Global patterns of moss diversity: taxonomic and molecular inferences

Taxonomic and molecular data were utilized to test the hypothesis that moss diversity is greatest near the equator. Species richness estimates from 86 taxonomic checklists representing global moss diversity do not support the hypothesis that, in general, mosses are more species-rich in the tropics than at higher latitudes

Phylogenetic significance of the rpoA loss in the chloroplast genome of mosses

A recent survey of arthrodontous mosses revealed that their chloroplast genome lacks the gene encoding the alpha subunit of the RNA polymerase (i.e., rpoA), and that at least in Physcomitrella patens the gene has been transferred to the nuclear genome. Subsequently the gene was recorded from the cytoplasmic genome in Takakia and Sphagnum. Here we extend the survey to representatives of all major lineages of mosses to determine when in the evolutionary history of the Bryophyta the loss took place. Amplifications using primers annealing to the flanking regions of the rpoA gene yield a product that contains the gene in Takakia, Sphagnum, Andreaea, Oedipodium, Polytrichaceae, and Buxbaumia. The gene is lacking in all arthrodontous mosses, including Diphyscium but also in both species of Tetraphis. Reconstruction of the transfer on the phylogeny of mosses suggests (a) that the rpoA gene was lost twice and (b) that the gene was lost after the divergence of Buxbaumiidae and prior to the divergence of Diphyscium from the remaining Bryopsida

Phylogeny, character evolution, and biogeography of the gondwanic moss family Hypopterygiaceae (Bryophyta)

Phylogenetic relationships among the seven genera of the Hypopterygiaceae, represented by 14 of the 21 species recognized in the family, were reconstructed based on variation in nucleotide sequences of six nuclear, mitochondrial, and plastid loci

Evolution of the major moss lineages: phylogenetic analyses based on multiple gene sequences and morphology

Evolutionary relationships of mosses are still poorly understood, with family, order, and subclass circumscription and relationships remaining especially obscure

Association analysis of two single-nucleotide polymorphisms of the RELN gene with autism in the South African population

BACKGROUND: Autism (MIM209850) is a neurodevelopmental disorder characterized by a triad of impairments, namely impairment in social interaction, impaired communication skills, and restrictive and repetitive behavior. A number of family and twin studies have demonstrated that genetic factors play a pivotal role in the etiology of autistic disorder. Various reports of reduced levels of reelin protein in the brain and plasma in autistic patients highlighted the role of the reelin gene (RELN) in autism. There is no such published study on the South African (SA) population. AIMS: The aim of the present study was to find the genetic association of intronic rs736707 and exonic rs362691 (single-nucleotide polymorphisms [SNPs] of the RELN gene) with autism in a SA population. METHODS: Genomic DNA was isolated from cheek cell swabs from autistic (136) as well as control (208) subjects. The TaqMan® Real-Time polymerase chain reaction and genotyping assay was utilized to determine the genotypes. RESULTS: A significant association of SNP rs736707, but not for SNP rs362691, with autism in the SA population is observed. CONCLUSION: There might be a possible role of RELN in autism, especially for SA populations. The present study represents the first report on genetic association studies on the RELN gene in the SA population.Web of Scienc

A modification of Representational Difference Analysis, with application to the cloning of a candidate in the Reelin signalling pathway

BACKGROUND: cDNA-RDA is one of the subtractive cloning techniques used to isolate differentially expressed genes between two complex cDNA populations. In the present study we present a modification of the protocol described by Hubank and Schatz. RESULTS: In the post-hybridization mix, the 5'-ends of homoduplexes of interest (tester-tester) are filled-in with α-thio-deoxynucleotides. Unprotected duplexes, as well as the single-stranded DNA fragments, are degraded using ExoIII and Mung Bean Nuclease, prior to PCR subtraction, resulting in less complex difference products. We illustrate this modification by the cloning of a new gene which is differentially expressed in normal, reelin and Dab1 mutant mice and is a candidate member of the Reelin signalling pathway involved in brain development. CONCLUSION: We propose a modification of cDNA-RDA that may reduce the complexity of the post-hybridization mix and thus facilitate the amplification of differentially expressed products

Role of p73 in Alzheimer disease: lack of association in mouse models or in human cohorts.

