The Collins-Roscoe mechanism and D-spaces

We prove that if a space X is well ordered $(\alpha A)$, or linearly semi-stratifiable, or elastic then X is a D-space

Overexpression of the Aspergillus nidulans histone 4 acetyltransferase EsaA increases activation of secondary metabolite production

This is the peer reviewed version of the following article: Soukup, A. A., Chiang, Y.-M., Bok, J. W., Reyes-Dominguez, Y., Oakley, B. R., Wang, C. C. C., Strauss, J. and Keller, N. P. (2012), Overexpression of the Aspergillus nidulans histone 4 acetyltransferase EsaA increases activation of secondary metabolite production. Molecular Microbiology, 86: 314–330. doi:10.1111/j.1365-2958.2012.08195.x, which has been published in final form at http://doi.org/10.1111/j.1365-2958.2012.08195.x. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.Regulation of secondary metabolite (SM) gene clusters in Aspergillus nidulans has been shown to occur through cluster specific transcription factors or through global regulators of chromatin structure such as histone methyltransferases, histone deacetylases, or the putative methyltransferase LaeA. A multi-copy suppressor screen for genes capable of returning SM production to the SM deficient ΔlaeA mutant resulted in identification of the essential histone acetyltransferase EsaA, able to complement an esa1 deletion in Saccharomyces cereviseae. Here we report that EsaA plays a novel role in SM cluster activation through histone 4 lysine 12 (H4K12) acetylation in four examined SM gene clusters (sterigmatocystin, penicillin, terrequinone, and orsellinic acid), in contrast to no increase in H4K12 acetylation of the housekeeping tubA promoter. This augmented SM cluster acetylation requires LaeA for full effect and correlates with both increased transcript levels and metabolite production relative to wild type. H4K12 levels may thus represent a unique indicator of relative production potential, notably of SMs

A LRRK2-Dependent EndophilinA Phosphoswitch Is Critical for Macroautophagy at Presynaptic Terminals.

Synapses are often far from the soma and independently cope with proteopathic stress induced by intense neuronal activity. However, how presynaptic compartments turn over proteins is poorly understood. We show that the synapse-enriched protein EndophilinA, thus far studied for its role in endocytosis, induces macroautophagy at presynaptic terminals. We find that EndophilinA executes this unexpected function at least partly independent of its role in synaptic vesicle endocytosis. EndophilinA-induced macroautophagy is activated when the kinase LRRK2 phosphorylates the EndophilinA-BAR domain and is blocked in animals where EndophilinA cannot be phosphorylated. EndophilinA-phosphorylation promotes the formation of highly curved membranes, and reconstitution experiments show these curved membranes serve as docking stations for autophagic factors, including Atg3. Functionally, deregulation of the EndophilinA phosphorylation state accelerates activity-induced neurodegeneration. Given that EndophilinA is connected to at least three Parkinson's disease genes (LRRK2, Parkin and Synaptojanin), dysfunction of EndophilinA-dependent synaptic macroautophagy may be common in this disorder

Ozone Exposure Increases Circulating Stress Hormones and Lipid Metabolites in Humans

Rationale: Air pollution has been associated with increased prevalence of type 2 diabetes; however, the mechanisms remain unknown. We have shown that acute ozone exposure in rats induces release of stress hormones, hyperglycemia, leptinemia, and glucose intolerance that are associated with global changes in peripheral glucose, lipid, and amino acid metabolism

The well-ordered (F) spaces are D-spaces

We studied the relationships between Collins-Roscoe mechanism and D-spaces, proved that well-ordered (F) spaces are D-spaces. This positively answered a question asked by D.Soukup and Y.Xu before.Comment: 6 page

Human vault-associated non-coding RNAs bind to mitoxantrone, a chemotherapeutic compound

Human vaults are the largest cytoplasmic ribonucleoprotein and are overexpressed in cancer cells. Vaults reportedly function in the extrusion of xenobiotics from the nuclei of resistant cells, but the interactions of xenobiotics with the vault-associated proteins or non-coding RNAs have never been directly observed. In the present study, we show that vault RNAs (vRNAs), specifically the hvg-1 and hvg-2 RNAs, bind to a chemotherapeutic compound, mitoxantrone. Using an in-line probing assay (spontaneous transesterification of RNA linkages), we have identified the mitoxantrone binding region within the vRNAs. In addition, we analyzed the interactions between vRNAs and mitoxantrone in the cellular milieu, using an in vitro translation inhibition assay. Taken together, our results clearly suggest that vRNAs have the ability to bind certain chemotherapeutic compounds and these interactions may play an important role in vault function, by participating in the export of toxic compounds

Parity Violation in Proton-Proton Scattering at 221 MeV

The parity-violating longitudinal analyzing power, Az, has been measured in pp elastic scattering at an incident proton energy of 221 MeV. The result obtained is Az =(0.84 +/- 0.29 (stat.) +/- 0.17 (syst.)) x 10^{-7}. This experiment is unique in that it selects a single parity violating transition amplitude, 3P2-1D2, and consequently directly constrains the weak meson-nucleon coupling constant h^pp_rho When this result is taken together with the existing pp parity violation data, the weak meson-nucleon coupling constants h^pp_rho and h^pp_omega can, for the first time, both be determined.Comment: 8 pages RevTeX4, 3 PostScript figures. Conclusion revised. New information about weak coupling constants adde

Parity Violation in Proton-Proton Scattering at 221 MeV

TRIUMF experiment 497 has measured the parity violating longitudinal analyzing power, A_z, in pp elastic scattering at 221.3 MeV incident proton energy. This paper includes details of the corrections, some of magnitude comparable to A_z itself, required to arrive at the final result. The largest correction was for the effects of first moments of transverse polarization. The addition of the result, A_z=(0.84 \pm 0.29 (stat.) \pm 0.17 (syst.)) \times 10^{-7}, to the pp parity violation experimental data base greatly improves the experimental constraints on the weak meson-nucleon coupling constants h^{pp}_\rho and h^{pp}_\omega, and has implications for the interpretation of electron parity violation experiments.Comment: 17 pages RevTeX, 14 PostScript figures. Revised version with additions suggested by Phys. Rev.