Etude de l’effet d’une source d’inoculum externe sur la propagation du CABMV (Cowpea aphid – borne mosaic virus) selon la proximité des parcelles voisines et la variété de niébé

Un champ ensemencé avec des semences de qualité peut se retrouver voisin avec un autre ensemencé avec des semences infectées par le virus de la mosaïque du niébé. Ce virus est transmis par les semences à des taux de 0 à 40% selon les variétés. Ces semences infectées donnent des jeunes plantes virosées à partir desquelles les pucerons vont propager la maladie. Ce travail a été effectué pour déterminer la distance minimale permettant d’éviter des contaminations à partir d’inoculum externe suivant la sensibilité de la variété. Ainsi, deux parcelles centrales de 300 m2 ont été semées avec des graines de Gorom local contaminées à 0,5% par le virus. Autour de la première parcelle centrale, 4 parcelles de 200 m2 chacune ont été semées avec des graines de Gorom local indemnes de virus aux distances respectives de 10 m, 15 m, 20 m et 25 m. Autour de la deuxième parcelle centrale, des semences indemnes de virus de Kvx61-1 ont été utilisées. Un dispositif similaire a été constitué pour les parcelles témoins avec des semences indemnes de virus. La propagation de la maladie a montré qu’elle est liée à la variété, aux pucerons et à la distance avec la source d’inoculum.© 2015 International Formulae Group. All rights reserved.Mots clés: Semences indemnes de virus, semences contaminées, distance minimale, puceronsEnglish Title: Study of the effect of external inoculum source on CABMV (Cowpea aphid – borne mosaic virus) spread in relation to the proximity of neighboring plots and the cowpea varietyEnglish AbstractA field sown with quality seeds can be closed to another one sown with seeds infected by cowpea mosaic virus which is seed transmitted at rates ranging from 0 to 40% depending on cowpea varieties. Infected seeds germinate and grow into virus-infected seedlings from which aphids will spread the disease. This  research was carried out in order to determine the minimum distance needed for avoiding contaminations from external virus inoculum sources, in relation with the susceptibility of cowpea varieties. Thus, two central plots of 300 m² have been sown with contaminated seeds at 0.5% by CABMV of cowpea variety Gorom local. Around the first central plot, four plots of 200 m² each were sown with virus-free seeds of Gorom local at respective distances of 10 m, 15 m, 20 m and 25 m. Around the second central plot, virus-free seeds of Kvx61- 1 have been used. A similar layout was done for the control plots with virus-free seeds. It was found that the spread of the disease was related to the cowpea variety, the aphids and the distance from the inoculum source.© 2015 International Formulae Group. All rights reserved.Keywords: Virus-free seeds, contaminated seeds, minimum distance, aphid

Gene induction during differentiation of human monocytes into dendritic cells: an integrated study at the RNA and protein levels

Changes in gene expression occurring during differentiation of human monocytes into dendritic cells were studied at the RNA and protein levels. These studies showed the induction of several gene classes corresponding to various biological functions. These functions encompass antigen processing and presentation, cytoskeleton, cell signalling and signal transduction, but also an increase in mitochondrial function and in the protein synthesis machinery, including some, but not all, chaperones. These changes put in perspective the events occurring during this differentiation process. On a more technical point, it appears that the studies carried out at the RNA and protein levels are highly complementary.Comment: website publisher: http://www.springerlink.com/content/ha0d2c351qhjhjdm

Phenotypic Studies of Natural Killer Cell Subsets in Human Transporter Associated with Antigen Processing Deficiency

Peripheral blood natural killer (NK) cells from patients with transporter associated with antigen processing (TAP) deficiency are hyporesponsive. The mechanism of this defect is unknown, but the phenotype of TAP-deficient NK cells is almost normal. However, we noticed a high percentage of CD56bright cells among total NK cells from two patients. We further investigated TAP-deficient NK cells in these patients and compared them to NK cells from two other TAP-deficient patients with no clinical symptoms and to individuals with chronic inflammatory diseases other than TAP deficiency (chronic lung diseases or vasculitis). Peripheral blood mononuclear cells isolated from venous blood were stained with fluorochrome-conjugated antibodies and the phenotype of NK cells was analyzed by flow cytometry. In addition, 51Chromium release assays were performed to assess the cytotoxic activity of NK cells. In the symptomatic patients, CD56bright NK cells represented 28% and 45%, respectively, of all NK cells (higher than in healthy donors). The patients also displayed a higher percentage of CD56dimCD16− NK cells than controls. Interestingly, this unusual NK cell subtype distribution was not found in the two asymptomatic TAP-deficient cases, but was instead present in several of the other patients. Over-expression of the inhibitory receptor CD94/NKG2A by TAP-deficient NK cells was confirmed and extended to the inhibitory receptor ILT2 (CD85j). These inhibitory receptors were not involved in regulating the cytotoxicity of TAP-deficient NK cells. We conclude that expansion of the CD56bright NK cell subtype in peripheral blood is not a hallmark of TAP deficiency, but can be found in other diseases as well. This might reflect a reaction of the immune system to pathologic conditions. It could be interesting to investigate the relative distribution of NK cell subsets in various respiratory and autoimmune diseases