BACKGROUND: P73 belongs to the p53 family of cell survival regulators with the corresponding locus Trp73 producing the N-terminally distinct isoforms, TAp73 and DeltaNp73. Recently, two studies have implicated the murine Trp73 in the modulation in phospho-tau accumulation in aged wild type mice and in young mice modeling Alzheimer's disease (AD) suggesting that Trp73, particularly the DeltaNp73 isoform, links the accumulation of amyloid peptides to the creation of neurofibrillary tangles (NFTs). Here, we reevaluated tau pathologies in the same TgCRND8 mouse model as the previous studies. RESULTS: Despite the use of the same animal models, our in vivo studies failed to demonstrate biochemical or histological evidence for misprocessing of tau in young compound Trp73+/- + TgCRND8 mice or in aged Trp73+/- mice analyzed at the ages reported previously, or older. Secondly, we analyzed an additional mouse model where the DeltaNp73 was specifically deleted and confirmed a lack of impact of the DeltaNp73 allele, either in heterozygous or homozygous form, upon tau pathology in aged mice. Lastly, we also examined human TP73 for single nucleotide polymorphisms (SNPs) and/or copy number variants in a meta-analysis of 10 AD genome-wide association datasets. No SNPs reached significance after correction for multiple testing and no duplications/deletions in TP73 were found in 549 cases of AD and 544 non-demented controls. CONCLUSION: Our results fail to support P73 as a contributor to AD pathogenesis.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Hybrid functional study of proper and improper multiferroics

We present a detailed study of the structural, electronic, magnetic and ferroelectric properties of prototypical \textit{proper} and \textit{improper} multiferroic (MF) systems such as BiFeO$_{3}$ and orthorhombic HoMnO$_{3}$, respectively, within density functional theory (DFT) and using the Heyd-Scuseria-Ernzerhof hybrid functional (HSE). By comparing our results with available experimental data as well as with state-of-the-art GW calculations, we show that the HSE formalism is able to account well for the relevant properties of these compounds and it emerges as an accurate tool for predictive first-principles investigations on multiferroic systems. We show that effects beyond local and semilocal DFT approaches (as provided by HSE) are necessary for a realistic description of MFs. For the electric polarization, a decrease is found for MFs with magnetically-induced ferroelectricity, such as HoMnO$_3$, where the calculated polarization changes from $\sim$ 6 $\mu C/cm^2$ using Perdew-Burke-Ernzerhof (PBE) to $\sim$ 2 $\mu C/cm^2$ using HSE. However, for \textit{proper} MFs, such as BiFeO$_{3}$, the polarization slightly increases upon introduction of exact exchange. Our findings therefore suggest that a general trend for the HSE correction to bare density functional cannot be extracted; rather, a specific investigation has to be carried out on each compound.Comment: Revised version. In press in PCC

Prevalence and mechanisms of resistance to carbapenems in Enterobacteriaceae

Objectives: To determine the point prevalence of carbapenem-non-susceptible Enterobacteriaceae (CNSE) and carbapenemase-producing Enterobacteriaceae (CPE) isolates among hospitalized patients in Belgium. Methods: Twenty-four hospital-based laboratories prospectively collected 200 non-duplicated Enterobacteriaceae isolates from clinical specimens of hospitalized patients over a 2 month period. All isolates were screened locally for decreased susceptibility to carbapenem drugs using a disc diffusion method according to CLSI interpretative criteria. CNSE strains were referred centrally for confirmation of carbapenemase by phenotypic and molecular testing. Results: From February to April 2012, 158 of the 4564 screened Enterobacteriaceae isolates were categorized as non-susceptible to carbapenems, resulting in a point prevalence of CNSE of 3.5% (95% CI: 2.9%–4.2%; range per centre: 0.5%–8.5%). Of the 125 referred CNSE isolates, 11 Klebsiella pneumoniae isolates [OXA-48 (n=7), KPC type (n=3) and NDM type (n=1)], 1 OXA-48-positive Escherichia coli isolate and 1 KPC-positive Klebsiella oxytoca isolate were detected in eight hospitals. None of the 72 carbapenem-non-susceptible Enterobacter spp. isolates were confirmed as CPE. The minimal estimated point prevalence of CPE isolates was 0.28% (13/ 4564; 95% CI: 0.13%–0.44%) overall (range per centre: 0%–1.5%). Conclusions: Despite the overall low prevalence of CNSE found in this study, the detection of CPE isolates in one-third of the participating centres raises concerns and highly suggests the spread and establishment of CPE in Belgian hospitals