The Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services (IPBES): getting involved

The Intergovernmental Science-Policy Platform for Biodiversity and Ecosystem Services (IPBES) held its 5th plenary session in Bonn during March 2017. After last year’s pollinator assessment, the biodiversity assessments currently being undertaken are shortly to be available for peer review. The scientific community can play an important role in both conducting assessments and in the peer-review process. Independent scientists can contribute to ensure that these assessments are comprehensive with respect to the current state and future trends of biodiversity and the ecosystem services. We outline possibilities for deeper involvement of the scientific community in the IPBES process and draw attention to upcoming reviews in 2017.     

Phenotypic responses of <Emphasis Type="Italic">Spartina anglica</Emphasis> to duration of tidal immersion

Although Spartina anglica C.E. Hubbard continues to be invasive in many countries, this species has experienced a drastic decline in coastal China over the last decade. We hypothesize that changes in the duration of tidal immersion were responsible for this decline because the elevation of the S. anglica-dominated area in coastal China has increased greatly over the last decade. We examined the effects of the duration of simulated tidal immersion and plant material provenance on growth, asexual reproduction, biomass accumulation, and allocation (percent of above-ground biomass to total biomass) of S. anglica in a greenhouse experiment. The provenance of S. anglica did not significantly affect any traits measured except for height, stalk diameter, and leaf area. However, all traits were affected by the duration of immersion. Plants grown under 6 h of immersion were taller and had more leaves, more roots, and larger leaf area than those under 2, 4, 8, and 10 h of immersion. Asexual traits and biomass of the plants grown under 6 h of immersion were significantly larger than those under other immersion durations. The results suggested that S. anglica benefits from tidal immersion and decreasing duration of tidal immersion may have resulted in the decline of the S. anglica populations in coastal China. Thus, controlling the duration of tidal immersion may be an effective way of controlling invasiveness of this species elsewhere in the world.     

Insights into the Renal Pathogenesis in Schimke Immuno-Osseous Dysplasia: A Renal Histological Characterization and Expression Analysis

Schimke immuno-osseous dysplasia (SIOD) is a pleiotropic disorder caused by mutations in the SWI/SNF2-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a-like-1 (SMARCAL1) gene, with multiple clinical features, notably end-stage renal disease. Here we characterize the renal pathology in SIOD patients. Our analysis of SIOD patient renal biopsies demonstrates the tip and collapsing variants of focal segmental glomerulosclerosis (FSGS). Additionally, electron microscopy revealed numerous glomerular abnormalities most notably in the podocyte and Bowman’s capsule. To better understand the role of SMARCAL1 in the pathogenesis of FSGS, we defined SMARCAL1 expression in the developing and mature kidney. In the developing fetal kidney, SMARCAL1 is expressed in the ureteric epithelium, stroma, metanephric mesenchyme, and in all stages of the developing nephron, including the maturing glomerulus. In postnatal kidneys, SMARCAL1 expression is localized to epithelial tubules of the nephron, collecting ducts, and glomerulus (podocytes and endothelial cells). Interestingly, not all cells within the same lineage expressed SMARCAL1. In renal biopsies from SIOD patients, TUNEL analysis detected marked increases in DNA fragmentation. Our results highlight the cells that may contribute to the renal pathogenesis in SIOD. Further, we suggest that disruptions in genomic integrity during fetal kidney development contribute to the pathogenesis of FSGS in SIOD patients.     

The Heterozygous Disproportionate Micromelia (Dmm) Mouse: Morphological Changes in Fetal Cartilage Precede Postnatal Dwarfism and Compared With Lethal Homozygotes Can Explain the Mild Phenotype

The disproportionate micromelia (Dmm) mouse has a mutation in the C-propeptide coding region of the Col2a1 gene that causes lethal dwarfism when homozygous (Dmm/Dmm) but causes only mild dwarfism observable ∼1-week postpartum when heterozygous (Dmm/+). The purpose of this study was 2-fold: first, to analyze and quantify morphological changes that precede the expression of mild dwarfism in Dmm/+ animals, and second, to compare morphological alterations between Dmm/+ and Dmm/Dmm fetal cartilage that may correlate with the marked skeletal differences between mild and lethal dwarfism. Light and electron transmission microscopy were used to visualize structure of chondrocytes and extracellular matrix (ECM) of fetal rib cartilage. Both Dmm/+ and Dmm/Dmm fetal rib cartilage had significantly larger chondrocytes, greater cell density, and less ECM per unit area than +/+ littermates. Quantitative RT-PCR showed a decrease in aggrecan mRNA in Dmm/+ vs +/+ cartilage. Furthermore, the cytoplasm of chondrocytes in Dmm/+ and Dmm/Dmm cartilage was occupied by significantly more distended rough endoplasmic reticulum (RER) compared with wild-type chondrocytes. Fibril diameters and packing densities of +/+ and Dmm/+ cartilage were similar, but Dmm/Dmm cartilage showed thinner, sparsely distributed fibrils. These findings support the prevailing hypothesis that a C-propeptide mutation could interrupt the normal assembly and secretion of Type II procollagen trimers, resulting in a buildup of proα1(II) chains in the RER and a reduced rate of matrix synthesis. Thus, intracellular entrapment of proα1(II) seems to be primarily responsible for the dominant-negative effect of the Dmm mutation in the expression of dwarfism. (J Histochem Cytochem 56:1003–1011, 2008)     