Quantum Symmetries and Strong Haagerup Inequalities

In this paper, we consider families of operators $\{x_r\}_{r \in \Lambda}$ in a tracial C$^\ast$-probability space $(\mathcal A, \phi)$, whose joint $\ast$-distribution is invariant under free complexification and the action of the hyperoctahedral quantum groups $\{H_n^+\}_{n \in \N}$. We prove a strong form of Haagerup's inequality for the non-self-adjoint operator algebra $\mathcal B$ generated by $\{x_r\}_{r \in \Lambda}$, which generalizes the strong Haagerup inequalities for $\ast$-free R-diagonal families obtained by Kemp-Speicher \cite{KeSp}. As an application of our result, we show that $\mathcal B$ always has the metric approximation property (MAP). We also apply our techniques to study the reduced C$^\ast$-algebra of the free unitary quantum group $U_n^+$. We show that the non-self-adjoint subalgebra $\mathcal B_n$ generated by the matrix elements of the fundamental corepresentation of $U_n^+$ has the MAP. Additionally, we prove a strong Haagerup inequality for $\mathcal B_n$, which improves on the estimates given by Vergnioux's property RD \cite{Ve}

IL-15 trans-presentation promotes human NK cell development and differentiation in vivo

The in vivo requirements for human natural killer (NK) cell development and differentiation into cytotoxic effectors expressing inhibitory receptors for self–major histocompatability complex class I (MHC-I; killer Ig-like receptors [KIRs]) remain undefined. Here, we dissect the role of interleukin (IL)-15 in human NK cell development using Rag2−/−γc−/− mice transplanted with human hematopoietic stem cells. Human NK cell reconstitution was intrinsically low in this model because of the poor reactivity to mouse IL-15. Although exogenous human IL-15 (hIL-15) alone made little improvement, IL-15 coupled to IL-15 receptor α (IL-15Rα) significantly augmented human NK cells. IL-15–IL-15Rα complexes induced extensive NK cell proliferation and differentiation, resulting in accumulation of CD16+KIR+ NK cells, which was not uniquely dependent on enhanced survival or preferential responsiveness of this subset to IL-15. Human NK cell differentiation in vivo required hIL-15 and progressed in a linear fashion from CD56hiCD16−KIR− to CD56loCD16+KIR−, and finally to CD56loCD16+KIR+. These data provide the first evidence that IL-15 trans-presentation regulates human NK cell homeostasis. Use of hIL-15 receptor agonists generates a robust humanized immune system model to study human NK cells in vivo. IL-15 receptor agonists may provide therapeutic tools to improve NK cell reconstitution after bone marrow transplants, enhance graft versus leukemia effects, and increase the pool of IL-15–responsive cells during immunotherapy strategies

HIV-1 Efficient Entry in Inner Foreskin Is Mediated by Elevated CCL5/RANTES that Recruits T Cells and Fuels Conjugate Formation with Langerhans Cells

Male circumcision reduces acquisition of HIV-1 by 60%. Hence, the foreskin is an HIV-1 entry portal during sexual transmission. We recently reported that efficient HIV-1 transmission occurs following 1 h of polarized exposure of the inner, but not outer, foreskin to HIV-1-infected cells, but not to cell-free virus. At this early time point, Langerhans cells (LCs) and T-cells within the inner foreskin epidermis are the first cells targeted by the virus. To gain in-depth insight into the molecular mechanisms governing inner foreskin HIV-1 entry, foreskin explants were inoculated with HIV-1-infeceted cells for 4 h. The chemokine/cytokine milieu secreted by the foreskin tissue, and resulting modifications in density and spatial distribution of T-cells and LCs, were then investigated. Our studies show that in the inner foreskin, inoculation with HIV-1-infected cells induces increased CCL5/RANTES (1.63-fold) and decreased CCL20/MIP-3-alpha (0.62-fold) secretion. Elevated CCL5/RANTES mediates recruitment of T-cells from the dermis into the epidermis, which is blocked by a neutralizing CCL5/RANTES Ab. In parallel, HIV-1-infected cells mediate a bi-phasic modification in the spatial distribution of epidermal LCs: attraction to the apical surface at 1 h, followed by migration back towards the basement membrane later on at 4 h, in correlation with reduced CCL20/MIP-3-alpha at this time point. T-cell recruitment fuels the continuous formation of LC-T-cell conjugates, permitting the transfer of HIV-1 captured by LCs. Together, these results reveal that HIV-1 induces a dynamic process of immune cells relocation in the inner foreskin that is associated with specific chemokines secretion, which favors efficient HIV-1 entry at this site

Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline

The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline

Сетевая система контроля технологического процесса выращивания полупроводниковых кристаллов и тонких пленок

Экспериментальное моделирование аппаратно-программного обеспечения показало достаточную надежность работы системы и значительное уменьшение трудоемкости контроля и управления параметрами технологического процесса

Defective germline reprogramming rewires the spermatogonial transcriptome.

Defective germline reprogramming in Piwil4 (Miwi2)- and Dnmt3l-deficient mice results in the failure to reestablish transposon silencing, meiotic arrest and progressive loss of spermatogonia. Here we sought to understand the molecular basis for this spermatogonial dysfunction. Through a combination of imaging, conditional genetics and transcriptome analysis, we demonstrate that germ cell elimination in the respective mutants arises as a result of defective de novo genome methylation during reprogramming rather than because of a function for the respective factors within spermatogonia. In both Miwi2-/- and Dnmt3l-/- spermatogonia, the intracisternal-A particle (IAP) family of endogenous retroviruses is derepressed, but, in contrast to meiotic cells, DNA damage is not observed. Instead, we find that unmethylated IAP promoters rewire the spermatogonial transcriptome by driving expression of neighboring genes. Finally, spermatogonial numbers, proliferation and differentiation are altered in Miwi2-/- and Dnmt3l-/- mice. In summary, defective reprogramming deregulates the spermatogonial transcriptome and may underlie spermatogonial dysfunction