Publications by authors named "Nolwenn Trinkler"

The mineral phase of shell repair in the Manila clam Venerupis philippinarum affected by brown ring disease (BRD) was characterised at various scales and at various stages of shell repair by confocal Raman microspectrometry and scanning electron microscopy. Spherulitic and quadrangular aragonite microstructures associated with polyene pigments were clearly observed. Von Kossa staining showed that at the beginning of shell repair, hemocytes are filled with insoluble calcium carbonate salts in all fluids and then are transported toward the extrapallial fluids and the repair sites.

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The shell of the Manila clam Venerupis philippinarum is composed of more than 99% calcium carbonate and of a small amount of organic matrix (around 0.2%). In this study, we developed one of the first proteomic approaches applied to mollusc shell in order to characterise the matrix proteins that are believed to be essential for the formation of the biomineral.

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For more than two decades, the Manila clam Ruditapes philippinarum has been regularly affected by Brown Ring Disease (BRD), an epizootic event caused by the bacterium Vibrio tapetis and characterized by the development of a brown deposit on the inner face of valves. Although BRD infection is often lethal, some clams recover by mineralizing a new repair shell layer, which covers the brown deposit and fully isolates it from living tissues. In order to understand this specific shell repair process, the microstructures of repaired zones were compared to those of shells unaffected by BRD.

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European stocks of the Manila clam Ruditapes philippinarum are affected by the Brown Ring Disease (BRD), which is caused by Vibrio tapetis. BRD is characterized by an accumulation of a brown organic matrix on the inner face of the shell. Clams that recover from BRD develop a white mineralized layer covering the brown matrix.

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Lamellarins, a family of hexacyclic pyrrole alkaloids originally isolated from marine invertebrates, display promising anti-tumor activity. They induce apoptotic cell death through multi-target mechanisms, including inhibition of topoisomerase I, interaction with DNA and direct effects on mitochondria. We here report that lamellarins inhibit several protein kinases relevant to cancer such as cyclin-dependent kinases, dual-specificity tyrosine phosphorylation activated kinase 1A, casein kinase 1, glycogen synthase kinase-3 and PIM-1.

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