Parasitism rates and parasitoid complexes of the wheat midges, <Emphasis Type="Italic">Sitodiplosis mosellana</Emphasis>, <Emphasis Type="Italic">Contarinia tritici</Emphasis> and <Emphasis Type="Italic">Haplodiplosis marginata</Emphasis>

Three species of cecidomyiid midges (Diptera: Cecidomyiidae), whose larvae overwinter in the soil, can cause significant yield losses on wheat in Europe: the orange wheat blossom midge, Sitodiplosis mosellana (Géhin), the yellow wheat blossom midge, Contarinia tritici (Kirby), and the saddle gall midge, Haplodiplosis marginata (von Roser). The biological control of wheat midges by their parasitoids can contribute to reduce the midge populations. Soil samples were collected in several fields in Belgium in 2012–2014 in order to characterize the parasitism rates and parasitoid complexes in overwintering larvae. The parasitism rates varied greatly between the sampled fields: 3–100, 0–100 and 2% for S. mosellana, H. marginata and C. tritici, respectively. The parasitism rate was not related to the larval density of wheat midge. The three wheat midges have totally distinct parasitoid complexes in Belgium. Eight species (Hymenoptera: Pteromalidae and Platygastridae) were found as parasitoid of S. mosellana: Macroglenes penetrans (Kirby), Amblypasis tritici (Walker), Euxestonotus error (Fitch), Euxestonutus sp. Fouts, Leptacis sp. Foerster, Platygaster gracilipes (Huggert), Platygaster nisus Walker, and Platygaster tuberosula (Kieffer). According to their abundance, M. penetrans, E. error and P. tuberosula appeared as the main parasitoids of S. mosellana in Belgium. For the two other wheat midges, only one species of the family Platygastridae was found for each midge: Platygaster equestris (Spittler) for H. marginata and Synopeas myles (Walker) for C. tritici.     

PSTPIP2 dysregulation contributes to aberrant terminal differentiation in GATA-1-deficient megakaryocytes by activating LYN

GATA1 mutations are tightly associated with transient myeloproliferative disorder (TMD) and acute megakaryoblstic leukemia (AMKL) in children with Down syndrome. Numerous genes are altered in GATA-1-deficient megakaryocytes, which may contribute to the hyperproliferation and abnormal terminal differentiation of these malignant cells. In this study, we demonstrate that Pstpip2 is a GATA-1-repressed gene that controls megakaryopoiesis. Ectopic expression of PSTPIP2 impaired megakaryocytic differentiation as evidenced by a decrease of CD41 expression and reduced DNA content in K562 cells. PSTPIP2 overexpression also caused enhanced activation of Src family kinases and subsequently reduced ERK phosphorylation. Consistently, PSTPIP2 knockdown showed the opposite effect on differentiation and signaling. Moreover, the W232A mutant of PSTPIP2, defective in its interaction with PEST family phosphatases that recruit c-Src terminal kinase (CSK) to suppress Src family kinases, failed to inhibit differentiation and lost its ability to enhance Src family kinases or reduce ERK phosphorylation. In fact, the W232A mutant of PSTPIP2 promoted megakaryocyte differentiation. These observations suggest that PSTPIP2 recruiting PEST phosphatases somehow blocked CSK activity and led to enhanced activation of Src family kinases and reduced ERK phosphorylation, which ultimately repressed megakaryocyte differentiation. Supporting this idea, PSTPIP2 interacted with LYN and the expression of a dominant negative LYN (LYN DN) overwhelmed the inhibitory effect of PSTPIP2 on differentiation and ERK signaling. In addition, a constitutively active LYN (LYN CA) normalized the enhanced megakaryocyte differentiation and repressed ERK signaling in PSTPIP2 knockdown cells. Finally, we found that PSTPIP2 repressed ERK signaling, differentiation, and proliferation and verified that PSTPIP2 upregulation repressed megakaryocyte development in primary mouse bone marrow cells. Our study thus reveals a novel mechanism by which dysregulation of PSTPIP2 due to GATA-1 deficiency may contribute to abnormal megakaryocyte proliferation and differentiation in pathogenesis of related diseases.     

Enzymatic Preparation of 32P-Labeled β-L-2′, 3′-dd-5′ ATP and Its Use as a High-Affinity,Conformation-Specific Ligand for Labeling Adenylyl Cyclases

Abstract

An enzymatic method was developed for the preparation of unlabeled and [β-³²P]-labeled β-L-2′,3′-dd-5′ATP from the monophosphate with near quantitative yields. β-L-2′,3′-dd-5′ATP was a competitive and potent inhibitor of adenylyl cyclases (IC₅ ～ 30 nM). Upon uvirradiation β-L-2′,3′-dd-[β-³²P]-5′ATP directly crosslinked to a chimeric construct of this enzyme. Data suggest that this is a pre-transition state inhibitor and contrasts with the equipotent 2′,5′-dd-3′ATP, a post-transition state, noncompetitive inhibitor.     