Altered mandibular development precedes the time of palate closure in mice homozygous for disproportionate micromelia: an oral clefting model supporting the Pierre-Robin sequence

BACKGROUND: Development of the human craniofacial anatomy involves a number of interrelated, genetically controlled components. The complexity of the interactions between these components suggests that interference with the spaciotemporal interaction of the expanding tongue and elongating Meckel's cartilage correlates with the appearance of cleft palate. Mice homozygous for the semi-dominant Col2a1 mutation Disproportionate micromelia (Dmm), presenting at birth with both cleft palate and micrognathia, provide the opportunity to test the hypothesis that mandibular growth retardation coincides with formation of the secondary palate as predicted from our understanding of the Pierre Robin sequence. The present study was conducted in embryonic day 14 (E14) mice, 1 day before palate closure, to describe the relationship between growth of the lower jaw/tongue complex versus genotype of the embryo. METHODS: Whole heads, isolated from E14.25, E14.5 and E14.75 wild-type and homozygous mutant embryos, were fixed in Bouin's solution, embedded in paraffin, and serially sectioned. Mid-sagittal sections, stained with toluidine blue, were used to estimate growth of both tongue and lower jaw (Meckel's cartilage length) during a 12-hr period preceding palate closure. RESULTS: In control embryos, the largest increase in Meckel's cartilage length occurred between E14.5 and E14.75. Compared to control, the mean Meckel's cartilage length in the mutant was similar at E14.25, but was significantly less at E14.5 and E14.75. Absolute tongue size in control embryos increased linearly during this period of E14.25 to E14.75. Relative to the rapidly growing Meckel's cartilage, however, relative tongue size in control embryos actually decreased over time. Absolute tongue size in the mutant was not significantly different from that of control at any of the embryonic stages examined, however, relative tongue size in the mutant was significantly greater at E14.75 compared to control. CONCLUSION: Mandibular growth retardation, coupled with relative macroglossia in E14 Dmm/Dmm mice, suggests that the concerted development of the palate and lower jaw complex in the mutant is aberrant. Detection of micrognathia and pseudomacroglossia in homozygotes, before the time of palate closure, supports the hypothesis that a relationship exists between growth retardation of Meckel's cartilage and malformation of the secondary palate, as predicted by the Pierre-Robin sequence.     

Nuclear variants of bone morphogenetic proteins

Background  

Bone morphogenetic proteins (BMPs) contribute to many different aspects of development including mesoderm formation, heart development, neurogenesis, skeletal development, and axis formation. They have previously been recognized only as secreted growth factors, but the present study detected Bmp2, Bmp4, and Gdf5/CDMP1 in the nuclei of cultured cells using immunocytochemistry and immunoblotting of nuclear extracts.     

Syntaxonomy of the Australian mangal refined through iterative ordinations

Mangal (tidal forest) communities vary with respect to position in the littoral sequence, and latitude. A previous classification of mangal from the southern and western coastlines of Australia has been subjected to a series of ordinations, in an attempt to produce a robust syntaxonomy. An iterative ordination process allowed for the progressive refinement of the syntaxonomic units. This process allows an ecologist to use critically a numerical technique to refine ecological assumptions developed from field work, and/or non-numerical analyses. Ordination analysis suggested a need for the classification to be refined, and allowed the construction of a final syntaxonomy. In conjunction with broad environmental data collected during the investigation, the ordinations allowed the development of some environmental perspectives. These suggested that littoral position is a stronger environmental influence on mangal communities than balance between salt and freshwater.     

A mobile surgery for single homeless people in London.

Little is known about the social and medical characteristics of people who regularly sleep rough, or whether medical care can be targeted at these people. In 1987 a mobile surgery was used to provide primary health care at two sites in central London where many single homeless people sleep outdoors. One hundred and forty six patients were seen with illnesses ranging from scabies to osteomyelitis and tuberculosis. Sociodemographic data showed the patients to be generally an isolated group with deprived and unstable backgrounds, often compounded by alcohol abuse. Over a third of the patients from one site attended a drop in surgery for homeless people in Soho within a month after seeing a doctor in the mobile surgery. This suggests that the project can be a first step in integrating this isolated group with health care facilities.