Spontaneous gelation of wheat gluten proteins in a food grade solvent

Structuring wheat gluten proteins into gels with tunable mechanical properties would provide more versatility for the production of plant protein-rich food products. Gluten, a strongly elastic protein material insoluble in water, is hardly processable. We use a novel fractionation procedure allowing the isolation from gluten of a water/ethanol soluble protein blend, enriched in glutenin polymers at an unprecedented high ratio (50%). We investigate here the viscoelasticity of suspensions of the protein blend in a water/ethanol (50/50 v/v) solvent, and show that, over a wide range of concentrations, they undergo a spontaneous gelation driven by hydrogen bonding. We successfully rationalize our data using percolation models and relate the viscoelasticity of the gels to their fractal dimension measured by scattering techniques. The gluten gels display self-healing properties and their elastic plateaus cover several decades, from 0.01 to 10000 Pa. In particular very soft gels as compared to standard hydrated gluten can be produced.Comment: Food Hydrocolloids, in pres

ETUDE MORPHO-GRANULOMETRIQUE ET STRUCTURALE DES SEMOULES DE BLE DUR PROPRIETES D'HYDRATATION ET D'AGGLOMERATION

International audienceLes propriétés d'hydratation et d'agglomération de la semoule de blé dur dépendent des caractéristiques de la matière à granuler, du liquide de granulation et de l'outil de granulation. Dans le procédé de fabrication des graines de couscous, la formation, la croissance et la densification des grains de semoule sont effectuées par addition d'eau, mélange et roulage. Une étude de caractérisation de la semoule de blé dur a été entreprise à différentes échelles d'observation : macroscopique, mésoscopique et moléculaire afin de comprendre les mécanismes d'hydratation et d'agglomération. La semoule de blé dur constitue une population de particules hétérogènes en granulométrie et en composition biochimique. Si cette hétérogénéité se traduit par des modifications des propriétés d'hydratation, d'autres études sont nécessaires pour mieux appréhender son influence sur les propriétés d'agglomération

Une exposition à de faibles doses d'alkylphénols entraine des altérations de épithélium mammaires et des défauts transgénérationnels mais n'augmente pas le potentiel tumorigénique des cellules cancéreuses mammaires

International audienceFetal and neonatal exposure to long chain alkylphenols has been suspected to promote breast developmental disorders and consequently to increase breast cancer risk. However, disease predisposition from developmental exposures remains unclear. In this work, human MCF-10A mammary epithelial cells were exposed in vitro to a low dose of a realistic [4-nonylphenol+4-tert-octylphenol] mixture. Transcriptome and cell phenotype analyses combined to functional and signaling network modeling indicated that long chain alkylphenols triggered enhanced proliferation, migration ability and apoptosis resistance and shed light on the underlying molecular mechanisms which involved the human estrogen receptor variant ERα36. A male mouse inherited transgenerational model of exposure to 3 environmentally relevant doses of the alkylphenol mix was set up in order to determine whether and how it would impact on mammary gland architecture. Mammary glands from F3 progeny obtained after intrabuccal chronic exposure of C57BL/6J P0 pregnant mice followed by F1 to F3 male inheritance displayed an altered histology which correlated with the phenotypes observed in vitro in human mammary epithelial cells. Since cellular phenotypes are similar in vivo and in vitro and involve the unique ERα36 human variant, such consequences of alkylphenol exposure could be extrapolated from mouse model to human. However, transient alkylphenol treatment combined to ERα36 overexpression in mammary epithelial cells were not sufficient to trigger tumorigenesis in xenografted Nude mice. Therefore, it remains to be determined if low dose alkylphenol transgenerational exposure and subsequent abnormal mammary gland development could account for an increased breast cancer susceptibility

Transgenerational effects of ERalpha36 over-expression on mammary gland development and molecular phenotype: clinical perspective for breast cancer risk and therapy.

