Anthropogenic impact on amorphous silica pools in temperate soils

Human land use changes perturb biogeochemical silica (Si) cycling in terrestrial ecosystems. This directly affects Si mobilisation and Si storage and influences Si export from the continents, although the magnitude of the impact is unknown. A major reason for our lack of understanding is that very little information exists on how land use affects amorphous silica (ASi) storage in soils. We have quantified and compared total alkali-extracted (PSi<sub>a</sub>) and easily soluble (PSi<sub>e</sub>) Si pools at four sites along a gradient of anthropogenic disturbance in southern Sweden. Land use clearly affects ASi pools and their distribution. Total PSi</sub>a</sub> and PSi<sub>e</sub> for a continuous forested site at Siggaboda Nature Reserve (66 900 ± 22 800 kg SiO<sub>2</sub> ha<sup>−1</sup> and 952 ± 16 kg SiO<sub>2</sub> ha<sup>−1</sup>) are significantly higher than disturbed land use types from the Råshult Culture Reserve including arable land (28 800 ± 7200 kg SiO<sub>2</sub> ha<sup>−1</sup> and 239 ± 91 kg SiO<sub>2</sub> ha<sup>−1</sup>), pasture sites (27 300 ± 5980 kg SiO<sub>2</sub> ha<sup>−1</sup> and 370 ± 129 kg SiO<sub>2</sub> ha<sup>−1</sup>) and grazed forest (23 600 ± 6370 kg SiO<sub>2</sub> ha<sup>−1</sup> and 346 ± 123 kg SiO<sub>2</sub> ha<sup>−1</sup>). Vertical PSi<sub>a</sub> and PSi<sub>e</sub> profiles show significant (<i>p</i> < 0.05) variation among the sites. These differences in size and distribution are interpreted as the long-term effect of reduced ASi replenishment, as well as changes in ecosystem specific pedogenic processes and increased mobilisation of the PSi<sub>a</sub> in disturbed soils. We have also made a first, though rough, estimate of the magnitude of change in temperate continental ASi pools due to human disturbance. Assuming that our data are representative, we estimate that total ASi storage in soils has declined by ca. 10 % since the onset of agricultural development (3000 BCE). Recent agricultural expansion (after 1700 CE) may have resulted in an average additional export of 1.1 ± 0.8 Tmol Si yr<sup>−1</sup> from the soil reservoir to aquatic ecosystems. This is ca. 20 % to the global land-ocean Si flux carried by rivers. It is necessary to update this estimate in future studies, incorporating differences in pedology, geology and climatology over temperate regions, but data are currently not sufficient. Yet, our results emphasize the importance of human activities for Si cycling in soils and for the land-ocean Si flux

Opal-CT precipitation in a clayey soil explained by geochemical transport model of dissolved Si (Blégny, Belgium)

Opal-CT precipitation controlling dissolved Si export Dissolved Si (DSi) exported by rivers are controlled by geological, hydrological and biological cycle processes [1]. The DSi concentrations measured in a river of an upstream catchment in eastern Belgium (Blégny, Land of Herve) don’t vary seasonally (6.91±0.94mgL-1; n=363). Si concentrations in pore water are often higher and vary more (8.65±3.65mgL-1; n=128). The decrease of DSi along the flowpath of water is due to sink processes, i.e. precipitation, adsorption or uptake by vegetation. As the DSi in the river does not show any seasonal variation, uptake by vegetation can be ruled out [1] whereas precipitation or adsorption can control the DSi drained by the stream water. This hypothesis is confirmed by XRD and DeMaster analysis. At 0.1m depth the soil is constituted of 62% quartz, 7% K-feldspar, 6% plagioclase, 3.2% carbonates, 18.9% Al-clay, 1.47% Kaolinite, 0.63% Chlorite and 0.2% amorphous Si, probably of biogenic origin. At 1.5m depth, the amounts of several minerals (35.8% quartz, 0.6% K-feldspars, 0.9% plagioclase, Al-clay 14.7%) drop drastically. Carbonates, chlorite and kaolinite are absent whereas 40.4% opal-CT appears. The precipitation of opal-CT controls the DSi export of this catchment. Development of geochemical transport model To descripe DSi export from a catchment a geochemical transport model is developped in HP1 which couples the water flux model Hydrus with the geochemical model PHREEQC [2]. Our model is based on the conceptual model developped in [3]. First results show different DSi export dynamics in the unsaturated zone than in the aquifer due to different pCO2 values and varying soil moisture conditions. Further development of the model will help to find out the reason of opal-CT precipitation in this setting. [1]Fulweiler, Nixon (2005) Biogeochemistry 74:115–130. [2] Simunek, Jacques, van Genuchten, Mallants (2006) JAWRA 42:1537-1547. [3] Ronchi et al. (2013). Silicon, 5(1), 115–133

