34 research outputs found

    Phylogenomic analysis of the Chlamydomonas genome unmasks proteins potentially involved in photosynthetic function and regulation

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    Chlamydomonas reinhardtii, a unicellular green alga, has been exploited as a reference organism for identifying proteins and activities associated with the photosynthetic apparatus and the functioning of chloroplasts. Recently, the full genome sequence of Chlamydomonas was generated and a set of gene models, representing all genes on the genome, was developed. Using these gene models, and gene models developed for the genomes of other organisms, a phylogenomic, comparative analysis was performed to identify proteins encoded on the Chlamydomonas genome which were likely involved in chloroplast functions (or specifically associated with the green algal lineage); this set of proteins has been designated the GreenCut. Further analyses of those GreenCut proteins with uncharacterized functions and the generation of mutant strains aberrant for these proteins are beginning to unmask new layers of functionality/regulation that are integrated into the workings of the photosynthetic apparatus

    Influence of Substrate Hydrophobicity on the Adsorption of Collagen in the Presence of Pluronic F68, Albumin, or Calf Serum

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    The influence of Pluronic F68 [a poly(ethylene oxide)-poly(propylene oxide)-poly(ethylene oxide) copolymer surfactant], serum albumin (HSA), and fetal calf serum (FCS) on the adsorption of type I collagen by polymer substrates was investigated using radiolabeling and XPS analysis. Three different kinds of polystyrene substrates with increasing level of hydrophobicity were used. Change in the state of hydration of the sorbent and protein surfaces appears to be the main driving force for collagen adsorption. Pluronic F68 strongly reduces collagen adsorption, the reduction being more pronounced with higher substrate hydrophobicity. This explains why epithelial cell adhesion on substrates preconditioned with a solution of Pluronic F68 and collagen is strongly influenced by substrate hydrophobicity. Collagen adsorption is also reduced in the presence of HSA and FCS, but the reduction and its sensitivity to substrate hydrophobicity are lower than with Pluronic F68

    Conceptual model of fracture-limited sea cliff erosion: erosion of the seaward tilted flyschs of Socoa, Basque Country, France

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    International audienceSea cliff morphology and erosion rates are modulated by several factors, including rock control that reflects both lithology and rock structure. Erosion is anticipated to preferentially exploit “fractures”, broadly meant as any discontinuity in an otherwise continuous medium, where the rock mass is weakest. Unpicking the direct control of such fractures on the spatial and temporal pattern of erosion remains, however, challenging. To analyze how such fractures control erosion, we monitored the evolution of a 400 m long stretch of highly-structured sedimentary cliffs in Socoa, Basque Country, France. The rock is known as the Socoa Flysch Formation. This formation combines decimeter-thick turbidites composed of repeat triplets of medium to strong calcareous sandstone, laminated siltstones and argillaceous marls. The sequence plunges at 45° into the sea with a shore-parallel strike. The cliffs are cross-cut by two normal and reverse fault families, with 10 – 100 m alongshore spacing, with primary and secondary strata bound fractures perpendicular to the bedding, which combined delimit the cliff rock mass into discrete blocks that are exploited by erosion process. Erosion, and sometimes plucking, of such beds and blocks on the cliff face was monitored using ground-based Structure-from-Motion (SfM) photogrammetry, over the course of 5.7 years between 2011 and 2017. To compare with longer time change, cliff-top retreat rate was assessed using SfM-orthorectified archive aerial photographs spanning 1954 - 2008. We show that the 13,250 m² cliff face released 4500 blocks exceeding 1.45 ×10-3 m3, removing a total volume of 170 m3. This equates to an average cliff erosion rate of 3.4 mm/yr, which is slightly slower than the 54-year-long local cliff top retreat (10.8 ± 1.8 mm/yr). The vertical distribution of erosion reflects the height of sea water inundation, where the maximum erosion intensity occurs ca. 2 m above high spring-tide water level. Alongshore, the distribution of rockfall scars is concentrated along bed edges bounding cross-cutting faults; the extent of block detachment is controlled by secondary tectonic joints, which may extend through several beds locally sharing similar mechanical strength; and, rockfall depth is always a multiple of bed thickness. Over the longer-term, we explain block detachment and resultant cliff collapse as a cycle. Erosion nucleates on readily exploitable fractures but elsewhere, the sea only meets defect free medium-strong to strong rock slabs offering few morphological features for exploitation. Structurally delimited blocks are quarried, and with sufficient time, carves semi-elliptic scars reaching progressively deeper strata to be eroded. Lateral propagation of erosion is directed along mechanical weaknesses in the bedding, and large episodic collapses affect the overhanging slabs via sliding on the weak marl beds. Collapse geometry is confined to one or several triplets of turbidite beds, but never reaches deeper into the cliff than the eroded depth at the foot. We contend that this fracture-limited model of sea-cliff erosion, inferred from the Socoa site dynamics and its peculiar sets of fractures, applies more broadly to other fractured cliff contexts, albeit with site specific geometries. The initiation of erosion, the propagation of incremental block release, and the ultimate full failure of the cliff, have each been shown to be fundamentally directly controlled by structure, which remains a vital control in understanding how cliffed coasts have changed in the past and will change in the future

    Adhesion of mammalian cells to polymer surfaces: from physical chemistry of surfaces to selective adhesion on defined patterns.

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    The study of the adsorption of type I collagen from a solution containing Pluronic F68 has shown that the latter prevents collagen adsorption on polystyrene and does not prevent it on surface-oxidized polystyrene. This explains the control of mammalian cell adhesion by substrate surface hydrophobicity and composition of pre-conditioning solution. On that basis, selective adhesion of different types of mammalian cells (PC12 pheochromocytoma, MSC80 schwannoma, Hep G2 hepatoblastoma, rat hepatocytes) on patterned surfaces was achieved. Therefore tracks (width in the range of a few tens of microm) of reduced hydrophobicity were produced on polystyrene by photolithography and oxygen plasma treatment. After conditioning by a solution containing both Pluronic F68 and extracellular matrix protein (collagen, fibronectin), the latter adsorbed selectively on these paths thus allowing selective adhesion of the cells

    Repression of ergosterol level during oxidative stress by fission yeast F-box protein Pof14 independently of SCF

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    We describe a new member of the F-box family, Pof14, which forms a canonical, F-box dependent SCF (Skp1, Cullin, F-box protein) ubiquitin ligase complex. The Pof14 protein has intrinsic instability that is abolished by inactivation of its Skp1 interaction motif (the F-box), Skp1 or the proteasome, indicating that Pof14 stability is controlled by an autocatalytic mechanism. Pof14 interacts with the squalene synthase Erg9, a key enzyme in ergosterol metabolism, in a membrane-bound complex that does not contain the core SCF components. pof14 transcription is induced by hydrogen peroxide and requires the Pap1 transcription factor and the Sty1 MAP kinase. Pof14 binds to and decreases Erg9 activity in vitro and a pof14 deletion strain quickly loses viability in the presence of hydrogen peroxide due to its inability to repress ergosterol synthesis. A pof14 mutant lacking the F-box and an skp1-3 ts mutant behave as wild type in the presence of oxidant showing that Pof14 function is independent of SCF. This indicates that modulation of ergosterol level plays a key role in adaptation to oxidative stress
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