The space of homogeneous probability measures on is compact: With an appendix by Jialun Li.

In this paper we prove that the space of homogeneous probability measures on the maximal Satake compactification of an arithmetic locally symmetric space is compact. As an application, we explain some consequences for the distribution of weakly special subvarieties of Shimura varieties.

Epigenetic Modulation of Class-Switch DNA Recombination to IgA by miR-146a Through Downregulation of Smad2, Smad3 and Smad4.

IgA is the predominant antibody isotype at intestinal mucosae, where it plays a critical role in homeostasis and provides a first line of immune protection. Dysregulation of IgA production, however, can contribute to immunopathology, particularly in kidneys in which IgA deposition can cause nephropathy. Class-switch DNA recombination (CSR) to IgA is directed by TGF-β signaling, which activates Smad2 and Smad3.

Lactate Elicits ER-Mitochondrial Mg Dynamics to Integrate Cellular Metabolism.

Mg is the most abundant divalent cation in metazoans and an essential cofactor for ATP, nucleic acids, and countless metabolic enzymes. To understand how the spatio-temporal dynamics of intracellular Mg (Mg) are integrated into cellular signaling, we implemented a comprehensive screen to discover regulators of Mg dynamics. Lactate emerged as an activator of rapid release of Mg from endoplasmic reticulum (ER) stores, which facilitates mitochondrial Mg (Mg) uptake in multiple cell types.

Mitochondrial pyruvate and fatty acid flux modulate MICU1-dependent control of MCU activity.

The tricarboxylic acid (TCA) cycle converts the end products of glycolysis and fatty acid β-oxidation into the reducing equivalents NADH and FADH Although mitochondrial matrix uptake of Ca enhances ATP production, it remains unclear whether deprivation of mitochondrial TCA substrates alters mitochondrial Ca flux. We investigated the effect of TCA cycle substrates on MCU-mediated mitochondrial matrix uptake of Ca, mitochondrial bioenergetics, and autophagic flux. Inhibition of glycolysis, mitochondrial pyruvate transport, or mitochondrial fatty acid transport triggered expression of the MCU gatekeeper MICU1 but not the MCU core subunit.

Blockade of MCU-Mediated Ca Uptake Perturbs Lipid Metabolism via PP4-Dependent AMPK Dephosphorylation.

Mitochondrial Ca uniporter (MCU)-mediated Ca uptake promotes the buildup of reducing equivalents that fuel oxidative phosphorylation for cellular metabolism. Although MCU modulates mitochondrial bioenergetics, its function in energy homeostasis in vivo remains elusive. Here we demonstrate that deletion of the Mcu gene in mouse liver (MCU) and in Danio rerio by CRISPR/Cas9 inhibits mitochondrial Ca (Ca) uptake, delays cytosolic Ca (Ca) clearance, reduces oxidative phosphorylation, and leads to increased lipid accumulation.