Effets de composts de déchets sur les propriétés chimiques du sol et la solubilité d’éléments minéraux sous deux régimes hydriques en conditions contrôlées au Togo

L'utilisation des composts de dechets en agriculture est lfune des voies principales dans la restauration de la fertilite des terres degradees. Cependant, les effets dfun compost dependent fortement de sa nature chimique et des conditions environnementales. Afin de mieux comprendre le mecanisme dfaction des composts de dechets sur les proprietes  chimiques du sol et la solubilite des ions, cinq types de composts de dechets ont ete testes selon un dispositif en blocs de Fischer repartis en trois repetitions par traitements. Les resultats obtenus revelent que les composts de dechets ont en general eleve le pH du sol de 2,13 unites et la conductivite electrique de 1301,9 µS/cm. Les traitements a engrais  synthetique NPK ont par contre reduit le pH de 0,51 unite. A lfexception du traitement a compost de dechets agroalimentaires, les traitements a compost ont en general reduit le potentiel Redox contrairement aux  traitements temoin et a engrais synthetiques. Ainsi, les traitements a engrais synthetique et a compost de dechets agroalimentaires sous deficit hydrique presentent respectivement des potentiels de 307,5 mV et 265 mV contre 262,5 mV pour le temoin absolu sous deficit hydrique. Lfetude de la fraction hydrosoluble des elements mineraux montre que la solubilite des cations essentiels (Ca, Mg et K) est liee fortement a leur concentration dans le substrat de culture contrairement aux elements traces metallique dont la solubilite depend essentiellement du pH et du potentiel Redox. Par ailleurs, le deficit hydrique a entraine lfelevation de la conductivite electrique chez les traitements a composts. Ces resultats seront utilises dans la phytoremediation des sols pollues.Mots cles : engrais organiques, amendements, parametres chimiques, ions, biodisponibilite

Correlations of Behavioral Deficits with Brain Pathology Assessed through Longitudinal MRI and Histopathology in the R6/2 Mouse Model of HD

Huntington's disease (HD) is caused by the expansion of a CAG repeat in the huntingtin (HTT) gene. The R6/2 mouse model of HD expresses a mutant version of exon 1 HTT and develops motor and cognitive impairments, a widespread huntingtin (HTT) aggregate pathology and brain atrophy. Despite the vast number of studies that have been performed on this model, the association between the molecular and cellular neuropathology with brain atrophy, and with the development of behavioral phenotypes remains poorly understood. In an attempt to link these factors, we have performed longitudinal assessments of behavior (rotarod, open field, passive avoidance) and of regional brain abnormalities determined through magnetic resonance imaging (MRI) (whole brain, striatum, cortex, hippocampus, corpus callosum), as well as an end-stage histological assessment. Detailed correlative analyses of these three measures were then performed. We found a gender-dependent emergence of motor impairments that was associated with an age-related loss of regional brain volumes. MRI measurements further indicated that there was no striatal atrophy, but rather a lack of striatal growth beyond 8 weeks of age. T2 relaxivity further indicated tissue-level changes within brain regions. Despite these dramatic motor and neuroanatomical abnormalities, R6/2 mice did not exhibit neuronal loss in the striatum or motor cortex, although there was a significant increase in neuronal density due to tissue atrophy. The deposition of the mutant HTT (mHTT) protein, the hallmark of HD molecular pathology, was widely distributed throughout the brain. End-stage histopathological assessments were not found to be as robustly correlated with the longitudinal measures of brain atrophy or motor impairments. In conclusion, modeling pre-manifest and early progression of the disease in more slowly progressing animal models will be key to establishing which changes are causally related. © 2013 Rattray et al

A Temporal Threshold for Formaldehyde Crosslinking and Fixation

Formaldehyde crosslinking is in widespread use as a biological fixative for microscopy and molecular biology. An assumption behind its use is that most biologically meaningful interactions are preserved by crosslinking, but the minimum length of time required for an interaction to become fixed has not been determined.Using a unique series of mutations in the DNA binding protein MeCP2, we show that in vivo interactions lasting less than 5 seconds are invisible in the microscope after formaldehyde fixation, though they are obvious in live cells. The stark contrast between live cell and fixed cell images illustrates hitherto unsuspected limitations to the fixation process. We show that chromatin immunoprecipitation, a technique in widespread use that depends on formaldehyde crosslinking, also fails to capture these transient interactions.Our findings for the first time establish a minimum temporal limitation to crosslink chemistry that has implications for many fields of research

