The Seagrass effect turned upside down changes the prospective of sea urchin survival and landscape implications

Habitat structure plays an important mediating role in predator-prey interactions. However the effects are strongly dependent on regional predator pools, which can drive predation risk in habitats with very similar structure in opposite directions. In the Mediterranean Sea predation on juvenile sea urchins is commonly known to be regulated by seagrass structure. In this study we test whether the possibility for juvenile Paracentrotus lividus to be predated changes in relation to the fragmentation of the seagrass Posidonia oceanica (four habitat classes: continuous, low-fragmentation, high-fragmentation and rocks), and to the spatial arrangement of such habitat classes at a landscape scale. Sea urchin predation risk was measured in a 20-day field experiment on tethered individuals placed in three square areas 35×35 m2 in size. Variability of both landscape and habitat structural attributes was assessed at the sampling grain 5×5 m2. Predation risk changed among landscapes, as it was lower where more ‘rocks’, and thus less seagrass, were present. The higher risk was found in the ‘continuous’ P. oceanica rather than in the low-fragmentation, high-fragmentation and rock habitats (p-values = 0.0149, 0.00008, and 0.0001, respectively). Therefore, the expectation that juvenile P. lividus survival would have been higher in the ‘continuous’ seagrass habitat, which would have served as shelter from high fish predation pressure, was not met. Predation risk changed across habitats due to different success between attack types: benthic attacks (mostly from whelks) were overall much more effective than those due to fish activity, the former type being associated with the ‘continuous’ seagrass habitat. Fish predation on juvenile sea urchins on rocks and ‘high-fragmentation’ habitat was less likely than benthic predation in the ‘continuous’ seagrass, with the low seagrass patch complexity increasing benthic activity. Future research should be aimed at investigating, derived from the complex indirect interactions among species, how top-down control in marine reserves can modify seagrass habitat effects

Impact assessment of fish cages on coralligenous reefs through the use of the STAR sampling procedure

The study aimed at contributing to the development of methods to assessing the effects of human disturbance on coralligenous reefs. The effects of the presence of a fish farm on coralligenous reefs were evaluated using the STAR (STAndaRdized coralligenous evaluation procedure) sampling procedure. An asymmetrical sampling design was used to compare the aquaculture site with two reference sites in areas unaffected by human pressure. The response of different ecological indices (ESCA, Ecological Status of Coralligenous Assemblages; ISLA, Integrated Sensitivity Level of coralligenous Assemblages; COARSE, COralligenous Assessment by Reef Scape Estimate) and descriptors (α-diversity, β-diversity and Sensitivity Level) of this kind of disturbance was compared. Results indicate that coralligenous reefs are vulnerable to aquaculture fish cages, and differences in the structure of coralligenous assemblages between the disturbed and the reference sites were mostly due to the decrease in β-diversity. On the contrary, no significant differences in the number of taxa/groups were highlighted. Encrusting Corallinales, erect Rhodophyta, Dictyotales, Fucales and Halimeda tuna were more abundant in reference sites than in disturbed site, while Peyssonnelia spp. and algal turfs had the opposite trend. Conversely, no significant differences between conditions were found in the abundance of sessile invertebrates. The study supports the suitability of the STAR approach to be employed in impact evaluation assessments, such as in monitoring programs. The present study is a first attempt to combine three different ecological indices (ESCA, ISLA and COARSE) within a unified approach, in order to assess the status of coralligenous reefs subjected to a moderate human-induced disturbance. The inconsistent response of the different indices highlights the advantage of applying different indices and descriptors to evaluate the variable human pressures on natural systems

Immanent conditions determine imminent collapses: nutrient regimes define the resilience of macroalgal communities

Este artículo contiene 9 páginas, 5 figuras.Predicting where state-changing thresholds lie can be inherently complex in ecosystems characterized by nonlinear dynamics. Unpacking the mechanisms underlying these transitions can help considerably reduce this unpredictability. We used empirical observations, field and laboratory experiments, and mathematical models to examine how differences in nutrient regimes mediate the capacity of macrophyte communities to sustain sea urchin grazing. In relatively nutrient-rich conditions, macrophyte systems were more resilient to grazing, shifting to barrens beyond 1 800 g m22 (urchin biomass), more than twice the threshold of nutrient-poor conditions. The mechanisms driving these differences are linked to how nutrients mediate urchin foraging and algal growth: controlled experiments showed that low-nutrient regimes trigger compensatory feeding and reduce plant growth, mechanisms supported by our consumer–resource model. These mechanisms act together to halve macrophyte community resilience. Our study demonstrates that by mediating the underlying drivers, inherent conditions can strongly influence the buffer capacity of nonlinear systems.The Spanish Ministry of Science and Innovation funded this research (projects CMT2010-22273-C02-01-02 and CMT2013- 48027-C03-R) and supported J.B. (scholarship BES-2011-043630) and D.A. (Ramon y Cajal fellowship). The Spanish National Research Council supported R.A.’s visitorship (CSIC-201330E062).Peer reviewe

