Tissue and skeletal changes in the scleractinian coral Stylophora pistillata Esper 1797 under phosphate enrichment

Long-term phosphate enrichments (0, 0.5, and 2.5 μmol L− 1; 4 to 11 weeks) were used to assess a possible limitation in phosphorus of zooxanthellae and to complement data on the effect of phosphate enrichment on calcification and elemental composition of the tissue in the scleractinian coral Stylophora pistillata. Phosphate addition mainly affected the coral symbionts. Indeed, at 2.5 μmol L− 1 P-enriched, zooxanthellae had a greater photosynthetic efficiency, their intracellular carbon and nitrogen contents increased by 70% and their phosphorus content by 190%, while their specific growth rate increased by 18%. C:P and N:P ratios in zooxanthellae were much higher than the Redfield ratios advocated for nutrient-repleted phytoplankton, and decreased with phosphate enrichment. Collectively, these results suggest a phosphorus limitation of the zooxanthellae growth in hospite. However, the increase in zooxanthellae specific growth rate did not lead to the building of a higher symbiont density, as zooxanthellae growth just matched the tissue and skeletal growth of the enriched corals. Benefits of phosphate supplementation were thus not substantial enough to lead to the building of higher zooxanthellae density and to their balanced growth, which suggests that symbiont growth was likely limited by another nutrient as well, probably nitrogen. At the host level, there were no changes in the elemental composition or in the protein levels, while skeletal growth rate increased by 31% between unenriched and 2.5 μmol L− 1 P-enriched corals. Phosphate-enriched corals also incorporated 1.7 times more phosphorus into their skeleton than did unenriched corals. These results evidenced that zooxanthellae and the skeleton are the two accumulation sites of inorganic phosphorus within the symbiotic association

New evidence of a mitochondrial genetic background paradox: Impact of the J haplogroup on the A3243G mutation

International audienceBackground: The A3243G mutation in the tRNALeu gene (UUR), is one of the most common pathogenic mitochondrial DNA (mtDNA) mutations in France, and is associated with highly variable and heterogeneous disease phenotypes. To define the relationships between the A3243G mutation and mtDNA backgrounds, we determined the haplogroup affiliation of 142 unrelated French patients – diagnosed as carriers of the A3243G mutation – by control-region sequencing and RFLP survey of their mtDNAs. Results: The analysis revealed 111 different haplotypes encompassing all European haplogroups, indicating that the 3243 site might be a mutational hot spot. However, contrary to previous findings, we observed a statistically significant underepresentation of the A3243G mutation on haplogroup J in patients (p = 0.01, OR = 0.26, C.I. 95%: 0.08–0.83), suggesting that might be due to a strong negative selection at the embryo or germ line stages. Conclusion: Thus, our study supports the existence of mutational hotspot on mtDNA and a "haplogroup J paradox," a haplogroup that may increase the expression of mtDNA pathogenic mutations, but also be beneficial in certain environmental contexts

Mécanismes impliqués dans la régulation de la biogenèse mitochondriale de tumeurs rénales (carcinomes à cellules claires et oncocytomes)

