Species,community, and ecosystem-level responses following the invasion of the red alga <Emphasis Type="Italic">Dasysiphonia japonica</Emphasis> to the western North Atlantic Ocean

Species invasions have been increasing in frequency worldwide, yet critical gaps remain in our understanding of how invaders affect community structure and ecosystem functioning, particularly during the initial stages of invasion. Even less is known about changes in the invader that may take place immediately following an invasion. This study examined the recent invasion of the red macroalga Dasysiphonia (formerly, Heterosiphonia) japonica to the western North Atlantic Ocean with the aim of filling in gaps in our understanding of the impacts that invasive seaweeds have at the species, community and ecosystem levels immediately following their establishment. Within 5 years of invasion, community composition had changed and biodiversity had decreased to nearly half of pre-invasion levels. In addition, the relative proportion of Dasysiphonia decreased by 35% over our four-year study from initially high levels shortly after establishment. We found evidence that functional traits of this initially aggressive invader changed over time, as it ultimately became a less aggressive, co-inhabiting member of the local algal community, particularly with respect to nutrient uptake and relative abundances, although native diversity remained low relative to pre-invasion levels. Using these realistic changes in community structure, including decreases in biodiversity, we also showed that nutrient uptake of algal assemblages changed over time, suggesting changes in the functional characteristics of invaded communities, with implications for ecosystem-level processes such as nutrient fluxes. This study provides rare empirical evidence about the successional stages occurring at the individual, community, and ecosystem levels during the first 5 years of an invasion.     

Histone H3 tails containing dimethylated lysine and adjacent phosphorylated serine modifications adopt a specific conformation during mitosis and meiosis

Condensation of chromatin, mediated in part by posttranslational modifications of histones, is essential for cell division during mitosis. Histone H3 tails are dimethylated on lysine (Kme2) and become phosphorylated on serine (Sp) residues during mitosis. We have explored the possibility that these double modifications are involved in the establishment of H3 tail conformations during the cell cycle. Here we describe a specific chromatin conformation occurring at Kme2 and adjacently phosphorylated S of H3 tails upon formation of a hydrogen bond. This conformation appears exclusively between early prophase and early anaphase of the mitosis, when chromatin condensation is highest. Moreover, we observed that the conformed H3Kme2Sp tail is present at the diplotene and metaphase stages in spermatocytes and oocytes. Our data together with results obtained by cryoelectron microscopy suggest that the conformation of Kme2Sp-modified H3 tails changes during mitosis and meiosis. This is supported by biostructural modeling of a modified histone H3 tail bound by an antibody, indicating that Kme2Sp-modified H3 tails can adopt at least two different conformations. Thus, the H3K9me2S10p and the H3K27me2S28p sites are involved in the acquisition of specific chromatin conformations during chromatin condensation for cell division.     

Analysis of LuPME3, a pectin methylesterase from Linum usitatissimum,revealed a variability in PME proteolytic maturation

Pectin methylesterase (PME) catalyzes the de-methylesterification of pectin in plant cell walls during cell elongation.¹ Pectins are mainly composed of α(1, 4)-D-galacturonosyl acid units that are synthesized in a methylesterified form in the Golgi apparatus to prevent any interaction with Ca²⁺ ions during their intracellular transport.² The highly methylesterified pectins are then secreted into the apoplasm³ and subsequently de-methylesterified in muro by PMEs. This can either induce the formation of pectin gels through the Ca²⁺ crosslinking of neighboring non-methylesterified chains or create substrates for pectin-degrading enzymes such as polygalacturonases and pectate lyases for the initiation of cell wall loosening.⁴ PMEs belong to a large multigene family. Sixty­six PME-related genes are predicted in the Arabidopsis genome.¹ Among them, we have recently shown that AtPME3 (At3g14310), a major basic PME isoform in A. thaliana, is ubiquitously expressed in vascular tissues and play a role in adventitious rooting.⁵ In flax (Linum usitatissimum), three genes encoding PMEs have been sequenced so far, including LuPME3, the ortholog of AtPME3. Analysis of the LuPME3 isoform brings new insights into the processing of these proteins.     

Mode and origin of replication of pSAM2, a conjugative integrating element of Streptomyces ambofaciens

pSAM2 is an 11 kb integrating element from Streptomyces ambofaciens that is capable of replication. It generates single-stranded DNA during replication, and is therefore the first Streptomyces integrating element to be described that may belong to the family of elements, called the ssDNA elements, that replicate by a rolling-circle mechanism. The direction of replication has been identified. The plus origin (ori) of replication and minus origin (M-O) have been located. Streptomyces lividans harbouring replicating pSAM2 also contain numerous small covalently closed circular DNA molecules (scm) derived from pSAM2. These scm contain ori and extend on both sides of the putative nick site. Sequences at the junction points of these scm are heterogeneous but short direct repeats were always found in the vicinity of these junctions.     

