Effet de deux types d’insecticides sur la mycorhization arbusculaire et le développement de deux variétés de pomme de terre (Solanum tuberosum)

Cette étude a été menée en serre pour évaluer l’effet de deux types d’insecticides sur la mycorhization et le développement de deux variétés de pomme de terre (Aïda et Atlas). Les insecticides carbofuran et chlorpyriphos-éthyl, respectivement systémiques et contacts, ont été appliqués au sol à différentes stades d’inoculation du champignon Glomus mosseae. Le pourcentage de mycorhization, la biomasse aérienne, lenombre et le calibre des minitubercules ont été évalués après 60 jours de culture. L’application du carbofuran ou du chlorpyriphos-éthyl 21 jours avant ou après l’inoculation du champignon induit une diminution significative du pourcentage de colonisation mycorhizienne chez toutes les deux variétés. Cependant, cette baisse est plus importante avec les  traitements de l’insecticide de contact après inoculation et de l’insecticidesystémique effectué avant inoculation. Cette tendance s’est répercutée sur la biomasse aérienne et le nombre des minitubercules. Le calibre des minitubercules présente une variabilité de réponse selon la variété de pomme de terre et le type d’insecticide. Ce travail a permis de déterminer le moment compatible de l’inoculation de Glomus mosseae avec  l’application des insecticides au sol chez les variétés Aïda et Atlas de la pomme de terre.© 2013 International Formulae Group. All rights reserved.Mots clés: Glomus mosseae, carbofuran, chlorpyriphos-éthyl, Aïda, Atlas

Responses of potatoes plants inoculated with arbuscular mycorrhizal fungi and litter in greenhouse

A pot experiment was set to examine the impact of the foliar litter (Hardwickia binata and Azadirachta indica) and an arbuscular mycorrhizal (AM) fungus on the development of two varieties of potato plants (Aida, Atlas). Three litter doses (0, 25 and 50 g) were applied to the pots after bedding plantlets. The plants were inoculated with AM, Glomus aggregatum. Mycorrhizal colonization, shoot dry weight, size and number of minitubers were evaluated after 12 weeks on the potato growth. Results show that shoot dry weight of plants was improved by litter of the H. binata at 25 and 50 g. Thus, A. indica litter increased size of plants Aida at 50 g and the minitubers numbers Atlas at 25 g. On the other hand, root colonization decreased with increase in the dose of litter with both varieties of potato.Key words: Arbuscular mycorrhizal fungi, potato, litter, micropropagation

Molecular Epidemiology of Endemic Human T-Lymphotropic Virus Type 1 in a Rural Community in Guinea-Bissau

Human T-Lymphotropic Virus type 1 (HTLV-1) affects millions of people worldwide. It is very similar to Simian T-Lymphotropic Virus, a virus that circulates in monkeys. HTLV-1 causes a lethal form of leukemia (Adult T-cell Leukemia) and a debilitating neurological syndrome (HTLV-associated myelopathy/tropical spastic paraparesis) in approximately 5% of infected people. Based on sequence variation, HTLV-1 can be divided into 7 subtypes (1a–1g) with the Cosmopolitan subtype 1a further subdivided into subgroups (A–E). We examined HTLV-1 diversity in a rural area in Guinea-Bissau, a country in West Africa with a high HTLV-1 prevalence (5%). We found that most viruses belong to the Cosmopolitan subtype 1a, subgroup D, but 2 viruses belonged to subtype 1g. This subtype had thus far only been found in monkey hunters in Cameroon, who were probably recently infected by monkeys. Our findings indicate that this subtype has spread beyond Central Africa. An important, unresolved question is whether persons with this subtype were infected by monkeys or through human-to-human transmission

Losartan Slows Pancreatic Tumor Progression and Extends Survival of SPARC-Null Mice by Abrogating Aberrant TGFβ Activation

Pancreatic adenocarcinoma, a desmoplastic disease, is the fourth leading cause of cancer-related death in the Western world due, in large part, to locally invasive primary tumor growth and ensuing metastasis. SPARC is a matricellular protein that governs extracellular matrix (ECM) deposition and maturation during tissue remodeling, particularly, during wound healing and tumorigenesis. In the present study, we sought to determine the mechanism by which lack of host SPARC alters the tumor microenvironment and enhances invasion and metastasis of an orthotopic model of pancreatic cancer. We identified that levels of active TGFβ1 were increased significantly in tumors grown in SPARC-null mice. TGFβ1 contributes to many aspects of tumor development including metastasis, endothelial cell permeability, inflammation and fibrosis, all of which are altered in the absence of stromal-derived SPARC. Given these results, we performed a survival study to assess the contribution of increased TGFβ1 activity to tumor progression in SPARC-null mice using losartan, an angiotensin II type 1 receptor antagonist that diminishes TGFβ1 expression and activation in vivo. Tumors grown in SPARC-null mice progressed more quickly than those grown in wild-type littermates leading to a significant reduction in median survival. However, median survival of SPARC-null animals treated with losartan was extended to that of losartan-treated wild-type controls. In addition, losartan abrogated TGFβ induced gene expression, reduced local invasion and metastasis, decreased vascular permeability and altered the immune profile of tumors grown in SPARC-null mice. These data support the concept that aberrant TGFβ1-activation in the absence of host SPARC contributes significantly to tumor progression and suggests that SPARC, by controlling ECM deposition and maturation, can regulate TGFβ availability and activation

Transcriptional Profiling in Pathogenic and Non-Pathogenic SIV Infections Reveals Significant Distinctions in Kinetics and Tissue Compartmentalization

Simian immunodeficiency virus (SIV) infection leads to AIDS in experimentally infected macaques, whereas natural reservoir hosts exhibit limited disease and pathology. It is, however, unclear how natural hosts can sustain high viral loads, comparable to those observed in the pathogenic model, without developing severe disease. We performed transcriptional profiling on lymph node, blood, and colon samples from African green monkeys (natural host model) and Asian pigtailed macaques (pathogenic model) to directly compare gene expression patterns during acute pathogenic versus non-pathogenic SIV infection. The majority of gene expression changes that were unique to either model were detected in the lymph nodes at the time of peak viral load. Results suggest a shift toward cellular stress pathways and Th1 profiles during pathogenic infection, with strong and sustained type I and II interferon responses. In contrast, a strong type I interferon response was initially induced during non-pathogenic infection but resolved after peak viral load. The natural host also exhibited controlled Th1 profiles and better preservation of overall cell homeostasis. This study identified gene expression patterns that are specific to disease susceptibility, tissue compartmentalization, and infection duration. These patterns provide a unique view of how host responses differ depending upon lentiviral infection outcome

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field