Synergy between intention recognition and commitments in cooperation dilemmas

Commitments have been shown to promote cooperation if, on the one hand, they can be sufficiently enforced, and on the other hand, the cost of arranging them is justified with respect to the benefits of cooperation. When either of these constraints is not met it leads to the prevalence of commitment free-riders, such as those who commit only when someone else pays to arrange the commitments. Here, we show how intention recognition may circumvent such weakness of costly commitments. We describe an evolutionary model, in the context of the one-shot Prisoner's Dilemma, showing that if players first predict the intentions of their co-player and propose a commitment only when they are not confident enough about their prediction, the chances of reaching mutual cooperation are largely enhanced. We find that an advantageous synergy between intention recognition and costly commitments depends strongly on the confidence and accuracy of intention recognition. In general, we observe an intermediate level of confidence threshold leading to the highest evolutionary advantage, showing that neither unconditional use of commitment nor intention recognition can perform optimally. Rather, our results show that arranging commitments is not always desirable, but that they may be also unavoidable depending on the strength of the dilemma.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

The Involvement of SMILE/TMTC3 in Endoplasmic Reticulum Stress Response

The state of operational tolerance has been detected sporadically in some renal transplanted patients that stopped immunosuppressive drugs, demonstrating that allograft tolerance might exist in humans. Several years ago, a study by Brouard et al. identified a molecular signature of several genes that were significantly differentially expressed in the blood of such patients compared with patients with other clinical situations. The aim of the present study is to analyze the role of one of these molecules over-expressed in the blood of operationally tolerant patients, SMILE or TMTC3, a protein whose function is still unknown.We first confirmed that SMILE mRNA is differentially expressed in the blood of operationally tolerant patients with drug-free long term graft function compared to stable and rejecting patients. Using a yeast two-hybrid approach and a colocalization study by confocal microscopy we furthermore report an interaction of SMILE with PDIA3, a molecule resident in the endoplasmic reticulum (ER). In accordance with this observation, SMILE silencing in HeLa cells correlated with the modulation of several transcripts involved in proteolysis and a decrease in proteasome activity. Finally, SMILE silencing increased HeLa cell sensitivity to the proteasome inhibitor Bortezomib, a drug that induces ER stress via protein overload, and increased transcript expression of a stress response protein, XBP-1, in HeLa cells and keratinocytes.In this study we showed that SMILE is involved in the endoplasmic reticulum stress response, by modulating proteasome activity and XBP-1 transcript expression. This function of SMILE may influence immune cell behavior in the context of transplantation, and the analysis of endoplasmic reticulum stress in transplantation may reveal new pathways of regulation in long-term graft acceptance thereby increasing our understanding of tolerance

Response of Jupiter's auroras to conditions in the interplanetary medium as measured by the Hubble Space Telescope and Juno

We present the first comparison of Jupiter's auroral morphology with an extended, continuous and complete set of near-Jupiter interplanetary data, revealing the response of Jupiter's auroras to the interplanetary conditions. We show that for ∼1-3 days following compression region onset the planet's main emission brightened. A duskside poleward region also brightened during compressions, as well as during shallow rarefaction conditions at the start of the program. The power emitted from the noon active region did not exhibit dependence on any interplanetary parameter, though the morphology typically differed between rarefactions and compressions. The auroras equatorward of the main emission brightened over ∼10 days following an interval of increased volcanic activity on Io. These results show that the dependence of Jupiter's magnetosphere and auroras on the interplanetary conditions are more diverse than previously thought

CARM1 Mediates Modulation of Sox2

Sox2 is a key component of the transcription factor network that maintains the pluripotent state of embryonic stem cells (ESCs). Sox2 is regulated by multiple post-translational modifications, including ubiquitination, sumoylation, acetylation and phosphorylation. Here we report that Sox2 is in association with and methylated by coactivator-associated arginine methyltransferase 1 (CARM1), a protein arginine methyltransferase that plays a pivotal role in ESCs. We found that CARM1 facilitates Sox2-mediated transactivation and directly methylates Sox2 at arginine 113. This methylation event enhances Sox2 self-association. Furthermore, the physiological retention of Sox2 on chromatin restricts the Sox2 methylation level. Our study reveals the direct regulation of Sox2 by CARM1 that sheds lights on how arginine methylation signals are integrated into the pluripotent transcription factor network