Directed evolution of recombinase specificity by split gene reassembly

The engineering of new enzymes that efficiently and specifically modify DNA sequences is necessary for the development of enhanced gene therapies and genetic studies. To address this need, we developed a robust strategy for evolving site-specific recombinases with novel substrate specificities. In this system, recombinase variants are selected for activity on new substrates based on enzyme-mediated reassembly of the gene encoding β-lactamase that confers ampicillin resistance to Escherichia coli. This stringent evolution method was used to alter the specificities of catalytic domains in the context of a modular zinc finger-recombinase fusion protein. Gene reassembly was detectable over several orders of magnitude, which allowed for tunable selectivity and exceptional sensitivity. Engineered recombinases were evolved to react with sequences from the human genome with only three rounds of selection. Many of the evolved residues, selected from a randomly-mutated library, were conserved among other members of this family of recombinases. This enhanced evolution system will translate recombinase engineering and genome editing into a practical and expedient endeavor for academic, industrial and clinical applications

High prevalence of chitotriosidase deficiency in Peruvian Amerindians exposed to chitin-bearing food and enteroparasites

The human genome encodes a gene for an enzymatically active chitinase (CHIT1) located in a single copy on Chromosome 1, which is highly expressed by activated macrophages and in other cells of the innate immune response. Several dysfunctional mutations are known in CHIT1, including a 24-bp duplication in Exon 10 causing catalytic deficiency. This duplication is a common variant conserved in many human populations, except in West and South Africans. Thus it has been proposed that human migration out of Africa and the consequent reduction of exposure to chitin from environmental factors may have enabled the conservation of dysfunctional mutations in human chitinases. Our data obtained from 85 indigenous Amerindians from Peru, representative of populations characterized by high prevalence of chitin-bearing enteroparasites and intense entomophagy, reveal a very high frequency of the 24-bp duplication (47.06%), and of other single nucleotide polymorphisms which are known to partially affect enzymatic activity (G102S: 42.7% and A442G/V: 25.5%). Our finding is in line with a founder effect, but appears to confute our previous hypothesis of a protective role against parasite infection and sustains the discussion on the redundancy of chitinolytic function

The Varicella-Zoster Virus ORF47 Kinase Interferes with Host Innate Immune Response by Inhibiting the Activation of IRF3

The innate immune response constitutes the first line of host defence that limits viral spread and plays an important role in the activation of adaptive immune response. Viral components are recognized by specific host pathogen recognition receptors triggering the activation of IRF3. IRF3, along with NF-κB, is a key regulator of IFN-β expression. Until now, the role of IRF3 in the activation of the innate immune response during Varicella-Zoster Virus (VZV) infection has been poorly studied. In this work, we demonstrated for the first time that VZV rapidly induces an atypical phosphorylation of IRF3 that is inhibitory since it prevents subsequent IRF3 homodimerization and induction of target genes. Using a mutant virus unable to express the viral kinase ORF47p, we demonstrated that (i) IRF3 slower-migrating form disappears; (ii) IRF3 is phosphorylated on serine 396 again and recovers the ability to form homodimers; (iii) amounts of IRF3 target genes such as IFN-β and ISG15 mRNA are greater than in cells infected with the wild-type virus; and (iv) IRF3 physically interacts with ORF47p. These data led us to hypothesize that the viral kinase ORF47p is involved in the atypical phosphorylation of IRF3 during VZV infection, which prevents its homodimerization and subsequent induction of target genes such as IFN-β and ISG15

