Photoacclimation in the marine alga Nannochloropsis sp. (Eustigmatophyte): a kinetic study

Exponentially growing cultures of Nannochloropsis sp. were transferredfrom high light (650 µ.mol quanta m^–2 s^–1)to low light (30 (µrnol quanta m^–2 s^–1). Thekinetics of changes in the various parameters of the photoacclimationprocess were followed until steady state was reached. In thisorganism, the observed 4.25 increase in cellular chlorophylla in the low-light-acclimated cells was linearly correlatedwith an increase in the number of photosynthetic units (PSU),while the PSU size remained constant. The new steady state wasreached after a transition period of 87 h and following an initialovershoot in the chlorophyll a concentration. During the processof photoacclimation, harvested and utilized light was increaseddue to a combination of increased cellular chlorophyll and anincrease of the quantum yield. These improvements in efficiencywere coupled with the reduction of respiration. The overalleffect of photoacclimation, therefore, amounted to reducingthe impact of low light on the growth rate of the algae. Ourstudy demonstrates the importance of the photoacclimation processin the context of the planktonic way of life. An index of the'effectiveness of photoacclimation' is proposed.     

Laminarin sulfate mimics the effects of heparin on smooth muscle cell proliferation and basic fibroblast growth factor-receptor binding and mitogenic activity

Heparin and heparin-like molecules may function, apart from their effect on hemostasis, as regulators of cell growth and neovascularization. We investigated whether similar effects are exerted by laminarin sulfate, an unrelated polysulfated saccharide isolated from the cell wall of seaweed and composed of chemically O-sulfated b?-(1,3)-linked glucose residues. Laminarin sulfate exhibits about 30% of the anticoagulant activity of heparin and is effective therapeutically in the prevention and treatment of cerebrovascular diseases. We characterized the effect of laminarin sulfate on interaction of the heparin-binding angiogenic factor, basic fibroblast growth factor (bFGF), with a naturally produced subendothelial extracellular matrix (ECM) and with cell surface receptor sites. Laminarin sulfate (1-2 m?g/ml) inhibited the binding of bFGF to ECM and to the surface of vascular smooth muscle cells (SMC) in a manner similar to that observed with heparin. Likewise, laminarin sulfate efficiently displaced both ECM-and cell-bound bFGF at concentrations as low as 1 m?g/ml. Both laminarin sulfate and heparin efficiently induced restoration of bFGF receptor binding in xylosyltransferase-deficient CHO cell mutants defective in initiation of glycosaminoglycan synthesis. Moreover, laminarin sulfate elicited bFGF receptor activation and mitogenic response in heparan sulfate(HS)-deficient, cytokine-dependent lymphoid cells. These results indicate that laminarin sulfate effectively replaced the need for heparin and HS in the induction of bFGF receptor binding and signaling. In other experiments, laminarin sulfate was found to inhibit the proliferation of vascular SMC in a manner similar to that observed with heparin. These effects of laminarin sulfate may have potential clinical applications in diverse situations such as wound healing, angiogenesis, and atherosclerosis. © 1995 Wiley-Liss, Inc.     

The Mexican Outsiders: A Community History of Marginalization and Discrimination

The Mexican Outsiders:. Community History of Marginalization and Discrimination. Martha Menchaca. Austin: University of Texas Press, 1995. 250 pp.     

S-phase and DNA-damage checkpoints: a tale of two yeasts

Many genes required for the S-phase and DNA-damage checkpoints have been identified in the yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe. This year many checkpoint genes have been sequenced, providing new information about the mechanism of checkpoint control. Several of these genes are conserved between the two yeasts but others are species-specific.     

Speciation,phenotypic plasticity,or ontogeny,the case of the genus Galkinius (Pyrgomatidae,Cirripedia, Crustacea)

Barnacles of the genus Galkinius occupy a large spectrum of host corals, making it one of the least host‐specific genera within the Pyrgomatidae. Molecular analyses show that within the genus Galkinius there are highly supported clades, suggesting that the genus Galkinius is a complex of evolutionarily significant units (ESUs). The morphology of the opercular valves has been used as the basis for the separation of species of Galkinius. In this study, morphological variability was found both between specimens within ESUs extracted from different host species and between specimens extracted from the same colony. Identifications based on the opercular valves cannot therefore be assigned to different species despite being genetically distinguishable. It is proposed that in many cases the differences between valve morphology of different species of Galkinius are the outcome of ontogeny. Allometric growth of the valves has resulted in differences in the proportions of the parts of the valve. © 2015 The Linnean Society of London     

