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A new species ofPseudospermais described based on collections recently made in Benin in West Africa.Pseudosperma brunneopilosumsp. nov. occurs in forests dominated by ectomycorrhizal FabaceaeIsoberliniaand PhyllanthaceaeUapacatrees. Phylogenetic analysis of combined ITS‐LSU‐RPB2‐TEF1 gene regions shows thatP. brunneopilosumis unrelated and distinct from several recently described species ofPseudospermaalso from West Africa. Complete descriptions and illustrations, including photographs and line drawings are presented. 

Inocybe is the largest genus in the family Inocybaceae, with approximately 1000 species worldwide. Basic data on the species diversity, geographic distribution, and the infrageneric framework of Inocybe are still incomplete because of the intricate nature of this genus, which includes numerous unrecognized taxa that exist around the world. A multigene phylogeny of the I. umbratica–paludinella group, initially designated as the “I. angustifolia subgroup”, was conducted using the ITS-28S-rpb2 nucleotide datasets. The seven species, I. alabamensis, I. angustifolia, I. argenteolutea, I. olivaceonigra, I. paludinella, I. subangustifolia, and I. umbratica, were confirmed as members of this species group. At the genus level, the I. umbratica–paludinella group is a sister to the lineage of the unifying I. castanea and an undescribed species. Inocybe sect. Umbraticae sect. nov. was proposed to accommodate species in the I. umbratica–paludinella group and the I. castanea lineage. This section now comprises eight documented species and nine new species from China, as described in this paper. Additionally, new geographical distributions of I. angustifolia and I. castanea in China are reported. The nine new species and I. angustifolia, I. castanea, I. olivaceonigra, and I. umbratica are described in detail and illustrated herein with color plates based on Chinese materials. A global key to 17 species in the section Umbraticae is provided. The results of the current study provide a more detailed basis for the accurate identification of species in the I. umbratica-paludinella group and a better understanding of their phylogenetic placement. 

Abstract DNA methylation at cytosine bases (5-methylcytosine, 5mC) is a heritable epigenetic mark regulating gene expression. While enzymes that metabolize 5mC are well-characterized, endogenous signaling molecules that regulate DNA methylation machinery have not been described. We report that physiological nitric oxide (NO) concentrations reversibly inhibit the DNA demethylases TET and ALKBH2 by binding to the mononuclear non-heme iron atom forming a dinitrosyliron complex (DNIC) and preventing cosubstrates from binding. In cancer cells treated with exogenous NO, or endogenously synthesizing NO, 5mC and 5-hydroxymethylcytosine (5hmC) increase, with no changes in DNA methyltransferase activity. 5mC is also significantly increased in NO-producing patient-derived xenograft tumors from mice. Genome-wide methylome analysis of cells chronically treated with NO (10 days) shows enrichment of 5mC and 5hmC at gene-regulatory loci, correlating with altered expression of NO-regulated tumor-associated genes. Regulation of DNA methylation is distinctly different from canonical NO signaling and represents a unique epigenetic role for NO. 

Motivated by the study of the growth rate of the number of geodesics in flat surfaces with bounded lengths, we study generalizations of such problems for K3 surfaces. In one gener- alization, we give a result regarding the upper bound on the asymptotics of the number of classes of irreducible special Lagrangians in K3 surfaces with bounded period integrals. In another generalization, we give the exact leading term in the asymptotics of the number of Mukai vectors of semistable coherent sheaves on algebraic K3 surfaces with bounded central charges, with respect to generic Bridgeland stability conditions. 

Abstract DNA methylation at cytosine bases of eukaryotic DNA (5-methylcytosine, 5mC) is a heritable epigenetic mark that can regulate gene expression in health and disease. Enzymes that metabolize 5mC have been well-characterized, yet the discovery of endogenously produced signaling molecules that regulate DNA methyl-modifying machinery have not been described. Herein, we report that the free radical signaling molecule nitric oxide (NO) can directly inhibit the Fe(II)/2-OG-dependent DNA demethylases ten-eleven translocation (TET) and human AlkB homolog 2 (ALKBH2). Physiologic NO concentrations reversibly inhibited TET and ALKBH2 demethylase activity by binding to the mononuclear non-heme iron atom which formed a dinitrosyliron complex (DNIC) preventing cosubstrates (2-OG and O₂) from binding. In cancer cells treated with exogenous NO, or cells endogenously synthesizing NO, there was a global increase in 5mC and 5-hydroxymethylcytosine (5hmC) in DNA, the substrates for TET, that could not be attributed to increased DNA methyltransferase activity. 5mC was also elevated in NO-producing cell-line-derived mouse xenograft and patient-derived xenograft tumors. Genome-wide DNA methylome analysis of cells chronically treated with NO (10 days) demonstrated enrichment of 5mC and 5hmC at gene-regulatory loci which correlated to changes in the expression of NO-regulated tumor-associated genes. Regulation of DNA methylation is distinctly different from canonical NO signaling and represents a novel epigenetic role for NO.