Pseudotumoural soft tissue lesions of the hand and wrist: a pictorial review

Mimickers of soft tissue tumours in the hand and wrist are more frequent than true neoplastic lesions. Pseudotumours belong to a large and heterogeneous group of disorders, varying from normal anatomical variants, cystic lesions, post-traumatic lesions, skin lesions, inflammatory and infectious lesions, non-neoplastic vascular lesions, metabolic disorders (crystal deposition disease and amyloidosis) and miscellaneous disorders. Although the imaging approach to pseudotumoural lesions is often very similar to the approach to “true” soft tissue tumoral counterparts, further management of these lesions is different. Biopsy should be performed only in doubtful cases, when the diagnosis is unclear. Therefore, the radiologist plays a pivotal role in the diagnosis of these lesions. Awareness of the normal anatomy and existence and common imaging presentation of these diseases, in combination with relevant clinical findings (clinical history, age, location and skin changes), enables the radiologist to make the correct diagnosis in most cases, thereby limiting the need for invasive procedures

Rewriting DNA Methylation Signatures at Will:The Curable Genome Within Reach?

DNA methyltransferases are important enzymes in a broad range of organisms. Dysfunction of DNA methyltransferases in humans leads to many severe diseases, including cancer. This book focuses on the biochemical properties of these enzymes, describing their structures and mechanisms in bacteria, humans and other species, including plants, and also explains the biological processes of reading of DNA methylation and DNA demethylation. It covers many emerging aspects of the biological roles of DNA methylation functioning as an essential epigenetic mark and describes the role of DNA methylation in diseases. Moreover, the book explains modern technologies, like targeted rewriting of DNA methylation by designed DNA methyltransferases, as well as technological applications of DNA methyltransferases in DNA labelling. Finally, the book summarizes recent methods for the analysis of DNA methylation in human DNA. Overall, this book represents a comprehensive state-of-the-art- work and is a must-have for advanced researchers in the field of DNA methylation and epigenetics

A Gammaherpesvirus Cooperates with Interferon-alpha/beta-Induced IRF2 to Halt Viral Replication, Control Reactivation, and Minimize Host Lethality

The gammaherpesviruses, including Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), establish latency in memory B lymphocytes and promote lymphoproliferative disease in immunocompromised individuals. The precise immune mechanisms that prevent gammaherpesvirus reactivation and tumorigenesis are poorly defined. Murine gammaherpesvirus 68 (MHV68) is closely related to EBV and KSHV, and type I (alpha/beta) interferons (IFNαβ) regulate MHV68 reactivation from both B cells and macrophages by unknown mechanisms. Here we demonstrate that IFNβ is highly upregulated during latent infection, in the absence of detectable MHV68 replication. We identify an interferon-stimulated response element (ISRE) in the MHV68 M2 gene promoter that is bound by the IFNαβ-induced transcriptional repressor IRF2 during latency in vivo. The M2 protein regulates B cell signaling to promote establishment of latency and reactivation. Virus lacking the M2 ISRE (ISREΔ) overexpresses M2 mRNA and displays uncontrolled acute replication in vivo, higher latent viral load, and aberrantly high reactivation from latency. These phenotypes of the ISREΔ mutant are B-cell-specific, require IRF2, and correlate with a significant increase in virulence in a model of acute viral pneumonia. We therefore identify a mechanism by which a gammaherpesvirus subverts host IFNαβ signaling in a surprisingly cooperative manner, to directly repress viral replication and reactivation and enforce latency, thereby minimizing acute host disease. Since we find ISREs 5′ to the major lymphocyte latency genes of multiple rodent, primate, and human gammaherpesviruses, we propose that cooperative subversion of IFNαβ-induced IRFs to promote latent infection is an ancient strategy that ensures a stable, minimally-pathogenic virus-host relationship