The impact of climate change on lakes in the Netherlands: a review

Climate change will alter freshwater ecosystems but specific effects will vary among regions and the type of water body. Here, we give an integrative review of the observed and predicted impacts of climate change on shallow lakes in the Netherlands and put these impacts in an international perspective. Most of these lakes are man-made and have preset water levels and poorly developed littoral zones. Relevant climatic factors for these ecosystems are temperature, ice-cover and wind. Secondary factors affected by climate include nutrient loading, residence time and water levels. We reviewed the relevant literature in order to assess the impact of climate change on these lakes. We focussed on six management objectives as bioindicators for the functioning of these ecosystems: target species, nuisance species, invading species, transparency, carrying capacity and biodiversity. We conclude that climate change will likely (i) reduce the numbers of several target species of birds; (ii) favour and stabilize cyanobacterial dominance in phytoplankton communities; (iii) cause more serious incidents of botulism among waterfowl and enhance the spreading of mosquito borne diseases; (iv) benefit invaders originating from the Ponto-Caspian region; (v) stabilize turbid, phytoplankton-dominated systems, thus counteracting restoration measures; (vi) destabilize macrophyte-dominated clear-water lakes; (vii) increase the carrying capacity of primary producers, especially phytoplankton, thus mimicking eutrophication; (viii) affect higher trophic levels as a result of enhanced primary production; (ix) have a negative impact on biodiversity which is linked to the clear water state; (x) affect biodiversity by changing the disturbance regime. Water managers can counteract these developments by reduction of nutrient loading, development of the littoral zone, compartmentalization of lakes and fisheries management.     

Variations in the composition and adsorption behavior of dissolved organic matter at a small, forested watershed

This study investigated the properties and sorption by goethite of bulk (unfractionated) dissolved organic matter (DOM) from surface and shallow groundwaters at McDonalds Branch, a small freshwater fen in the New Jersey Pine Barrens (USA). Water samples were collected in the spring and fall seasons from two surface-water sampling sites, an upstream potential recharge area and a downstream discharge area, as well as from a set of in-stream nested wells in the upstream potential recharge area. Changes in DOM concentration, molecular weight distribution, and molar absorptivity at 280 nm were measured. Surface and shallow (1.6 m below land surface) groundwater samples collected in spring 1997 in the potential recharge zone (actual recharge impeded by an extensive clay lens) were found to be very similar in terms of DOM concentrations and physicochemical properties and is believe to originate from a common source. Samples taken in fall 1997 yielded no surface water because of drought conditions, and the shallow groundwater DOM collected from the recharge well contained significantly less and chemically altered DOM. This change in chemical properties is believed to be caused in part by fractionation resulting from sorption to mineral phases. Batch isotherm experiments show that sorption by goethite of the DOM from both spring surface and shallow groundwaters in the potential recharge area were similar, whereas the fall groundwater possessed a much lower affinity for the sorbent. This study demonstrated that shallow groundwaters collected under different climatic and hydrologic conditions (spring, high flow versus fall, drought conditions) resulted in different physicochemical properties and adsorption affinities.     

A single mutation that causes phosphatidylglycerol deficiency impairs synthesis of photosystem II cores in Chlamydomonas reinhardtii.

Two mutants of Chlamydomonas reinhardtii, mf1 and mf2, characterized by a marked reduction in their phosphatidylglycerol content together with a complete loss in its Delta3-trans hexadecenoic acid-containing form, also lost photosystem II (PSII) activity. Genetic analysis of crosses between mf2 and wild-type strains shows a strict cosegregation of the PSII and lipid deficiencies, while phenotypic analysis of phototrophic revertant strains suggests that one single nuclear mutation is responsible for the pleiotropic phenotype of the mutants. The nearly complete absence of PSII core is due to a severely decreased synthesis of two subunits, D1 and apoCP47, which is not due to a decrease in translation initiation. Trace amounts of PSII cores that were detected in the mutants did not associate with the light-harvesting chlorophyll a/b-binding protein antenna (LHCII). We discuss the possible role of phosphatidylglycerol in the coupled process of cotranslational insertion and assembly of PSII core subunits.     

Identification of somatic chromosomal abnormalities in hypothalamic hamartoma tissue at the GLI3 locus

Hypothalamic hamartomas (HH) are rare, benign congenital tumors associated with intractable epilepsy. Most cases are sporadic and nonsyndromic. Approximately 5% of HH cases are associated with Pallister-Hall syndrome (PHS), which is caused by haploinsufficiency of GLI3. We have investigated the possibility that HH pathogenesis in sporadic cases is due to a somatic (tumor-only) mutation in GLI3. We isolated genomic DNA from peripheral blood and surgically resected HH tissue in 55 patients with sporadic HH and intractable epilepsy. A genome-wide screen for loss of heterozygosity (LOH) and chromosomal abnormalities was performed with parallel analysis of blood and HH tissue with Affymetrix 10K SNP microarrays. Additionally, resequencing and fine mapping with SNP genotyping were completed for the GLI3 gene with comparisons between peripheral blood and HH tissue pairs. By analyzing chromosomal copy-number data for paired samples on the Affymetrix 10K array, we identified a somatic chromosomal abnormality on chromosome 7p in one HH tissue sample. Resequencing of GLI3 did not identify causative germline mutations but did identify LOH within the GLI3 gene in the HH tissue samples of three patients. Further genotyping of 28 SNPs within and surrounding GLI3 identified five additional patients exhibiting LOH. Together, these data provide evidence that the development of chromosomal abnormalities within GLI3 is associated with the pathogenesis of HH lesions in sporadic, nonsyndromic patients with HH and intractable epilepsy. Chromosomal abnormalities including the GLI3 locus were seen in 8 of 55 (15%) of the resected HH tissue samples. These somatic mutations appear to be highly variable.     

