From topography to hydrology—The modifiable area unit problem impacts freshwater species distribution models

Species distribution models (SDMs) are statistical tools to identify potentially suitable habitats for species. For SDMs in river ecosystems, species occurrences and predictor data are often aggregated across subcatchments that serve as modeling units. The level of aggregation (i.e., model resolution) influences the statistical relationships between species occurrences and environmental predictors—a phenomenon known as the modifiable area unit problem (MAUP), making model outputs directly contingent on the model resolution. Here, we test how model performance, predictor importance, and the spatial congruence of species predictions depend on the model resolution (i.e., average subcatchment size) of SDMs. We modeled the potential habitat suitability of 50 native fish species in the upper Danube catchment at 10 different model resolutions. Model resolutions were derived using a 90‐m digital‐elevation model by using the GRASS‐GIS module r.watershed. Here, we decreased the average subcatchment size gradually from 632 to 2 km². We then ran ensemble SDMs based on five algorithms using topographical, climatic, hydrological, and land‐use predictors for each species and resolution. Model evaluation scores were consistently high, as sensitivity and True Skill Statistic values ranged from 86.1–93.2 and 0.61–0.73, respectively. The most contributing predictor changed from topography at coarse, to hydrology at fine resolutions. Climate predictors played an intermediate role for all resolutions, while land use was of little importance. Regarding the predicted habitat suitability, we identified a spatial filtering from coarse to intermediate resolutions. The predicted habitat suitability within a coarse resolution was not ported to all smaller, nested subcatchments, but only to a fraction that held the suitable environmental conditions. Across finer resolutions, the mapped predictions were spatially congruent without such filter effect. We show that freshwater SDM predictions can have consistently high evaluation scores while mapped predictions differ significantly and are highly contingent on the underlying subcatchment size. We encourage building freshwater SDMs across multiple catchment sizes, to assess model variability and uncertainties in model outcomes emerging from the MAUP.     

The common hepatic branch of the vagus is not required to mediate the glycemic and food intake suppressive effects of glucagon-like-peptide-1

The incretin and food intake suppressive effects of intraperitoneally administered glucagon-like peptide-1 (GLP-1) involve activation of GLP-1 receptors (GLP-1R) expressed on vagal afferent fiber terminals. Central nervous system processing of GLP-1R-driven vagal afferents results in satiation signaling and enhanced insulin secretion from pancreatic-projecting vagal efferents. As the vast majority of endogenous GLP-1 is released from intestinal l-cells following ingestion, it stands to reason that paracrine GLP-1 signaling, activating adjacent GLP-1R expressed on vagal afferent fibers of gastrointestinal origin, contributes to glycemic and food intake control. However, systemic GLP-1R-mediated control of glycemia is currently attributed to endocrine action involving GLP-1R expressed in the hepatoportal bed on terminals of the common hepatic branch of the vagus (CHB). Here, we examine the hypothesis that activation of GLP-1R expressed on the CHB is not required for GLP-1's glycemic and intake suppressive effects, but rather paracrine signaling on non-CHB vagal afferents is required to mediate GLP-1's effects. Selective CHB ablation (CHBX), complete subdiaphragmatic vagal deafferentation (SDA), and surgical control rats received an oral glucose tolerance test (2.0 g glucose/kg) 10 min after an intraperitoneal injection of the GLP-1R antagonist, exendin-(9-39) (Ex-9; 0.5 mg/kg) or vehicle. CHBX and control rats showed comparable increases in blood glucose following blockade of GLP-1R by Ex-9, whereas SDA rats failed to show a GLP-1R-mediated incretin response. Furthermore, GLP-1(7-36) (0.5 mg/kg ip) produced a comparable suppression of 1-h 25% glucose intake in both CHBX and control rats, whereas intake suppression in SDA rats was blunted. These findings support the hypothesis that systemic GLP-1R mediation of glycemic control and food intake suppression involves paracrine-like signaling on GLP-1R expressed on vagal afferent fibers of gastrointestinal origin but does not require the CHB.     