Impact of phosphate concentration on the metabolome of biofilms of the marine bacterium Pseudoalteromonas lipolytica

Metabolomics - Recent advances in high-throughput methodologies in the ‘omics’ and synthetic biology fields call for rapid and sensitive workflows in the metabolic phenotyping of...     

Alfalfa response to elevated atmospheric CO2 varies with the symbiotic rhizobial strain

Increased atmospheric CO₂ was shown to affect a variety of physiological processes in plants, including photosynthesis and growth with repercussions on crop yield and nutritive value. Perennial alfalfa (Medicago sativa L.) is a sustainable crop with a deep root system, living in symbiosis with rhizobium for nitrogen (N) fixation. The objective of the project was to determine the combined effects of elevated CO₂ and rhizobial strains on photosynthesis, growth, N fixation, and nutritive value of alfalfa, and on soil microflora. Alfalfa inoculated with two different strains of rhizobia (Sinorhizobium meliloti strains A2 and NRG34) was grown 2 months at day/night temperatures of 22/17°C under either 400 (near ambient) or 800 (elevated) μmol mol⁻¹ of CO₂. The photosynthetic response of alfalfa to elevated CO₂ differed according to the rhizobial strain. At the end of the experiment, elevated CO₂ stimulated photosynthetic rates by 50% in plants associated with A2 but there was no significant increase in plants nodulated with NRG34. Nitrogenase activity (+38%) and shoot growth (+60%) were stimulated under 800 μmol mol⁻¹ of CO₂ for alfalfa inoculated with both strains. Root dry weight was significantly higher at 800 μmol mol⁻¹ of CO₂ only with strain A2. Fibre concentration decreased in response to elevated atmospheric CO₂ in alfalfa inoculated with strain A2 resulting in plant material with greater nutritive value when inoculated with A2 compared to NRG34. In the soil, elevated CO₂ increased the proportion of fungi in the microbial community while decreasing Gram⁻ bacteria. For alfalfa inoculated with rhizobial strain A2, photosynthetic rates, nitrogenase activity, and growth were all stimulated by increased atmospheric CO₂ compared to less consistently positive responses to elevated CO₂ when inoculated with NRG34. Our results show that it is possible to identify rhizobial strains to improve plant performance under predicted future CO₂ concentrations with no negative effect on nutritive value. The Canadian Government’s right to retain a non-exclusive, royalty-free license in and to any copyright is acknowledged.     

The mitochondrial complex I inhibitor rotenone triggers a cerebral tauopathy

Reduced activity of the mitochondrial respiratory chain--particularly complex I--may be implicated in the etiology of both Parkinson's disease and progressive supranuclear palsy, although these neurodegenerative diseases differ substantially as to their distinctive pattern of neuronal cell loss and the predominance of cerebral alpha-synuclein or tau protein pathology. To determine experimentally whether chronic generalized complex I inhibition has an effect on the distribution of alpha-synuclein or tau, we infused rats systemically with the plant-derived isoflavonoid rotenone. Rotenone-treated rats with a pronounced metabolic impairment had reduced locomotor activity, dystonic limb posture and postural instability. They lost neurons in the substantia nigra and in the striatum. Spherical deposits of alpha-synuclein were observed in a few cells, but cells with abnormal cytoplasmic accumulations of tau immunoreactivity were significantly more numerous in the striatum of severely lesioned rats. Abnormally high levels of tau immunoreactivity were found in the cytoplasm of neurons, oligodendrocytes and astrocytes. Ultrastructurally, tau-immunoreactive material consisted of straight 15-nm filaments decorated by antibodies against phosphorylated tau. Many tau+ cell bodies also stained positive for thioflavin S, nitrotyrosine and ubiquitin. Some cells with abnormal tau immunoreactivity contained activated caspase 3. Our data suggest that chronic respiratory chain dysfunction might trigger a form of neurodegeneration in which accumulation of hyperphosphorylated tau protein predominates over deposits of alpha-synuclein.     

Generation and characterization of Smac/DIABLO-deficient mice

The mitochondrial proapoptotic protein Smac/DIABLO has recently been shown to potentiate apoptosis by counteracting the antiapoptotic function of the inhibitor of apoptosis proteins (IAPs). In response to apoptotic stimuli, Smac is released into the cytosol and promotes caspase activation by binding to IAPs, thereby blocking their function. These observations have suggested that Smac is a new regulator of apoptosis. To better understand the physiological function of Smac in normal cells, we generated Smac-deficient (Smac(-/-)) mice by using homologous recombination in embryonic stem (ES) cells. Smac(-/-) mice were viable, grew, and matured normally and did not show any histological abnormalities. Although the cleavage in vitro of procaspase-3 was inhibited in lysates of Smac(-/-) cells, all types of cultured Smac(-/-) cells tested responded normally to all apoptotic stimuli applied. There were also no detectable differences in Fas-mediated apoptosis in the liver in vivo. Our data strongly suggest the existence of a redundant molecule or molecules capable of compensating for a loss of Smac function.