Diversity of Bacterial Endosymbionts of Environmental Acanthamoeba Isolates

Free-living amoebae are frequent hosts for bacterial endosymbionts. In this study, the symbionts of eight novel environmental Acanthamoeba strains isolated from different locations worldwide were characterized. Phylogenetic analysis revealed that they were related to one of four evolutionary lineages of amoeba symbionts recognized previously. This study provides evidence for the existence of only a small number of phylogenetically well-separated groups of obligate intracellular endosymbionts of acanthamoebae with global distribution.     

Separation of carvedilol enantiomers in very small volumes of human plasma by capillary electrophoresis with laser-induced fluorescence

A sensitive capillary electrophoretic method for the determination of carvedilol enantiomers in 100 μl of human plasma has been developed and validated. Carvedilol and the internal standard carazolol are isolated from plasma samples by liquid–liquid extraction using diethylether. A sensitive and selective detection is provided by helium–cadmium laser-induced fluorescence. The total analysis time is 17.5 min, about 30 min are needed for the sample preparation. The linearity of the assay ranges from 1.56 to 50 ng/ml per carvedilol enantiomer. The limits of quantification (LOQ) for the carvedilol enantiomers in 100 μl of human plasma are 1.56 ng/ml. The inter-day accuracy for R-carvedilol is between 95.8 and 103% (104% at LOQ) and for S-carvedilol between 97.1 and 103% (107% at LOQ); the inter-day precision values are between 3.81 and 8.64% (10.9% at LOQ) and between 5.47 and 7.86% (7.91% at LOQ) for R- and S-carvedilol, respectively. The small sample volume needed is especially advantageous for the application in clinical studies in pediatric patients. As an application of the assay concentration/time profiles of the carvedilol enantiomers in a 5-year-old patient receiving a test dose of 0.09 mg/kg carvedilol are reported.     

Functional characterization of the mouse organic-anion-transporting polypeptide 2

We have isolated and functionally characterized an additional murine member of the organic-anion-transporting polypeptide (Oatp) family of membrane transport proteins from mouse liver. The 3.6 kb cDNA insert contains an open reading frame of 2010 bp coding for a 670 amino acid protein. Based on its amino acid identity of 88% to the rat Oatp2, it is considered the mouse Oatp2 orthologue. Functional expression in Xenopus laevis oocytes demonstrated that mouse Oatp2 transports several general Oatp substrates such as estrone-3-sulfate, dehydroepiandrosterone sulfate (DHEAS), ouabain and BQ-123 but hardly any taurocholate nor rocuronium or deltorphin II. The high-affinity rat Oatp2 substrate digoxin is transported with a rather low affinity with an apparent K_m value of 5.7 μM. Bromosulfophthalein (BSP), a substrate not transported by the rat Oatp2, is transported very well by mouse Oatp2. Northern blot analysis demonstrated a predominant expression in the liver with additional signals in kidney and brain. Using fluorescence in situ hybridization, the Oatp2 gene (gene symbol Slc21a5) was mapped to chromosome 6G1-G3.     

Uncoupling of protein-3 induces an uncontrolled uncoupling of mitochondria after expression in muscle derived L6 cells.

The uncoupling proteins (UCPs) are thought to uncouple oxidative phosphorylation in the mitochondria and thus generate heat. One of the UCP isoforms, UCP3, is abundantly expressed in skeletal muscle, the major thermogenic tissue in humans. UCP3 has been overexpressed at high levels in yeast systems, where it leads to the uncoupling of cell respiration, suggesting that UCP3 may indeed be capable of dissipating the mitochondrial proton gradient. This effect, however, was recently shown to be a consequence of the high level of expression and incorrect folding of the protein and not to its intrinsic uncoupling activity. In the present study, we investigated the properties of UCP3 overexpressed in a relevant mammalian host system such as the rat myoblast L6 cell line. UCP3 was expressed in relatively low levels (< 1 microg x mg(-1) membrane protein) with the help of an adenovirus vector. Immunofluorescence microscopy of transduced L6 cells showed that UCP3 was expressed in more than 90% of the cells and that its staining pattern was characteristic for mitochondrial localization. The oxygen consumption of L6 cells under nonphosphorylating conditions increased concomitantly with the levels of UCP3 expression. However, uncoupling was associated with an inhibition of the maximal respiratory capacity of mitochondria and was not affected by purine nucleotides and free fatty acids. Moreover, recombinant UCP3 was resistant to Triton X-100 extraction under conditions that fully solubilize membrane bound proteins. Thus, UCP3 can be uniformly overexpressed in the mitochondria of a relevant muscle-derived cell line resulting in the expected increase of mitochondrial uncoupling. However, our data suggest that the protein is present in an incompetent conformation.