K562 cell proliferation is modulated by PLCβ1 through a PKCα-mediated pathway

Phospholipase C β1 (PLCβ1) is known to play an important role in cell proliferation. Previous studies reported aninvolvement of PLCβ1 in G0-G1/S transition and G2/M progression in Friend murine erythroleukemia cells (FELC). However,little has been found about its role in human models. Here, we used K562 cell line as human homologous of FELC inorder to investigate the possible key regulatory role of PLCβ1 during cell proliferation of this humancell line. Our studies on the effects of the overexpression of both these isoforms showed a specific and positive connection between cyclinD3 and PLCβ1 in K562 cells, which led to a prolonged S phase of the cell cycle and a delay in cell proliferation. In order to shed light on this mechanism, we decided to study the possible involvement of protein kinases C (PKC), known to be direct targets of PLC signaling and important regulators of cell proliferation. Our data showed a peculiar decrease of PKCα levels in cells overexpressing PLCβ1. Moreover, when we silenced PKCα, by RNAi technique, in order to mimic the effects of PLCβ1, we caused the same upregulation of cyclin D3 levels and the same decrease of cell proliferation found in PLCβ1-overexpressing cells. The key features emerging from our studies in K562 cells is that PLCβ1 targets cyclin D3, likely through a PKCα-mediated-pathway, and that, as a downstream effect of its activity, K562 cells undergo an accumulation in the S phase of the cell cycle

PI3Kα-selective inhibitor alpelisib (BYL719), may be effective as anticancer agents in Rhabdomyosarcoma

Rhabdomyosarcoma (RMS) is a highly malignant and metastatic pediatric cancer that arises from the skeletal muscle. Recent studies have identified an important role of AKT signaling in RMS progression. This suggests targeting components of the PI3K/Akt pathway may be an effective therapeutic strategy. Here, we investigated the in vitro activity of the class I PI3K inhibitors [1] in human rhabdomyosarcoma cell lines (embryonal rhabdomyosarcoma RD and A204, alveolar rhabdomyosarcoma SJCRH30). We used a panel of four compounds which specifically target PI3K isoforms including the PI3Kα-selective (p110α ) inhibitor alpelisib BYL719, currently in clinical development by Novartis Oncology, the p110β TGX-221 inhibitor, the p110γ CZC24832, the p110δ CAL-101inhibitor and the dual p110α/p110δ inhibitor AZD8835. The effects of single drugs and of several drug combinations were analyzed to assess cytotoxicity by MTT assays, cell cycle by flow cytometry , apoptosis by caspase 3/7 assay and Western blot, as well as the phosphorylation status of the pathway. BYL719 treatment resulted in G1 phase cell cycle arrest and apoptosis. BYL719 administered in combination with CAL-101, for 48 h and 72h, decreased cell viability and induced apoptosis in a marked synergistic manner. Taken together, our findings indicate that BYL719, either alone or in combination with p110δ CAL-101inhibitor, may be an efficient treatment for human rhabdomyosarcoma cells that have aberrant upregulation of the PI3K signaling pathway for their proliferation and survival

Modeling macroalgal forest distribution at Mediterranean scale : present status, drivers of changes and insights for conservation and management

Macroalgal forests are one of the most productive and valuable marine ecosystems, but yet strongly exposed to fragmentation and loss. Detailed large-scale information on their distribution is largely lacking, hindering conservation initiatives. In this study, a systematic effort to combine spatial data on Cystoseira C. Agardh canopies (Fucales, Phaeophyta) was carried out to develop a Habitat Suitability Model (HSM) at Mediterranean scale, providing critical tools to improve site prioritization for their management, restoration and protection. A georeferenced database on the occurrence of 20 Cystoseira species was produced collecting all the available information from published and grey literature, web data portals and co-authors personal data. Data were associated to 55 predictor variable layers in the (ASCII) raster format and were used in order to develop the HSM by means of a Random Forest, a very effective Machine Learning technique. Knowledge about the distribution of Cystoseira canopies was available for about the 14% of the Mediterranean coastline. Absence data were available only for the 2% of the basin. Despite these gaps, our HSM showed high accuracy levels in reproducing Cystoseira distribution so that the first continuous maps of the habitat across the entire basin was produced. Misclassification errors mainly occurred in the eastern and southern part of the basin, where large gaps of knowledge emerged. The most relevant drivers were the geomorphological ones, followed by anthropogenic variables proxies of pollution and urbanization. Our model shows the importance of data sharing to combine a large number of spatial and environmental data, allowing to individuate areas with high probability of Cystoseira occurrence as suitable for its presence. This approach encourages the use of this modeling tool for the prediction of Cystoseira distribution and for supporting and planning conservation and management initiatives. The step forward is to refine the spatial information of presence-absence data about Cystoseira canopies and of environmental predictors in order to address species-specific assessments.peer-reviewe