International audienceGrowing source of evidence suggests that exposure to estrogen mimicking agents is a risk factor for breast cancer onset and progression. Long chain alkylphenols are man made compounds still present in household products, industrial and agricultural processes, leading to a global environmental and human contamination. These molecules are known to exert estrogen -like activities through binding to classical estrogen receptors. Recently, we have demonstrated that a realistic mixture of 4 tert - octylphenol and 4 - nonylphenol can stimulate proliferation and modulate epigenetic status of testicular cancer germ cells through a rapid, Estrogen Receptor alpha 36 (ERα36) -dependent non genomic pathway (Ajj et al, 2013; doi: 10.1371/journal.pone.0061758). In a retrospective study of breast tumor samples, we also validated ERα36 expression as a reliable prognostic factor for cancer progression from an estrogen dependent prolifera tive tumor toward an estrogen dispensable metastatic disease (Chamard - Jovenin et al, 2015; doi: 10.1186/s12918 - 015 - 0178 - 7). Since high ERα36 expression enhances expression of migration/invasion markers in breast tumors, we addressed the question of its involvement in response to alkylphenol exposure in vitro (MCF -10A mammary epithelial cell line and MCF -7 estrogen -sensitive cancer cells) and in vivo ( C57BL mice). A male inherited transgenerational model of exposure to environmentally relevant doses of an alkylphenol mix was set up in C57BL/6J mice to determine whether and how it impacts on mammary gland morphogenesis. Human mammary epithelial MCF -10A cells were exposed to similar doses to decipher the molecular mechanisms involved by a combination of transcriptomic study, cell phenotype analyses, functional and signaling network modeling. The relevance of mouse phenotype extrapolation to human risk is discussed. Mouse mammary gland exposed transgenerationally to the alkylphenol mix displayed a neoplastic -like histology. This phenotype was correlated with the enhanced proliferation, migration ability and apoptosis resistance observed in vitro on human mammary epithelial cells and mediated by the estrogen receptor variant ERα36. Since cellular phenotypes are similar in vivo and in vitro and involve the unique ERα36 human variant , such consequences of alkylphenol exposure could be extrapolated from mouse model to human. Low dose alkylphenol transgenerational exposure could promote abnormal mammary gland development and subsequently increase the risk of breast cancer at ageing

Genomic changes during the evolution of the Coxiella genus along the parasitism-mutualism continuum

The Coxiellaceae family is composed of five genera showing lifestyles ranging from free-living to symbiosis. Among them, Coxiella burnetii is a well-known pathogen causing Q fever in humans. This bacterium presents both intracellular (parasitic) and environmental (resistant) forms. Recently, several environmental Coxiella genomes have been reported, among which several have come from intracellular mutualistic symbionts of ticks, termed Coxiella-like endosymbionts. We sequenced two new Coxiella-LE genomes from Dermacentor marginatus (CLEDm) and Ornithodoros maritimus (CLEOmar) ticks, the latter belonging to the C. burnetii lineage. Using these newly sequenced Coxiella-LEs and 43 Coxiellaceae genomes, we conducted comparative genomic and phylogenomic analyses to increase our knowledge of C. burnetii pathogenicity and the emergence of Coxiella-LEs. Results highlight the probably parasitic nature of the common ancestor of the Coxiellaceae. Indeed, the virulence factor Dot/Icm T4 Secretion System is present in most, but not all, Coxiellaceae. Whereas it is part of a putative pathogenic island in C. burnetii, it has been entirely lost or inactivated in Coxiella-LEs, suggesting its importance in pathogenesis. Additionally, we found that a Sha/Mrp antiporter was laterally acquired in the C. burnetii lineage. This antiporter might be involved in alkali resistance and the development of the resistant form that is able to persist in the environment for long periods of time. The Sha operon is eroded or absent in Coxiella-LEs. Finally, we found that all Coxiella representatives produce B vitamins and co-factors indicating a pre-adaptation of Coxiella to mutualism with hematophagous arthropods. Accordingly, the ancestor of C. burnetii and Coxiella-LEs was likely a parasitic bacterium able to manipulate its host cell and to produce vitamins and co-factors for its own use