Is the 6 kDa tobacco etch viral protein a bona fide ERES marker?

The claim that the 6 kDa viral protein (VP) of Tobacco Etch Virus is a marker for ER exit sites (ERES) has been investigated. When transiently expressed as a CFP tagged fusion construct in tobacco mesophyll protoplasts, this integral membrane protein co-localizes with both the COPII coat protein YFP-SEC24 and the Golgi marker Man1-RFP. However, when over-expressed the VP locates to larger spherical structures which co-localize with neither ER nor Golgi markers. Nevertheless, deletion of the COPII interactive N-terminal D(X)E motif causes it to be broadly distributed throughout the ER, supporting the notion that this protein could be an ERES marker. Curiously, whereas brefeldin A (BFA) caused a typical Golgi-stack response (redistribution into the ER) of the VP in leaf epidermal cells, in protoplasts it resulted in the formation of structures identical to those formed by over-expression. However, anomalous results were obtained with protoplasts: when co-expressed with the non-cycling cis-Golgi marker Man1-RFP, a BFA-induced redistribution of the VP-CFP signal into the ER was observed, but, in the presence of the cycling Golgi marker ERD2-YFP, this did not occur. High resolution images of side-on views of Golgi stacks in epidermal cells showed that the 6 kDa VP-CFP signal overlapped considerably more with YFP-SEC24 than with Man1-RFP, indicating that the VP is proportionately more associated with ERES. However, based on a consideration of the structure of its cytoplasmic tail, the scenario that the VP collects at ERES and is transported to the cis-Golgi before being recycled back to the ER, is supported.     

1-Butanol targets the Golgi apparatus in tobacco BY-2 cells, but in a different way to Brefeldin A

The effects of 1-butanol on the organelles of the early secretory pathway in tobacco BY-2 cells have been examined, because this primary alcohol is known to interfere with phospholipase D an enzyme whose activity contributes to COPI-vesicle formation. Since the fungal lactone Brefeldin A (BFA) also prevents COPI-vesicle production by the Golgi apparatus, the sequential and simultaneous application of these two inhibitors was also investigated. 1-Butanol, but not 2-butanol caused rapid changes in the morphology of the BY-2 Golgi apparatus resulting in extended curved cisternae. By contrast with BFA-treated cells, ER cisternae did not attach laterally to these structures, and ER-Golgi fusion hybrids were not obtained with 1-butanol. However, immunofluorescence microscopy revealed that 1-butanol, like BFA, elicited the release of the GTPase ARF1 from Golgi membranes. Washing out the butanol resulted in re-attachment of ARF1 and a recovery of Golgi stack morphology. BY-2 cells treated sequentially with 1-butanol then BFA (each 30 min), did not reveal any BFA-typical changes in Golgi structure. Cells treated first with BFA, then 1-butanol retained the typical ER-Golgi sandwich morphology induced by BFA, but were larger. When 1-butanol and BFA were added together (for a 30 min period), even larger Golgi aggregates were formed with, again, no ER attachments. Thus, although both inhibitors had the Golgi apparatus as their principle cytological target and both interfere with coatomer attachment, they differ in their ability to induce an interaction with the ER.     

Chromosome-breakage genomic instability and chromothripsis in breast cancer

Background

Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome.

Results

We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers.

Conclusions

Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.

Electronic supplementary material

The online version of this article (doi:10.1186/1471-2164-15-579) contains supplementary material, which is available to authorized users.     

Development and characterization of highly polymorphic long TC repeat microsatellite markers for genetic analysis of peanut

Background

The immune system has paradoxical roles during cancer development and the prognostic significance of immune modulating factors is controversial. The aim of this study was to determine the expression of cyclooxygenase 2 (COX-2), transforming growth factor-beta (TGF- beta), interleukin-10 (IL-10) and their prognostic significance in breast cancers. Ki67 was included as a measure of growth fraction of tumor cells.

Methods

On immunohistochemical stained slides from 38 breast cancer patients, we performed digital video analysis of tumor cell areas and adjacent tumor stromal areas from the primary tumors and their corresponding lymph node metastases. COX-2 was recorded as graded staining intensity.

