Plastid Transcript Editing across Dinoflagellate Lineages Shows Lineage-Specific Application but Conserved Trends.

Dinoflagellates are a group of unicellular protists with immense ecological and evolutionary significance and cell biological diversity. Of the photosynthetic dinoflagellates, the majority possess a plastid containing the pigment peridinin, whereas some lineages have replaced this plastid by serial endosymbiosis with plastids of distinct evolutionary affiliations, including a fucoxanthin pigment-containing plastid of haptophyte origin. Previous studies have described the presence of widespread substitutional RNA editing in peridinin and fucoxanthin plastid genes. Because reports of this process have been limited to manual assessment of individual lineages, global trends concerning this RNA editing and its effect on the biological function of the plastid are largely unknown. Using novel bioinformatic methods, we examine the dynamics and evolution of RNA editing over a large multispecies data set of dinoflagellates, including novel sequence data from the peridinin dinoflagellate Pyrocystis lunula and the fucoxanthin dinoflagellate Karenia mikimotoi. We demonstrate that while most individual RNA editing events in dinoflagellate plastids are restricted to single species, global patterns, and functional consequences of editing are broadly conserved. We find that editing is biased toward specific codon positions and regions of genes, and generally corrects otherwise deleterious changes in the genome prior to translation, though this effect is more prevalent in peridinin than fucoxanthin lineages. Our results support a model for promiscuous editing application subsequently shaped by purifying selection, and suggest the presence of an underlying editing mechanism transferred from the peridinin-containing ancestor into fucoxanthin plastids postendosymbiosis, with remarkably conserved functional consequences in the new lineage

LA N-GLYCOSYLATION:MARQUEUR PRECOCE DE LA DIFFERENCIATION ENTEROCYTAIRE DES CELLULES HT-29

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HL 60 leukaemia cells chemically induced to differentiate retain some surface glycan features of undifferentiated cells not found in normal leukocytes.

International audienceHuman HL 60 myeloid leukaemia cells have the potential to differentiate into either macrophage-like cells or granulocyte-like cells under the stimulus of chemical treatments. Using glycotechnology procedures, the glycosylation patterns of differentiated and undifferentiated HL 60 cells were analysed and compared with those of normal human peripheral monocytes. Both in vitro differentiations result in significant morphologic and functional changes, but we observed that the glycosylation patterns of undifferentiated and differentiated HL 60 cells exhibit several common glycosidic features that are absent in normal peripheral monocytes: the presence of (i) bisecting beta-N-acetylglucosamine attached at the C-4 position of the beta-mannose of polyantennary complex-type carbohydrate chains and (ii) complex-type carbohydrate chains enriched with non-reducing terminal beta-N-acetylglucosamine residues. Moreover, the three populations of HL 60 cells express small amounts of biantennary complex-type structures ( 20% of such structures. Thus, the cell glycosylation pattern could reflect the pathological state of the HL 60 cells

Cell spreading on laminin substrate involves Con A-binding proteins

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Dual effect of 1-deoxymannojirimycin on the mannose uptake and on the N-glycan processing of the human colon cancer cell line HT-29.

International audience1-Deoxymannojirimycin (dMM), a specific alpha-mannosidase I inhibitor, completely blocks the conversion of Man9-8GlcNAc2 into Man7-5-GlcNAc2 in both differentiated and undifferentiated human adenocarcinoma HT-29 cells. Besides this well known effect on N-glycan trimming, we describe here a novel effect of this inhibitor on the D-[2-3H]mannose uptake that is exclusively observed in differentiated intestinal cells, i.e. cells that display a functional apical brush border membrane. This inhibition of D-[2-3H]mannose uptake was shown to be dose-dependent and reversible. Moreover, using microsomal fractions we showed that this effect depends only on the integrity of the brush border and is unrelated to the classical inhibitory effect of dMM on N-glycan processing. Furthermore, another N-glycan trimming inhibitor 1-deoxynojirimycin, an epimer of dMM, did not interfere with D-[2-3H]mannose uptake. This observation was in good agreement with the specificity of the effect induced by dMM. These results demonstrate a novel effect of dMM on highly differentiated intestinal cells and suggest that a carrier-mediated mannose transport could exist in those cells. Such an interaction between cell morphology and the biological effect of dMM should lead to a careful use of drugs acting on N-glycan processing