La gestion des ressources forestières au Maroc: Une approche par le capital social

Social capital appears only very rarely in the nomenclature related to the management of forest resources in Morocco. Far from being a semantic detail, this lexical omission comes as a revelation of a policy change. Public authorities have established, in spite of the positive externalities that social capital generates, a bureaucratic management source of heaviness and ineffectiveness. The proof is a recession of the wooded surfaces accompanied by an irreversible degradation of the natural environment on one hand and of the intrinsic quality of the forests on the other hand. This political position raises questions. Thereby, we suggest that the management of forest resources could be optimized if handled through an approach coming from social capital. Our hypothesis is to set forth that this caesura took place through the disappearance of the local traditional organizations, certainly a vector of social capital but also protector of the natural environment. It is possible, by questioning the past, to find an opening in the forest crisis by rehabilitating the Jemaâ in a modern vision.Common management, Forestry, Jemaâ, Morocco, Social capital

Author Correction: LKB1 loss links serine metabolism to DNA methylation and tumorigenesis

Erratum for: LKB1 loss links serine metabolism to DNA methylation and tumorigenesis. [Nature. 2016

Droits de propriété en économie pastorale. Le raisonnement hardinien est-il crédible ?

Les débats autours de l’allocation optimale des ressources forestières ont mis en évidence la forte dépendance entre leur soutenabilité et les régimes de propriété. Pour privilégier la solution privative, les tenants de l’École des droits de propriété ont d’abord opté pour la remise en cause de la propriété commune qu’ils considèrent comme facteur accélérant la détérioration de la ressource. Si leurs arguments sont multiples, le plus célèbre reste l’article de Hardin relative à la tragédie des communs. L’auteur propose d’imaginer une communauté d’éleveur partageant un pré en commun. Tenté par la maximisation de sa propre utilité, chaque éleveur continuera d’élargir la taille de son troupeau pour augmenter son rendement, ce qui se traduira par une détérioration tragique de la ressource. La solution est donc de privatiser le pré. L’auteur tentera de soumettre ce raisonnement à la réalité pour évaluer sa crédibilité.The debate goshawks of the optimal allowance of forest resources brought to light the fort dependence between their sustainability and the property regimes. To privilege the privative solution, the upholders of the “property rights” opted at first for the depreciation of the common property considered as factor which accelerates the deterioration of the resource. If their arguments are multiple, the most famous is Hardin’s article relative to the tragedy of the commons. The author suggests imagining a breeder’s community who shares and exploits a meadow. To maximize his own utility, every breeder will continue to widen the size of his herd to increase his return, what will be translated by a tragic deterioration of the resource. According to Hardin, the only solution is the privatization of the meadow. We would try to examine this reasoning in reality in the purpose of estimate its credibility

Gene therapy restores adipose tissue and metabolic health in a pre-clinical mouse model of lipodystrophy

The authors are extremely grateful to Dr Donna MacCallum (University of Aberdeen) for assistance with AAV vector i.v. tail vein injections and Pat Bain (University of Aberdeen) for design and generation of the graphical abstract. The authors would also like to thank the staff at the University of Aberdeen’s Microscopy and Histology Core Facility and the Medical Research Facility for support with animal breeding and maintenance. This research was supported by funding from the EFSD/Lilly Young Investigator Research Award Programme, Wellcome Trust ISSF Fellowship Support Fund, and Diabetes UK RD Lawrence Fellowship (21/0006280) awarded to G.D.M. and Diabetes UK (18/0005884) awarded to J.J.R.Peer reviewedPublisher PD

Bscl2 Deficiency Does Not Directly Impair the Innate Immune Response in a Murine Model of Generalized Lipodystrophy

Funding: Work was supported by Diabetes UK (JJR;18/0005884, MD;17/0005621) the Medical Research Council (JJR; MR/L002620/1, MC/PC/15077), the British Heart Foundation (MD; PG/14/43/30889), The Agency for Science, Technology and Research, Singapore (A*STAR) (WH), The Wellcome Trust (ISSF Funding to GDM) and the European Union’s Horizon 2020 ERC consolidator award (MB:2016-726152-TYPHI).Peer reviewedPublisher PD

Oligomers of the lipodystrophy protein seipin may co-ordinate GPAT3 and AGPAT2 enzymes to facilitate adipocyte differentiation

Abstract: Seipin deficiency causes severe congenital generalized lipodystrophy (CGL) and metabolic disease. However, how seipin regulates adipocyte development and function remains incompletely understood. We previously showed that seipin acts as a scaffold protein for AGPAT2, whose disruption also causes CGL. More recently, seipin has been reported to promote adipogenesis by directly inhibiting GPAT3, leading to the suggestion that GPAT inhibitors could offer novel treatments for CGL. Here we investigated the interactions between seipin, GPAT3 and AGPAT2. We reveal that seipin and GPAT3 associate via direct interaction and that seipin can simultaneously bind GPAT3 and AGPAT2. Inhibiting the expression of seipin, AGPAT2 or GPAT3 led to impaired induction of early markers of adipocyte differentiation in cultured cells. However, consistent with normal adipose mass in GPAT3-null mice, GPAT3 inhibition did not prevent the formation of mature adipocytes. Nonetheless, loss of GPAT3 in seipin-deficient preadipocytes exacerbated the failure of adipogenesis in these cells. Thus, our data indicate that GPAT3 plays a modest positive role in adipogenesis and argue against the potential of GPAT inhibitors to rescue white adipose tissue mass in CGL2. Overall, our study reveals novel mechanistic insights regarding the molecular pathogenesis of severe lipodystrophy caused by mutations in either seipin or AGPAT2

LKB1 loss links serine metabolism to DNA methylation and tumorigenesis

Intermediary metabolism generates substrates for chromatin modification, enabling the potential coupling of metabolic and epigenetic states. Here we identify a network linking metabolic and epigenetic alterations that is central to oncogenic transformation downstream of the liver kinase B1 (LKB1, also known as STK11) tumour suppressor, an integrator of nutrient availability, metabolism and growth. By developing genetically engineered mouse models and primary pancreatic epithelial cells, and employing transcriptional, proteomics, and metabolic analyses, we find that oncogenic cooperation between LKB1 loss and KRAS activation is fuelled by pronounced mTOR-dependent induction of the serine-glycine-one-carbon pathway coupled to S-adenosylmethionine generation. At the same time, DNA methyltransferases are upregulated, leading to elevation in DNA methylation with particular enrichment at retrotransposon elements associated with their transcriptional silencing. Correspondingly, LKB1 deficiency sensitizes cells and tumours to inhibition of serine biosynthesis and DNA methylation. Thus, we define a hypermetabolic state that incites changes in the epigenetic landscape to support tumorigenic growth of LKB1-mutant cells, while resulting in potential therapeutic vulnerabilities

Adipose Loss and Metabolic Disease Due to Seipin Deficiency: Systemic Versus Tissue Specific Effects

This thesis aimed to understand the molecular mechanisms via which BSCL2 disruption causes metabolic disease in congenital generalised lipodystrophy type 2. The results presented provide evidence that seipin has significant roles in adipose tissue, by regulating lipolysis, but also in pancreatic ß-cells where it influences insulin secretion. This work also reveals an interaction between seipin and glucagon-like peptide 1 receptor. This thesis demonstrates the therapeutic potential of liraglutide to treat metabolic disease in CGL2 patients