An extensive study of dynamical friction in dwarf galaxies: the role of stars, dark matter, halo profiles and MOND

We investigate the in-spiraling timescales of globular clusters in dwarf spheroidal (dSph) and dwarf elliptical (dE) galaxies, due to dynamical friction. We address the problem of these timescales having been variously estimated in the literature as much shorter than a Hubble time. Using self-consistent two-component (dark matter and stars) models, we explore mechanisms which may yield extended dynamical friction timescales in such systems in order to explain why dwarf galaxies often show globular cluster systems. As a general rule, dark matter and stars both give a comparable contribution to the dynamical drag. By exploring various possibilities for their gravitational make-up, it is shown that these studies help constrain the parameters of the dark matter haloes in these galaxies, as well as to test alternatives to dark matter. Under the assumption of a dark haloes having a constant density core, dynamical friction timescales are naturally extended upwards of a Hubble time. Cuspy dark haloes yield timescales $\lesssim$ 4.5 Gyr, for any dark halo parameters in accordance with observations of stellar line-of-sight velocity dispersion in dwarf spheroidal galaxies. We find that under the hypothesis of MOND dynamics, due to the enhanced dynamical drag of the stars, the dynamical friction timescales would be extremely short. Taking the well-measured structural parameters of the Fornax dSph and its globular cluster system as a case study, we conclude that requiring dynamical friction timescales comparable to the Hubble time strongly favours dark haloes with a central core.Comment: 18 pages, four figures, final version, accepted in MNRA

The impact of dark matter cusps and cores on the satellite galaxy population around spiral galaxies

(Abridged) We use N-body simulations to study the effects that a divergent (i.e. "cuspy") dark matter (DM) profile introduces on the tidal evolution of dwarf spheroidal galaxies (dSphs). Our models assume cosmologically-motivated initial conditions where dSphs are DM-dominated systems on eccentric orbits about a host galaxy composed of a dark halo and a baryonic disc. We find that the resilience of dSphs to tidal stripping is extremely sensitive to the halo cuspiness; whereas dwarfs with a cored profile can be easily destroyed by the host disc, those with cusps always retain a bound remnant. For a given halo profile the evolution of the structural parameters as driven by tides is controlled solely by the total amount of mass lost. This information is used to construct a semi-analytic code that simulates the hierarchical build-up of spiral galaxies assuming different halo profiles and disc masses. We find that tidal encounters with discs tend to decrease the average mass of satellites at all galactocentric radii. Interestingly, satellites accreted before re-ionization (z>6), which may be singled out by anomalous metallicity patterns, survive only if haloes are cuspy. We show that the size-mass relation established from Milky Way (MW) dwarfs strongly supports the presence of cusps in the majority of these systems, as cored models systematically underestimate the masses of the known Ultra-Faint dSphs. Our models also indicate that a massive M31 disc may explain why many of its dSphs fall below the size-mass relationship derived from MW dSphs. We use our models to constrain the mass threshold below which star formation is suppressed in DM haloes, finding that luminous satellites must be accreted with masses above 10^8--10^9 M_sol in order to explain the size-mass relation observed in MW dwarfs.Comment: 17 pages, 14 figures, MNRAS accepted after minor revisio

Abnormalities in fronto-striatal connectivity within language networks relate to differences in grey-matter heterogeneity in Asperger syndrome

Abstract Asperger syndrome (AS) is an Autism Spectrum Disorder (ASD) characterised by qualitative impairment in the development of emotional and social skills with relative preservation of general intellectual abilities, including verbal language. People with AS may nevertheless show atypical language, including rate and frequency of speech production. We previously observed that abnormalities in grey matter homogeneity (measured with texture analysis of structural MR images) in AS individuals when compared with controls are also correlated with the volume of caudate nucleus. Here, we tested a prediction that these distributed abnormalities in grey matter compromise the functional integrity of brain networks supporting verbal communication skills. We therefore measured the functional connectivity between caudate nucleus and cortex during a functional neuroimaging study of language generation (verbal fluency), applying psycho-physiological interaction (PPI) methods to test specifically for differences attributable to grey matter heterogeneity in AS participants. Furthermore, we used dynamic causal modelling (DCM) to characterise the causal directionality of these differences in interregional connectivity during word production. Our results revealed a diagnosis-dependent influence of grey matter heterogeneity on the functional connectivity of the caudate nuclei with right insula/inferior frontal gyrus and anterior cingulate, respectively with the left superior frontal gyrus and right precuneus. Moreover, causal modelling of interactions between inferior frontal gyri, caudate and precuneus, revealed a reliance on bottom-up (stimulus-driven) connections in AS participants that contrasted with a dominance of top-down (cognitive control) connections from prefrontal cortex observed in control participants. These results provide detailed support for previously hypothesised central disconnectivity in ASD and specify discrete brain network targets for diagnosis and therapy in ASD

Failure of SOX9 Regulation in 46XY Disorders of Sex Development with SRY, SOX9 and SF1 Mutations

In human embryogenesis, loss of SRY (sex determining region on Y), SOX9 (SRY-related HMG box 9) or SF1 (steroidogenic factor 1) function causes disorders of sex development (DSD). A defining event of vertebrate sex determination is male-specific upregulation and maintenance of SOX9 expression in gonadal pre-Sertoli cells, which is preceded by transient SRY expression in mammals. In mice, Sox9 regulation is under the transcriptional control of SRY, SF1 and SOX9 via a conserved testis-specific enhancer of Sox9 (TES). Regulation of SOX9 in human sex determination is however poorly understood.We show that a human embryonal carcinoma cell line (NT2/D1) can model events in presumptive Sertoli cells that initiate human sex determination. SRY associates with transcriptionally active chromatin in NT2/D1 cells and over-expression increases endogenous SOX9 expression. SRY and SF1 co-operate to activate the human SOX9 homologous TES (hTES), a process dependent on phosphorylated SF1. SOX9 also activates hTES, augmented by SF1, suggesting a mechanism for maintenance of SOX9 expression by auto-regulation. Analysis of mutant SRY, SF1 and SOX9 proteins encoded by thirteen separate 46,XY DSD gonadal dysgenesis individuals reveals a reduced ability to activate hTES.We demonstrate how three human sex-determining factors are likely to function during gonadal development around SOX9 as a hub gene, with different genetic causes of 46,XY DSD due a common failure to upregulate SOX9 transcription

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Cohort Profile: Pregnancy And Childhood Epigenetics (PACE) Consortium.

Development Psychopathology in context: famil