A Mediterranean Diet Mix Has Chemopreventive Effects in a Murine Model of Colorectal Cancer Modulating Apoptosis and the Gut Microbiota

Objectives: Unhealthy dietary patterns have been associated with colorectal cancer (CRC) onset while Mediterranean Diet (MD) has been proposed for CRC prevention. This study evaluated the effect of a Mediterranean Diet Mix (MD-MIX) on colonic tumors development in A/J mice fed a low-fat (LFD) or a high-fat western diet (HFWD), and injected with the procarcinogen azoxymethane (AOM).Materials and Methods: Forty A/J male mice were randomly assigned into four feeding arms (10 mice/arm; LFD, LFD-MD-MIX, HFWD, HFWD-MD-MIX) to be treated with AOM. Ten mice were exposed to the diets alone (Healthy LFD and Healthy HFWD) to be used as control. Tumor incidence and multiplicity were evaluated at sacrifice. Mucosal fatty acid content and urinary phenolic compounds were assayed by mass spectrometry. Apoptosis was evaluated by TUNEL assay and gene expression markers. Cell proliferation was evaluated by Ki67 immunohistochemistry. Microbiota composition was assessed at different time points by 16S RNA sequencing.Results: A tumor incidence of 100% was obtained in AOM-treated mice. The MD-MIX supplementation was able to reduce the number of colonic lesions in both LFD and HFWD-fed mice and to induce apoptosis, in particular in the LFD-MD-MIX arm. Moreover, a preventive effect on low-grade dysplasia and macroscopical lesions (>1 mm) development was found in HFWD-fed mice together with a regulation of the AOM-driven intestinal dysbiosis.Conclusions: MD-MIX was able to counteract CRC development in mice under different dietary backgrounds through the regulation of apoptosis and gut microbiota

Epigenetic regulation of Delta-Like1 controls Notch1 activation in gastric cancer

The Notch signaling pathway drives proliferation, differentiation, apoptosis, cell fate, and maintenance of stem cells in several tissues. Aberrant activation of Notch signaling has been described in several tumours and in gastric cancer (GC), activated Notch1 has been associated with de-differentiation of lineage-committed stomach cells into stem progenitors and GC progression. However, the specific role of the Notch1 ligand (DLL1) in GC has not yet been elucidated. To assess the role of DLL1 in GC cancer, the expression of Notch1 and its ligands DLL1 and Jagged1, was analyzed in 8 gastric cancer cell lines (KATOIII, SNU601, SNU719, AGS, SNU16, MKN1, MKN45, TMK1). DLL1 expression was absent in KATOIII, SNU601, SNU719 and AGS. The lack of DLL1 expression in these cells was associated with promoter hypermethylation and 5-aza-2’deoxycitidine caused up-regulation of DLL1. The increase in DLL1 expression was associated with activation of Notch1 signalling, with an increase in cleaved Notch1 intracellular domain (NICD) and Hes1, and down-regulation in Hath1. Concordantly, Notch1 signalling was activated with the overexpression of DLL1. Moreover, Notch1 signalling together with DLL1 methylation were evaluated in samples from 52 GC patients and 21 healthy control as well as in INS-GAS mice infected with H. pylori and randomly treated with eradication therapy. In GC patients, we found a correlation between DLL1 and Hes1 expression, while DLL1 methylation and Hath1 expression were associated with the diffuse and mixed type of gastric cancer. Finally, none of the samples from INS-GAS mice infected with H. pylori, a model of intestinal-type gastric tumorigenesis, showed promoter methylation of DLL1. This study shows that Notch1 activity in gastric cancer is controlled by the epigenetic silencing of the ligand DLL1, and that Notch1 inhibition is associated with the diffuse type of gastric cancer