Dew formation on the surface of biological soil crusts in central European sand ecosystems

Dew formation was investigated in three developmental stages of biological soil crusts (BSC), which were collected along a catena of an inland dune and in the initial substrate. The Penman equation, which was developed for saturated surfaces, was modified for unsaturated surfaces and used for prediction of dewfall rates. The levels of surface saturation required for this approach were predicted using the water retention functions and the thicknesses of the BSCs. During a first field campaign (2–3 August 2011), dewfall increased from 0.042 kg m<sup>−2</sup> for the initial sandy substrate to 0.058, 0.143 and 0.178 kg m<sup>−2</sup> for crusts 1 to 3, respectively. During a second field campaign (17–18 August 2011), where dew formation was recorded in 1.5 to 2.75-h intervals after installation at 21:30 CEST, dewfall increased from 0.011 kg m<sup>−2</sup> for the initial sandy substrate to 0.013, 0.028 and 0.055 kg m<sup>−2</sup> for crusts 1 to 3, respectively. Dewfall rates remained on low levels for the substrate and for crust 1, and decreased overnight for crusts 2 and 3 (with crust 3 > crust 2 > crust 1 throughout the campaign). Dew formation was well reflected by the model response. The suggested mechanism of dew formation involves a delay in water saturation in near-surface soil pores and extracellular polymeric substances (EPS) where the crusts were thicker and where the water capacity was high, resulting in elevated vapor flux towards the surface. The results also indicate that the amount of dewfall was too low to saturate the BSCs and to observe water flow into deeper soil. Analysis of the soil water retention curves revealed that, despite the sandy mineral matrix, moist crusts clogged by swollen EPS pores exhibited a clay-like behavior. It is hypothesized that BSCs gain double benefit from suppressing their competitors by runoff generation and from improving their water supply by dew collection. Despite higher amounts of dew, the water availability to the crust community decreases with crust development, which may be compensated by ecophysiological adaptation of crust organisms, and which may further suppress higher vegetation or mosses

PIP5KIβ Selectively Modulates Apical Endocytosis in Polarized Renal Epithelial Cells

Localized synthesis of phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] at clathrin coated pits (CCPs) is crucial for the recruitment of adaptors and other components of the internalization machinery, as well as for regulating actin dynamics during endocytosis. PtdIns(4,5)P2 is synthesized from phosphatidylinositol 4-phosphate by any of three phosphatidylinositol 5-kinase type I (PIP5KI) isoforms (α, β or γ). PIP5KIβ localizes almost exclusively to the apical surface in polarized mouse cortical collecting duct cells, whereas the other isoforms have a less polarized membrane distribution. We therefore investigated the role of PIP5KI isoforms in endocytosis at the apical and basolateral domains. Endocytosis at the apical surface is known to occur more slowly than at the basolateral surface. Apical endocytosis was selectively stimulated by overexpression of PIP5KIβ whereas the other isoforms had no effect on either apical or basolateral internalization. We found no difference in the affinity for PtdIns(4,5)P2-containing liposomes of the PtdIns(4,5)P2 binding domains of epsin and Dab2, consistent with a generic effect of elevated PtdIns(4,5)P2 on apical endocytosis. Additionally, using apical total internal reflection fluorescence imaging and electron microscopy we found that cells overexpressing PIP5KIβ have fewer apical CCPs but more internalized coated structures than control cells, consistent with enhanced maturation of apical CCPs. Together, our results suggest that synthesis of PtdIns(4,5)P2 mediated by PIP5KIβ is rate limiting for apical but not basolateral endocytosis in polarized kidney cells. PtdIns(4,5)P2 may be required to overcome specific structural constraints that limit the efficiency of apical endocytosis. © 2013 Szalinski et al

Focal structural variants revealed by whole genome sequencing disrupt the histone demethylase KDM4C in B cell lymphomas