Le but de ce travail était de comprendre les mécanismes liés aux déficiences mitochondriales dans les cancers.Dans des tumeurs rénales graves, les CRCC, l absence du gène vhl fonctionnel est corrélée à la diminution des complexes des OXPHOS. La stabilisation du facteur de transcription HIF ("Hypoxia-inducible factor") due à la déficience de vhl doit être associée à une augmentation de la production de ROS pour induire ce phénomène. Si HIF est stabilisé par du CoCl2, celui-ci peut exercer un effet toxique additionnel en inhibant le clivage du précurseur d'une sous unité de la cytochrome c oxydase, la COX4, et empêcher ainsi l'assemblage de ce complexe. Dans les oncocytomes rénaux, tumeurs bénignes caractérisées par une prolifération mitochondriale, l'identification de mutations de l'ADN mitochondrial du complexe I et/ou du complexe IV suggère que la prolifération soit due à une induction de la biogenèse similaire à celle observée dans des pathologies mitochondriales typiquesThis thesis aimed at better understanding the origins of mitochondrial disorders in renal tumors. The CRCC that are often associated with poor prognosis in patients, and characterized by vhl invalidation, exhibit a decrease in OXPHOS complexes. This phenomenon could be due both to HIF (Hypoxia-inducible factor) stabilization induced by the lack of pVHL in CRCC and to an increase in ROS production. HIF can also be stabilized by cobalt treatment but this compound brings additional toxic effects, since it inhibits the processing of a precursor of the cytochrome c oxidase 4 subunit and therefore prevents the cytochrome c oxidase assembly.On the opposite, renal oncocytoma, that are non-malignant tumors are characterized by mitochondrial proliferation. We identified mutations in mitochondrial DNA genes of complex I or IV, which might suggest that the mitochondrial proliferation in these tumors is similar to that observed in typical mitochondrial pathologiesLYON1-BU.Sciences (692662101) / SudocSudocFranceF

Étude des déficiences en cytochrome c oxydase et en ATPase-ATPsynthétase dans des pathologies mitochondriales humaines et chez le nématode C. elegans

Les pathologies mitochondriales dues à un défaut dans la synthèse d'ATP causé par une déficience d'une enzyme des OXPHOS peuvent avoir de graves manifestations pouvant aller jusqu'à une mort précoce. Tout d'abord, nous avons étudié le complexe IV (COX) dont le déficit est surtout dû à des mutations de SURF1. Diverses analyses réalisées sur des cellules de patients mutés pour ce gène se sont avérées très utiles pour la mise en place de diagnostics pré et post-natals pour le Syndrome de Leigh, mais aussi pour mieux comprendre l'assemblage de la COX. Un modèle C. elegans de ces déficiences à été réalisé en inhibant par RNAi l'expression de protéines constitutives ou d'assemblage de l'enzyme. Il ne reste plus maintenant qu'à mettre en place un test pharmacologique à haut débit sur ces animaux. D'autre part, l'étude d'un patient portant le codon d'initiation GUG pour la traduction de la sous-unité 6 du complexe V apporte de nouveaux éléments sur le mécanisme traductionnel mitochondrialLYON1-BU.Sciences (692662101) / SudocSudocFranceF

Binding of L-glutamate to glutamate dehydrogenase in the presence of 1,4,5,6-tetrahydronicotinamide adenine dinucleotide

International audienceIn a previous work with Julliard, a lipid-protein complex showing a high affinity for glutamate was extracted from pig heart mitochondrial membranes; it exhibited many properties expected from a glutamate translocator [ 11. From its protein composition it was suggested..

Iodine uptake in brown seaweed exposed to radioactive liquid discharges from the reprocessing plant of ORANO La Hague

International audienceIodine-129 is present in controlled liquid radioactive waste routinely released in seawater by the ORANO nuclear fuel reprocessing plant in La Hague (Normandy, France). Brown algae are known for their exceptional ability to concentrate iodine from seawater. They also potentially emit volatile iodine compounds in response to various stresses, such as during emersion at low tide. For these reasons, brown seaweed is routinely collected for radioactivity monitoring in the marine environment (Fucus serratus and Laminaria digitata). Despite the high concentration ratio, the exact mechanism of iodine uptake is still unclear. Chemical imaging by laser desorption/ionization mass spectrometry provided evidence that iodine is stored by kelps as I−. In this study we investigate in vivo iodine uptake in kelps (L. digitata) with an emphasis on seawater iodine chemical speciation. Our results showed that kelp plantlets were able to take up iodine in the forms of both IO3− and I−. We also observed transient net efflux of I− back to seawater but no IO3− efflux. Since the seaweed stores I− but takes up both IO3− and I−, IO3− was likely to be converted into I− at some point in the plantlet. One major outcome of our experiments was the direct observation of the kelp-based biogenic conversion of seawater IO3− into I−. On the basis of both IO3− and I− uptakes by the seaweed, we propose new steps in the possible iodine concentration mechanism used by brown algae