A Relationship Between Stellar Metallicity Gradients and Galaxy Age in Dwarf Galaxies

We explore the origin of stellar metallicity gradients in simulated and observed dwarf galaxies. We use FIRE-2 cosmological baryonic zoom-in simulations of 26 isolated galaxies as well as existing observational data for 10 Local Group dwarf galaxies. Our simulated galaxies have stellar masses between $10^{5.5}$ and 10^{8.6} \msun. Whilst gas-phase metallicty gradients are generally weak in our simulated galaxies, we find that stellar metallicity gradients are common, with central regions tending to be more metal-rich than the outer parts. The strength of the gradient is correlated with galaxy-wide median stellar age, such that galaxies with younger stellar populations have flatter gradients. Stellar metallicty gradients are set by two competing processes: (1) the steady "puffing" of old, metal-poor stars by feedback-driven potential fluctuations, and (2) the accretion of extended, metal-rich gas at late times, which fuels late-time metal-rich star formation. If recent star formation dominates, then extended, metal-rich star formation washes out pre-existing gradients from the "puffing" process. We use published results from ten Local Group dwarf galaxies to show that a similar relationship between age and stellar metallicity-gradient strength exists among real dwarfs. This suggests that observed stellar metallicity gradients may be driven largely by the baryon/feedback cycle rather than by external environmental effects.Comment: 14 pages, 13 figures, submitted to MNRA

HDAC6 Regulates LPS-Tolerance in Astrocytes

Inflammatory tolerance is a crucial mechanism that limits inflammatory responses in order to avoid prolonged inflammation that may damage the host. Evidence that chronic inflammation contributes to the neuropathology of prevalent neurodegenerative and psychiatric diseases suggests that inflammatory tolerance mechanisms are often inadequate to control detrimental inflammation in the central nervous system. Thus, identifying mechanisms that regulate neuroinflammatory tolerance may reveal opportunities for bolstering tolerance to reduce chronic inflammation in these diseases. Examination of tolerance after repeated lipopolysaccharide (LPS) treatment of mouse primary astrocytes demonstrated that histone deacetylase (HDAC) activity promoted tolerance, opposite to the action of glycogen synthase kinase-3 (GSK3), which counteracts tolerance. HDAC6 in particular was found to be critical for tolerance induction, as its deacetylation of acetyl-tubulin was increased during LPS tolerance, this was enhanced by inhibition of GSK3, and the HDAC6 inhibitor tubacin completely blocked tolerance and the promotion of tolerance by inhibition of GSK3. These results reveal opposing interactions between HDAC6 and GSK3 in regulating tolerance, and indicate that shifting the balance between these two opposing forces on inflammatory tolerance can obliterate or enhance tolerance to LPS in astrocytes

Bacterial Niche-Specific Genome Expansion Is Coupled with Highly Frequent Gene Disruptions in Deep-Sea Sediments

The complexity and dynamics of microbial metagenomes may be evaluated by genome size, gene duplication and the disruption rate between lineages. In this study, we pyrosequenced the metagenomes of microbes obtained from the brine and sediment of a deep-sea brine pool in the Red Sea to explore the possible genomic adaptations of the microbes in response to environmental changes. The microbes from the brine and sediments (both surface and deep layers) of the Atlantis II Deep brine pool had similar communities whereas the effective genome size varied from 7.4 Mb in the brine to more than 9 Mb in the sediment. This genome expansion in the sediment samples was due to gene duplication as evidenced by enrichment of the homologs. The duplicated genes were highly disrupted, on average by 47.6% and 70% for the surface and deep layers of the Atlantis II Deep sediment samples, respectively. The disruptive effects appeared to be mainly due to point mutations and frameshifts. In contrast, the homologs from the Atlantis II Deep brine sample were highly conserved and they maintained relatively small copy numbers. Likely, the adaptation of the microbes in the sediments was coupled with pseudogenizations and possibly functional diversifications of the paralogs in the expanded genomes. The maintenance of the pseudogenes in the large genomes is discussed

Disease- and age-related changes in histone acetylation at gene promoters in psychiatric disorders

Increasing evidence suggests that epigenetic factors have critical roles in gene regulation in neuropsychiatric disorders and in aging, both of which are typically associated with a wide range of gene expression abnormalities. Here, we have used chromatin immunoprecipitation-qPCR to measure levels of acetylated histone H3 at lysines 9/14 (ac-H3K9K14), two epigenetic marks associated with transcriptionally active chromatin, at the promoter regions of eight schizophrenia-related genes in n=82 postmortem prefrontal cortical samples from normal subjects and those with schizophrenia and bipolar disorder. We find that promoter-associated ac-H3K9K14 levels are correlated with gene expression levels, as measured by real-time qPCR for several genes, including, glutamic acid decarboxylase 1 (GAD1), 5-hydroxytryptamine receptor 2C (HTR2C), translocase of outer mitochondrial membrane 70 homolog A (TOMM70A) and protein phosphatase 1E (PPM1E). Ac-H3K9K14 levels of several of the genes tested were significantly negatively associated with age in normal subjects and those with bipolar disorder, but not in subjects with schizophrenia, whereby low levels of histone acetylation were observed in early age and throughout aging. Consistent with this observation, significant hypoacetylation of H3K9K14 was detected in young subjects with schizophrenia when compared with age-matched controls. Our results demonstrate that gene expression changes associated with psychiatric disease and aging result from epigenetic mechanisms involving histone acetylation. We further find that treatment with a histone deacetylase (HDAC) inhibitor alters the expression of several candidate genes for schizophrenia in mouse brain. These findings may have therapeutic implications for the clinical use of HDAC inhibitors in psychiatric disorders

A relationship between stellar metallicity gradients and galaxy age in dwarf galaxies

We explore the origin of stellar metallicity gradients in simulated and observed dwarf galaxies. We use FIRE-2 cosmological baryonic zoom-in simulations of 26 isolated galaxies as well as existing observational data for 10 Local Group dwarf galaxies. Our simulated galaxies have stellar masses between 105.5 and 108.6 MO. Whilst gas-phase metallicty gradients are generally weak in our simulated galaxies, we find that stellar metallicity gradients are common, with central regions tending to be more metal-rich than the outer parts. The strength of the gradient is correlated with galaxy-wide median stellar age, such that galaxies with younger stellar populations have flatter gradients. Stellar metallicty gradients are set by two competing processes: (1) the steady 'puffing' of old, metal-poor stars by feedback-driven potential fluctuations and (2) the accretion of extended, metal-rich gas at late times, which fuels late-time metal-rich star formation. If recent star formation dominates, then extended, metal-rich star formation washes out pre-existing gradients from the 'puffing' process. We use published results from ten Local Group dwarf galaxies to show that a similar relationship between age and stellar metallicity-gradient strength exists among real dwarfs. This suggests that observed stellar metallicity gradients may be driven largely by the baryon/feedback cycle rather than by external environmental effects