Histone methylation-modifiers, like EZH2 and KMT2D, are recurrently altered in B-cell lymphomas. To comprehensively describe the landscape of alterations affecting genes encoding histone methylation-modifiers in lymphomagenesis we investigated whole genome and transcriptome data of 186 mature B-cell lymphomas sequenced in the ICGC MMML-Seq project. Besides confirming common alterations of KMT2D (47% of cases), EZH2 (17%), SETD1B (5%), PRDM9 (4%), KMT2C (4%), and SETD2 (4%) also identified by prior exome or RNAseq studies, we here unravel KDM4C in chromosome 9p24, encoding a histone demethylase, to be recurrently altered. Focal structural variation was the main mechanism of KDM4C alterations, which was independent from 9p24 amplification. We identified KDM4C alterations also in lymphoma cell lines including a focal homozygous deletion in a classical Hodgkin lymphoma cell line. By integrating RNAseq and genome sequencing data we predict KDM4C structural variants to result in loss-of-function. By functional reconstitution studies in cell lines, we provide evidence that KDM4C can act as tumor suppressor. Thus, we show that identification of structural variants in whole genome sequencing data adds to the comprehensive description of the mutational landscape of lymphomas and, moreover, establish KDM4C as putative tumor suppressive gene recurrently altered in subsets of B-cell derived lymphomas

Fair Value Measurement Under Level 2 Inputs: Do Market and Transaction Multiples Catch Firm-Specific Risk Factors?

This paper focuses on fair value measurement under the IFRS 13 assumptions and the reliability of the market and transaction multiples evaluations (\u201cLevel 2\u201d methods). We test the reliability of multiples evaluation approaches in different economic sectors, by comparing the fair value of 1678 companies estimated by multiples with the effective market capitalization over 15 years. Multiples\u2019 fair value does not provide a reliable measure of a company\u2019s value, with a gap that varies depending upon portfolios and time. In the case of observable Level 2 fair value indicators for a market, such as market multiples, the company\u2019s fair value is not consistent with the real market value. Thus, whenever Level 2 indicators are not observable, the method is increasing volatility and intrinsic evaluation risk

Androgen Receptor Function Links Human Sexual Dimorphism to DNA Methylation

Sex differences are well known to be determinants of development, health and disease. Epigenetic mechanisms are also known to differ between men and women through X-inactivation in females. We hypothesized that epigenetic sex differences may also result from sex hormone functions, in particular from long-lasting androgen programming. We aimed at investigating whether inactivation of the androgen receptor, the key regulator of normal male sex development, is associated with differences of the patterns of DNA methylation marks in genital tissues. To this end, we performed large scale array-based analysis of gene methylation profiles on genomic DNA from labioscrotal skin fibroblasts of 8 males and 26 individuals with androgen insensitivity syndrome (AIS) due to inactivating androgen receptor gene mutations. By this approach we identified differential methylation of 167 CpG loci representing 162 unique human genes. These were significantly enriched for androgen target genes and low CpG content promoter genes. Additional 75 genes showed a significant increase of heterogeneity of methylation in AIS compared to a high homogeneity in normal male controls. Our data show that normal and aber

DNA-Methylation Profiling of Fetal Tissues Reveals Marked Epigenetic Differences between Chorionic and Amniotic Samples

Epigenetic mechanisms including DNA methylation are supposed to play a key role in fetal development. Here we have investigated fetal DNA-methylation levels of 27,578 CpG loci in 47 chorionic villi (CVS) and 16 amniotic cell (AC) samples. Methylation levels differed significantly between karyotypically normal AC and CVS for 2,014 genes. AC showed more extreme DNA-methylation levels of these genes than CVS and the differentially methylated genes are significantly enriched for processes characteristic for the different cell types sampled. Furthermore, we identified 404 genes differentially methylated in CVS with trisomy 21. These genes were significantly enriched for high CG dinucleotid (CpG) content and developmental processes associated with Down syndrome. Our study points to major tissue-specific differences of fetal DNA-methylation and gives rise to the hypothesis that part of the Down syndrome phenotype is epigenetically programmed in the first trimester of pregnancy