Vertical Migration and Mortality of Marine Benthos in Dredged Material: A Synthesis

This account describes the comparative response of four species of benthic invertebrates to burial in terms of vertical migration and mortality, and provides a synthesis of studies and recommendations upon which to assess future impacts. The species featured were the bivalve Mercenaries mercenaria, the amphipod crustacean Parahaustorius longimerus, and the polychaetes Scoloplos fragilis and Nereis succinea. There was evidence of synergistic effects on burrowing activity and mortality with changes in time of burial, sediment depth, sediment type and temperature. In sediment with silt-clay, N. succinea was the most resistant species followed by M. mercenaria, S. fragilis and P. longimerus. In sediment without silt-clay the order of percent mortality was reversed. Studies of surface water chemistry and sediment geochemistry showed that dissolved oxygen decreased significantly and ammonia and sulfide increased significantly between the surface and below 2.0 cm within a 15-day period. Based on these results and physiological tolerances from the literature it was concluded that M. mercenaria and N. succinea would be relatively resistant to chemical effects of spoil disposal, whereas S. fragilis and P. longimerus would be less resistant to such effects. Vertical migration of benthic invertebrates through dredge disposal can be a viable mechanism of recolonization under certain conditions. Some effects of burial of benthos can be predicted based on morphology, behavior and physiology. These biological features were discussed with examples dealing with molluscs, crustaceans, and polychaetes. Finally, recommendations were made concerning the type of studies to provide additional data to aid management agencies in decision making about future dredging and disposal practices.     

Preparative use of isolated CYP102 monooxygenases -- a critical appraisal

Isolated P450 monooxygenases have for long been neglected catalysts in enzyme technology. This is surprising as they display a remarkable substrate specificity catalyzing reactions, which represent a challenge for classic organic chemistry. On the other hand, many P450 monooxygenases are membrane bound, depend on rather complicated electron transfer systems and require expensive cofactors such as NAD(P)H. Their activities are low, and stability leaves much to be desired. The use of bacterial P450 monooxygenases from CYP102 family allows overcoming some of these handicaps. They are soluble and their turnovers are high, presumably because their N-terminal heme monooxygenase and their C-terminal diflavin reductase domain are covalently linked. In recent years, protein engineering approaches have been successfully used to turn CYP102 monooxgenases into powerful biocatalysts.     

Potential causes of linkage disequilibrium in a European maize breeding program investigated with computer simulations

Knowledge about the forces generating and conserving linkage disequilibrium (LD) is important for drawing conclusions about the prospects and limitations of association mapping. The objectives of our research were to examine the importance of (1) selection, (2) mutation, and (3) genetic drift for generating LD in a typical maize breeding program. We conducted computer simulations based on genotypic data of Central European maize open-pollinated varieties which have played an important role as founders of the European flint heterotic group. The breeding scheme and the dimensioning underlying our simulations reflect essentially the maize breeding program of the University of Hohenheim. Results suggested that in a plant breeding program of the examined dimension and breeding scheme, genetic drift and selection are major forces generating LD. The currently used population-based association mapping tests do not explicitly correct for LD caused by these two forces. Therefore, increased type I error rates are expected if these tests are applied to plant breeding populations. As a consequence, we recommend to use family-based association tests for association mapping approaches in plant breeding populations.     

Penicillin-binding protein 2x of Streptococcus pneumoniae: three new mutational pathways for remodelling an essential enzyme into a resistance determinant

Mutations in the transpeptidase domain of penicillin-binding protein 2x (PBP2x) of Streptococcus pneumoniae that reduce the affinity to beta-lactams are important determinants of resistance to these antibiotics. We have now analyzed in vitro and in vivo properties of PBP2x variants from cefotaxime-resistant laboratory mutants and a clinical isolate. The patterns of two to four resistance-specific mutations present in each of the proteins, all of which are placed between 6.6 and 24 Å around the active site, fall into three categories according to their positions in the three-dimensional structure. The first PBP2x group is characterized by mutations at the end of helix α11 and carries the well-known T550A change and/or one mutation on the surface of the penicillin-binding domain in close contact with the C-terminal domain. All group I proteins display very low acylation efficiencies, ≤ 1700 M^− 1 s^− 1, for cefotaxime. The second class represented by PBP2x of the mutant C505 shows acylation efficiencies below 100 M^− 1 s^− 1 for both cefotaxime and benzylpenicillin and contains the mutation L403F at a critical site close to the active serine. PBP2x of the clinical isolate 669 reveals a third mutational pathway where at least the two mutations Q552E and S389L are important for resistance, and acylation efficiency is reduced for both beta-lactams to around 10,000 M^− 1 s^− 1. In each group, at least one mutation is located in close vicinity to the active site and mediates a resistance phenotype in vivo alone, whereas other mutations might exhibit secondary effects only in context with other alterations.     