Results

The expression of TGF-beta, IL-10 and Ki67 were recorded in tumor cell areas and adjacent tumor stromal areas. In both primary tumors and metastases, the expression of COX-2 was higher in the tumor stromal areas than in the tumor cell areas (both P < 0.001). High stromal staining intensity in the primary tumors was associated with a 3.9 (95% CI 1.1-14.2) times higher risk of death compared to the low staining group (P = 0.036). The expression of TGF-beta was highest in the tumor cell areas of both primary tumors and metastases (both P < 0.001). High stromal expression of TGF-beta was associated with increased mortality. For IL-10, the stromal expression was highest in the primary tumors (P < 0.001), whereas in the metastases the expression was highest in tumor cell areas (P < 0.001). High IL-10 expression in tumor- and stromal cell areas of primary tumors predicted mortality. Ki67 was higher expressed in tumor stromal areas of the metastases, and in tumor cell areas of the primary tumors (P < 0.001). Ki67 expression in tumor cell areas and stromal areas of the metastases was independently associated with breast cancer mortality.

Conclusions

Stromal expression of COX-2, TGF-beta and Ki67 may facilitate tumor progression in breast cancer.     

The role of timing, duration, and frequency of inundation in controlling leaf litter decomposition in a river-floodplain ecosystem (Tagliamento, northeastern Italy)

Despite growing recognition of the importance of a natural flow regime in river-floodplain systems, researchers struggle to quantify ecosystem responses to altered hydrological regimes. How do frequency, timing, and duration of inundation affect fundamental ecosystem processes such as leaf litter decomposition? Along the semi-natural Tagliamento River corridor, located in northeastern Italy, we employed in situ experiments to separate effects of different inundation components on breakdown rates of black poplar (Populus nigra). We used a litter-bag method with two different mesh sizes to investigate how fungi and macroinvertebrates influence leaf breakdown rates. Ten treatments, each representing a specific combination of duration and frequency of inundation, were deployed in two seasons (summer, winter) to mimic complex inundation patterns. After 30 days of exposure, mean percentage of remaining leaf litter (ash free dry mass) ranged between 51% (permanent wet) and 88% (permanent dry). Leaf breakdown was significantly faster in winter than in summer. Duration of inundation was the main inundation component that controlled leaf breakdown rates. Leaf-shredding macroinvertebrates played only a role in the permanent wet treatment. Fungal parameters explained the faster leaf breakdown in winter. Our study suggests that modifications of the inundation regime will directly modify established decomposition processes. Factors reducing duration of inundation will decelerate leaf breakdown rates, whereas a decrease in flow variation will reduce leaf breakdown heterogeneity.     

Role of auxin in regulating Arabidopsis flower development

To elucidate the role of auxin in flower morphogenesis, its distribution patterns were studied during flower development in Arabidopsis thaliana (L.) Heynh. Expression of DR5::GUS was regarded to reflect sites of free auxin, while immunolocalization with auxin polyclonal antibodies visualized conjugated auxin distribution. The youngest flower bud was loaded with conjugated auxin. During development, the apparent concentration of free auxin increased in gradual patterns starting at the floral-organ tip. Anthers are major sites of high concentrations of free auxin that retard the development of neighboring floral organs in both the acropetal and basipetal directions. The IAA-producing anthers synchronize flower development by retarding petal development and nectary gland activity almost up to anthesis. Tapetum cells of young anthers contain free IAA which accumulates in pollen grains, suggesting that auxin promotes pollen-tube growth towards the ovules. High amounts of free auxin in the stigma induce a wide xylem fan immediately beneath it. After fertilization, the developing embryos and seeds show elevated concentrations of auxin, which establish their axial polarity. This developmental pattern of auxin production during floral-bud development suggests that young organs which produce high concentrations of free IAA inhibit or retard organ-primordium initiation and development at the shoot tip. Electronic Supplementary Material Supplementary material is available for this article at This paper is dedicated to Orna Aloni for continuous support and management over many years.