Impact of the contamination level and the background flora on the growth of Listeria monocytogenes in ready-to-eat diced poultry.

UNLABELLED: The food safety criteria that have been incorporated in European regulation (EC) No2073/2005 (Official Journal of the European Union L, 338, 2005, 1), for Listeria monocytogenes in ready-to eat (RTE) foods, specify a maximum allowable concentration of 100 CFU g(-1) or ml(-1) . Some factors such as pH, salt and modified atmosphere packaging (MAP) are used to prevent the growth of L. monocytogenes in order to comply with the limit. Interactions between background microflora (BM) and L. monocytogenes may limit the growth of L. monocytogenes. The aim of this study was to investigate the mechanisms behind the observed inhibition by natural BM of the growth of L. monocytogenes in ready-to-eat diced poultry meat whose pH and water activity were favourable to its growth. The dynamics of L. monocytogenes and natural BM were therefore monitored in mono-culture and co-culture experiments with various combinations of contamination levels. In the absence of BM, the growth potential of L. monocytogenes depended only on the initial inoculum. With both BM and L. monocytogenes, whatever the combination of concentrations studied, the growth potentials of L. monocytogenes were lower than in a mono-culture through a partial Jameson effect. Thus, the use-by date of this product can be optimized by using models that take into account interactions with BM. SIGNIFICANCE AND IMPACT OF THE STUDY: The study of the growth of Listeria monocytogenes in a diced poultry meat, a matrix whose pH and water activity characteristics are favourable to L. monocytogenes growth, showed that it was inhibited by natural background microflora. This highlights the importance of knowing the product's composition, and in particular the natural background microflora, which can impact the use-by date.

Valvular dystrophy associated filamin A mutations reveal a new role of its first repeats in small-GTPase regulation.

Filamin A (FlnA) is a ubiquitous actin binding protein which anchors various transmembrane proteins to the cell cytoskeleton and provides a scaffold to many cytoplasmic signaling proteins involved in actin cytoskeleton remodeling in response to mechanical stress and cytokines stimulation. Although the vast majority of FlnA binding partners interact with the carboxy-terminal immunoglobulin like (Igl) repeats of FlnA, little is known on the role of the amino-N-terminal repeats. Here, using cardiac mitral valvular dystrophy associated FlnA-G288R and P637Q mutations located in the N-terminal Igl repeat 1 and 4 respectively as a model, we identified a new role of FlnA N-terminal repeats in small Rho-GTPases regulation. Using FlnA-deficient melanoma and HT1080 cell lines as expression systems we showed that FlnA mutations reduce cell spreading and migration capacities. Furthermore, we defined a signaling network in which FlnA mutations alter the balance between RhoA and Rac1 GTPases activities in favor of RhoA and provided evidences for a role of the Rac1 specific GTPase activating protein FilGAP in this process. Together our work ascribed a new role to the N-terminal repeats of FlnA in Small GTPases regulation and supports a conceptual framework for the role of FlnA mutations in cardiac valve diseases centered around signaling molecules regulating cellular actin cytoskeleton in response to mechanical stress.

Expression of the familial cardiac valvular dystrophy gene, filamin-A, during heart morphogenesis.

Myxoid degeneration of the cardiac valves is a common feature in a heterogeneous group of disorders that includes Marfan syndrome and isolated valvular diseases. Mitral valve prolapse is the most common outcome of these and remains one of the most common indications for valvular surgery. While the etiology of the disease is unknown, recent genetic studies have demonstrated that an X-linked form of familial cardiac valvular dystrophy can be attributed to mutations in the Filamin-A gene. Since these inheritable mutations are present from conception, we hypothesize that filamin-A mutations present at the time of valve morphogenesis lead to dysfunction that progresses postnatally to clinically relevant disease. Therefore, by carefully evaluating genetic factors (such as filamin-A) that play a substantial role in MVP, we can elucidate relevant developmental pathways that contribute to its pathogenesis. In order to understand how developmental expression of a mutant protein can lead to valve disease, the spatio-temporal distribution of filamin-A during cardiac morphogenesis must first be characterized. Although previously thought of as a ubiquitously expressed gene, we demonstrate that filamin-A is robustly expressed in non-myocyte cells throughout cardiac morphogenesis including epicardial and endocardial cells, and mesenchymal cells derived by EMT from these two epithelia, as well as mesenchyme of neural crest origin. In postnatal hearts, expression of filamin-A is significantly decreased in the atrioventricular and outflow tract valve leaflets and their suspensory apparatus. Characterization of the temporal and spatial expression pattern of filamin-A during cardiac morphogenesis is a crucial first step in our understanding of how mutations in filamin-A result in clinically relevant valve disease.