Epigenetic acquisition of inducibility of type III cytotoxicity in P. aeruginosa

Background  

Pseudomonas aeruginosa, an opportunistic pathogen, is often encountered in chronic lung diseases such as cystic fibrosis or chronic obstructive pneumonia, as well as acute settings like mechanical ventilation acquired pneumonia or neutropenic patients. It is a major cause of mortality and morbidity in these diseases. In lungs, P. aeruginosa settles in a biofilm mode of growth with the secretion of exopolysaccharides in which it is encapsulated, enhancing its antibiotic resistance and contributing to the respiratory deficiency of patients. However, bacteria must first multiply to a high density and display a cytotoxic phenotype to avoid the host's defences. A virulence determinant implicated in this step of infection is the type III secretion system (TTSS), allowing toxin injection directly into host cells. At the beginning of the infection, most strains isolated from patients' lungs possess an inducible TTSS allowing toxins injection or secretion upon in vivo or in vitro activation signals. As the infection persists most of the bacteria permanently loose this capacity, although no mutations have been evidenced. We name "non inducible" this phenotype. As suggested by the presence of a positive feedback circuit in the regulatory network controlling TTSS expression, it may be due to an epigenetic switch allowing heritable phenotypic modifications without genotype's mutations.     

A spatial statistical model for landscape genetics

Landscape genetics is a new discipline that aims to provide information on how landscape and environmental features influence population genetic structure. The first key step of landscape genetics is the spatial detection and location of genetic discontinuities between populations. However, efficient methods for achieving this task are lacking. In this article, we first clarify what is conceptually involved in the spatial modeling of genetic data. Then we describe a Bayesian model implemented in a Markov chain Monte Carlo scheme that allows inference of the location of such genetic discontinuities from individual geo-referenced multilocus genotypes, without a priori knowledge on populational units and limits. In this method, the global set of sampled individuals is modeled as a spatial mixture of panmictic populations, and the spatial organization of populations is modeled through the colored Voronoi tessellation. In addition to spatially locating genetic discontinuities, the method quantifies the amount of spatial dependence in the data set, estimates the number of populations in the studied area, assigns individuals to their population of origin, and detects individual migrants between populations, while taking into account uncertainty on the location of sampled individuals. The performance of the method is evaluated through the analysis of simulated data sets. Results show good performances for standard data sets (e.g., 100 individuals genotyped at 10 loci with 10 alleles per locus), with high but also low levels of population differentiation (e.g., F_ST < 0.05). The method is then applied to a set of 88 individuals of wolverines (Gulo gulo) sampled in the northwestern United States and genotyped at 10 microsatellites.     

Automated pollen monitoring system using laser optics for observing seasonal changes in the concentration of total airborne pollen

The development of a simple and automatic pollen measurement methodology is required to manage allergic problems caused by airborne pollen. We developed a device and algorithm to automatically monitor airborne pollen by using basic laser optics technology. The device measures the sideward and forward scattering intensities of laser light from each particle. Because this device provides detailed temporal variation in the pollen concentration, the dispersal dynamics of airborne pollen can be effectively analyzed. We compared the pollen counts obtained with the automated method and standard Hirst-type method. Scatter-plot graphs were constructed of the forward and sideward scattering intensities of the observed particles. An extract window methodology was used to estimate the concentrations of the major allergenic pollens. The extract window parameters were obtained for major types of allergenic pollen. The results suggest the possibility of developing a device for monitoring several types of airborne pollen simultaneously. We determined the standard extract window to be used for estimating the concentration of all types of airborne pollen together. A field experiment was performed to evaluate the automated monitoring system with the standard extract window. The estimated temporal variation pattern of the total airborne pollen concentration agreed well with the observed temporal variation pattern for the whole pollen season. The pollen monitor was able to estimate the overall features of seasonal changes in the total airborne pollen concentration.     

Carbon partitioning in forage crops

The paper describes the conceptual models used to understand the processes determining plant growth rates in response to environmental changes. A series of experiments and growth models were used at three organizational levels: the specific plant organs, the whole plant and the plant canopy. The energy conversion efficiency and the total plant carbon balance were first examined. The carbon partitioning amongst the plant parts was then studied. The energy conversion efficiency is generally understood. In modelling carbon partitioning it was first necessary to establish the carbon demand for each plant organ. The carbon partitioned amongst plant organs was then calculated in two ways. The first one based on empirical data consisted in defining which organ received the carbon prior to other organs. The second one was based on the relationship between the carbon mass of specific organs and their trophic activity. This hypothesis allowed the optimization of the carbon partitioning in order to maximize the whole plant growth rate. The opportunities to use these theoretical approaches in plant growth modelling are discussed.     

A multi-approach study to reveal eel life-history traits in an obstructed catchment before dam removal

Hydrobiologia - River fragmentation is expected to impact not only movement patterns and distribution of eels within catchment, but also their life-history traits. Here, we used otolith...