity of Fornax galaxies to those in the Virgo cluster and in the field. Methods: Our sample consists of 582 galaxies from the Fornax main cluster and Fornax A group. We quantified the light distributions of each galaxy based on a combination of aperture photometry, Sérsic+PSF (point spread function) and multi-component decompositions, and non-parametric measures of morphology. From these analyses, we derived the galaxy colours, structural parameters, non-parametric morphological indices (Concentration C; Asymmetry A, Clumpiness S; Gini G; second order moment of light M20), and structural complexity based on multi-component decompositions. These quantities were then compared between the Fornax main cluster and Fornax A group. The structural complexity of Fornax galaxies were also compared to those in Virgo and in the field. Results: We find significant (Kolmogorov-Smirnov test p-value < α = 0.05) differences in the distributions of quantities derived from Sérsic profiles (g′‒r′, r′‒i′, Re, and μ̄e,r′), and non-parametric indices (A and S) between the Fornax main cluster and Fornax A group. Fornax A group galaxies are typically bluer, smaller, brighter, and more asymmetric and clumpy. Moreover, we find significant cluster-centric trends with r′‒i′, Re, and μ̄e,r′, as well as A, S, G, and M20 for galaxies in the Fornax main cluster. This implies that galaxies falling towards the centre of the Fornax main cluster become fainter, more extended, and generally smoother in their light distribution. Conversely, we do not find significant group-centric trends for Fornax A group galaxies. We find the structural complexity of galaxies (in terms of the number of components required to fit a galaxy) to increase as a function of the absolute r′-band magnitude (and stellar mass), with the largest change occurring between ‒14 mag ≲Mr′ ≲ ‒19 mag (7.5 ≲ log10(M*/M⊙) ≲ 9.7). This same trend was found in galaxy samples from the Virgo cluster and in the field, which suggests that the formation or maintenance of morphological structures (e.g., bulges, bar) are largely due to the stellar mass of the galaxies, rather than the environment they reside in. Full Tables 2, 3, and I.1 are only available at the CDS via anonymous ftp to cdsarc.u-strasbg.fr (ftp://130.79.128.5) or via http://cdsarc.u-strasbg.fr/viz-bin/cat/J/A+A/647/A10

Microcapteurs électrochimiques pour des mesures durables en Environnement-Santé et Agroalimentaire

National audienc

Genetic testing among high-risk individuals in families with hereditary nonpolyposis colorectal cancer

Hereditary nonpolyposis colorectal cancer (HNPCC) is frequently associated with constitutional mutations in a class of genes involved in DNA mismatch repair. We identified 32 kindreds, with germline mutations in one of three genes hMSH2, hMLH1 or hMSH6. In this study, we purposed to evaluate how many high-risk individuals in each family underwent genetic testing: moreover, we assessed how many mutation-positive unaffected individuals accepted colonoscopic surveillance and the main findings of the recommended follow-up. Families were identified through a population-based registry, or referred from other centres. Members of the families were invited for an education session with two members of the staff. When a kindred was consistent with HNPCC, neoplastic tissues were examined for microsatellite instability (MSI) and immunohistochemical expression of MSH2, MLH1 and MSH6 proteins. Moreover, constitutional mutations were searched by SSCP or direct sequencing of the whole genomic region. Of the 164 subjects assessed by genetic testing, 89 were gene carriers (66 affected - that is, with HNPCC-related cancer diagnosis - and 23 unaffected) and 75 tested negative. Among the 23 unaffected gene carriers, 18 (78.3%) underwent colonoscopy and four declined. On a total of 292 first degree at risk of cancer, 194 (66.4%) did not undergo genetic testing. The main reasons for this were: (a) difficulty to reach family members at risk, (b) lack of collaboration, (c) lack of interest in preventive medicine or 'fatalistic' attitude towards cancer occurrence. The number of colorectal lesions detected at endoscopy in gene carriers was significantly (P<0.01) higher than in controls (noncarriers). We conclude that a large fraction of high-risk individuals in mutation-positive HNPCC families does not undergo genetic testing, despite the benefits of molecular screening and endoscopic surveillance. This clearly indicates that there are still barriers to genetic testing in HNPCC, and that we are unable to provide adequate protection against cancer development in these families

Galaxy mapping with the SAURON integral-field spectrograph: The star formation history of NGC 4365