Monoallelic and Biallelic Variants in EMC1 Identified in Individuals with Global Developmental Delay,Hypotonia, Scoliosis,and Cerebellar Atrophy

The paradigm of a single gene associated with one specific phenotype and mode of inheritance has been repeatedly challenged. Genotype-phenotype correlations can often be traced to different mutation types, localization of the variants in distinct protein domains, or the trigger of or escape from nonsense-mediated decay. Using whole-exome sequencing, we identified homozygous variants in EMC1 that segregated with a phenotype of developmental delay, hypotonia, scoliosis, and cerebellar atrophy in three families. In addition, a de novo heterozygous EMC1 variant was seen in an individual with a similar clinical and MRI imaging phenotype. EMC1 encodes a member of the endoplasmic reticulum (ER)-membrane protein complex (EMC), an evolutionarily conserved complex that has been proposed to have multiple roles in ER-associated degradation, ER-mitochondria tethering, and proper assembly of multi-pass transmembrane proteins. Perturbations of protein folding and organelle crosstalk have been implicated in neurodegenerative processes including cerebellar atrophy. We propose EMC1 as a gene in which either biallelic or monoallelic variants might lead to a syndrome including intellectual disability and preferential degeneration of the cerebellum.     

The effects of proteasomal inhibition on synaptic proteostasis

Synaptic function crucially depends on uninterrupted synthesis and degradation of synaptic proteins. While much has been learned on synaptic protein synthesis, little is known on the routes by which synaptic proteins are degraded. Here we systematically studied how inhibition of the ubiquitin‐proteasome system (UPS) affects the degradation rates of thousands of neuronal and synaptic proteins. We identified a group of proteins, including several proteins related to glutamate receptor trafficking, whose degradation rates were significantly slowed by UPS inhibition. Unexpectedly, however, degradation rates of most synaptic proteins were not significantly affected. Interestingly, many of the differential effects of UPS inhibition were readily explained by a quantitative framework that considered known metabolic turnover rates for the same proteins. In contrast to the limited effects on protein degradation, UPS inhibition profoundly and preferentially suppressed the synthesis of a large number of synaptic proteins. Our findings point to the importance of the UPS in the degradation of certain synaptic proteins, yet indicate that under basal conditions most synaptic proteins might be degraded through alternative pathways.     

Optimization of the All-D Peptide D3 for Aβ Oligomer Elimination

The aggregation of amyloid-β (Aβ) is postulated to be the crucial event in Alzheimer’s disease (AD). In particular, small neurotoxic Aβ oligomers are considered to be responsible for the development and progression of AD. Therefore, elimination of thesis oligomers represents a potential causal therapy of AD. Starting from the well-characterized d-enantiomeric peptide D3, we identified D3 derivatives that bind monomeric Aβ. The underlying hypothesis is that ligands bind monomeric Aβ and stabilize these species within the various equilibria with Aβ assemblies, leading ultimately to the elimination of Aβ oligomers. One of the hereby identified d-peptides, DB3, and a head-to-tail tandem of DB3, DB3DB3, were studied in detail. Both peptides were found to: (i) inhibit the formation of Thioflavin T-positive fibrils; (ii) bind to Aβ monomers with micromolar affinities; (iii) eliminate Aβ oligomers; (iv) reduce Aβ-induced cytotoxicity; and (v) disassemble preformed Aβ aggregates. The beneficial effects of DB3 were improved by DB3DB3, which showed highly enhanced efficacy. Our approach yielded Aβ monomer-stabilizing ligands that can be investigated as a suitable therapeutic strategy against AD.     

The role of recombination in the evolvement of the fragile X mutation

Summary The frequency of recombination in the regions adjacent to the fragile X locus was studied in two groups of carriers: daughters of transmitting males and transmitters of maternally inherited fragile X chromosomes. Approximately one-half of the offspring of the former and one quarter of the off-spring of the latter are recombinant. Recombinants and parentals are equally distributed among affected and normal off-spring in the two groups. These results indicate that crossing-over at or around the fragile X locus occurs in every meiosis in doughters of transmitting males, although the recombinant chromatids do not necessarily carry the fragile X mutation. Hence, crossing-over is unequivocally associated with, but is not the direct cause of, the transition from the primary genetic lesion to the final mutation.