Degradation of a cytosolic protein requires endoplasmic reticulum-associated degradation machinery

Protein misfolding is monitored by a variety of cellular "quality control" systems. Endoplasmic reticulum (ER) quality control handles misfolded secretory and membrane proteins and is well characterized. However, less is known about the quality control of misfolded cytosolic proteins (CytoQC). To study CytoQC, we have employed a genetic system in Saccharomyces cerevisiae using a transplantable degron, CL1 (1). Attachment of CL1 to the cytosolic protein Ura3p destabilizes Ura3p, targeting it for rapid proteasomal degradation. We have performed a comprehensive analysis of Ura3p-CL1 degradation requirements. As shown previously, we observe that the ER-localized ubiquitin E2 (Ubc6p, Ubc7p, and Cue1p) and E3 (Doa10p) machinery involved in ER-associated degradation (ERAD) are also responsible for the degradation of the cytosolic substrate Ura3p-CL1. Importantly, we find that the cytosol/ER membrane-localized chaperones Ydj1p and Ssa1p, known to be necessary for the ERAD of membrane proteins with misfolded cytosolic domains, are also required for the ubiquitination and degradation of Ura3p-CL1. In addition, we show a role for the Cdc48p-Npl4p-Ufd1p complex in the degradation of Ura3p-CL1. When ubiquitination is blocked, a portion of Ura3p-CL1 is ER membrane-localized. Furthermore, access to the cytosolic face of the ER is required for the degradation of CL1 degron-containing proteins. The ER is distributed throughout the cytosol, and our data, together with previous studies, suggest that the cytosolic face of the ER membrane serves as a "platform" for the degradation of Ura3p-CL1, which may also be the case for other CytoQC substrates.     

Psoriasis patients are enriched for genetic variants that protect against HIV-1 disease

An important paradigm in evolutionary genetics is that of a delicate balance between genetic variants that favorably boost host control of infection but which may unfavorably increase susceptibility to autoimmune disease. Here, we investigated whether patients with psoriasis, a common immune-mediated disease of the skin, are enriched for genetic variants that limit the ability of HIV-1 virus to replicate after infection. We analyzed the HLA class I and class II alleles of 1,727 Caucasian psoriasis cases and 3,581 controls and found that psoriasis patients are significantly more likely than controls to have gene variants that are protective against HIV-1 disease. This includes several HLA class I alleles associated with HIV-1 control; amino acid residues at HLA-B positions 67, 70, and 97 that mediate HIV-1 peptide binding; and the deletion polymorphism rs67384697 associated with high surface expression of HLA-C. We also found that the compound genotype KIR3DS1 plus HLA-B Bw4-80I, which respectively encode a natural killer cell activating receptor and its putative ligand, significantly increased psoriasis susceptibility. This compound genotype has also been associated with delay of progression to AIDS. Together, our results suggest that genetic variants that contribute to anti-viral immunity may predispose to the development of psoriasis.     

Neurons and Neuronal Stem Cells Survive in Glucose-Free Lactate and in High Glucose Cell Culture Medium During Normoxia and Anoxia

Several questions concerning the survival of isolated neurons and neuronal stem and progenitor cells (NPCs) have not been answered in the past: (1) If lactate is discussed as a major physiological substrate of neurons, do neurons and NPCs survive in a glucose-free lactate environment? (2) If elevated levels of glucose are detrimental to neuronal survival during ischemia, do high concentrations of glucose (up to 40 mmol/L) damage neurons and NPCs? (3) Which is the detrimental factor in oxygen glucose deprivation (OGD), lack of oxygen, lack of glucose, or the combination of both? Therefore, in the present study, we exposed rat cortical neurons and NPCs to different concentrations of d-glucose ranging from 0 to 40 mmol/L, or 10 and 20 mmol/L l-lactate under normoxic and anoxic conditions, as well as in OGD. After 24 h, we measured cellular viability by biochemical assays and automated cytochemical morphometry, pH values, bicarbonate, lactate and glucose concentrations in the cell culture media, and caspases activities. We found that (1) neurons and NPCs survived in a glucose-free lactate environment at least up to 24 h, (2) high glucose concentrations >5 mmol/L had no effect on cell viability, and (3) cell viability was reduced in normoxic glucose deprivation to 50% compared to 10 mmol/L glucose, whereas cell viability in OGD did not differ from that in anoxia with lactate which reduced cell viability to 30%. Total caspases activities were increased in the anoxic glucose groups only. Our data indicate that (1) neurons and NPCs can survive with lactate as exclusive metabolic substrate, (2) the viability of isolated neurons and NPCs is not impaired by high glucose concentrations during normoxia or anoxia, and (3) in OGD, low glucose concentrations, but not low oxygen levels are detrimental for neurons and NPCs.     

Graphene Doping Induced Tunability of Nanoparticles Plasmonic Resonances

Interest in graphene has been widely increasing since its discovery in 2004. Research on graphene for plasmonic applications has also boomed due to the high potential of these systems. In this article, we discuss the possible interaction between metallic NPs and graphene monolayer. We show how the contact between metallic NPs and graphene results in graphene doping. More importantly, we experimentally put into evidence the possible modulation of the plasmonic resonance of NPs by graphene doping. Understanding and evidencing this interaction is highly important both from a fundamental point of view and for specific applications such as active plasmonic devices.

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