We report the first wide-field mapping of the kinematics and stellar populations in the E3 galaxy NGC 4365. The velocity maps extend previous long-slit work. They show two independent kinematic subsystems: the central 300 x 700 pc rotates about the projected minor axis, and the main body of the galaxy, 3 x 4 kpc, rotates almost at right angles to this. The line-strength maps show that the metallicity of the stellar population decreases from a central value greater than solar, to one-half solar at a radius of 2 kpc. The decoupled core and main body of the galaxy have the same luminosity-weighted age, of ~14 Gyr, and the same elevated magnesium-to-iron ratio. The two kinematically distinct components have thus shared a common star formation history. We infer that the galaxy underwent a sequence of mergers associated with dissipative star formation that ended >12 Gyr ago. The misalignment between the photometric and kinematic axes of the main body is unambiguous evidence of triaxiality. The similarity of the stellar populations in the two components suggests that the observed kinematic structure has not changed substantially in 12 Gyr.Comment: 5 pages, accepted for publication in ApJ Letter

OPA1 mutations induce mitochondrial DNA instability and optic atrophy ‘plus’ phenotypes

Mutations in OPA1, a dynamin-related GTPase involved in mitochondrial fusion, cristae organization and control of apoptosis, have been linked to non-syndromic optic neuropathy transmitted as an autosomal-dominant trait (DOA). We here report on eight patients from six independent families showing that mutations in the OPA1 gene can also be responsible for a syndromic form of DOA associated with sensorineural deafness, ataxia, axonal sensory-motor polyneuropathy, chronic progressive external ophthalmoplegia and mitochondrial myopathy with cytochrome c oxidase negative and Ragged Red Fibres. Most remarkably, we demonstrate that these patients all harboured multiple deletions of mitochondrial DNA (mtDNA) in their skeletal muscle, thus revealing an unrecognized role of the OPA1 protein in mtDNA stability. The five OPA1 mutations associated with these DOA ‘plus’ phenotypes were all mis-sense point mutations affecting highly conserved amino acid positions and the nuclear genes previously known to induce mtDNA multiple deletions such as POLG1, PEO1 (Twinkle) and SLC25A4 (ANT1) were ruled out. Our results show that certain OPA1 mutations exert a dominant negative effect responsible for multi-systemic disease, closely related to classical mitochondrial cytopathies, by a mechanism involving mtDNA instability

The 3-methylglutaconic acidurias: what’s new?

The heterogeneous group of 3-methylglutaconic aciduria (3-MGA-uria) syndromes includes several inborn errors of metabolism biochemically characterized by increased urinary excretion of 3-methylglutaconic acid. Five distinct types have been recognized: 3-methylglutaconic aciduria type I is an inborn error of leucine catabolism; the additional four types all affect mitochondrial function through different pathomechanisms. We provide an overview of the expanding clinical spectrum of the 3-MGA-uria types and provide the newest insights into the underlying pathomechanisms. A diagnostic approach to the patient with 3-MGA-uria is presented, and we search for the connection between urinary 3-MGA excretion and mitochondrial dysfunction

CLUH couples mitochondrial distribution to the energetic and metabolic status

Mitochondrial dynamics and distribution are critical for supplying ATP in response to energy demand. CLUH is a protein involved in mitochondrial distribution whose dysfunction leads to mitochondrial clustering, the metabolic consequences of which remain unknown. To gain insight into the role of CLUH on mitochondrial energy production and cellular metabolism, we have generated CLUH-knockout cells using CRISPR/Cas9. Mitochondrial clustering was associated with a smaller cell size and with decreased abundance of respiratory complexes, resulting in oxidative phosphorylation (OXPHOS) defects. This energetic impairment was found to be due to the alteration of mitochondrial translation and to a metabolic shift towards glucose dependency. Metabolomic profiling by mass spectroscopy revealed an increase in the concentration of some amino acids, indicating a dysfunctional Krebs cycle, and increased palmitoylcarnitine concentration, indicating an alteration of fatty acid oxidation, and a dramatic decrease in the concentrations of phosphatidylcholine and sphingomyeline, consistent with the decreased cell size. Taken together, our study establishes a clear function for CLUH in coupling mitochondrial distribution to the control of cell energetic and metabolic status