From plant neighbourhood to landscape scales: how grazing modifies native and exotic plant species richness in grassland

The interactive effect of grazing and soil resources on plant species richness and coexistence has been predicted to vary across spatial scales. When resources are not limiting, grazing should reduce competitive effects and increase colonisation and richness at fine scales. However, at broad scales richness is predicted to decline due to loss of grazing intolerant species. We examined these hypotheses in grasslands of southern Australia that varied in resources and ungulate grazing intensity since farming commenced 170 years ago. Fine-scale species richness was slightly greater in more intensively grazed upper slope sites with high nutrients but low water supply compared to those that were moderately grazed, largely due to a greater abundance of exotic species. At broader scales, exotic species richness declined with increasing grazing intensity whether nutrients or water supply were low or high. Native species richness declined at all scales in response to increasing grazing intensity and greater resource supply. Grazing also reduced fine-scale heterogeneity in native species richness and although exotics were also characterised by greater heterogeneity at fine scales, grazing effects varied across scales. In these grasslands patterns of plant species richness did not match predictions at all scales and this is likely to be due to differing responses of native and exotic species and their relative abundance in the regional species pool. Over the past 170 years intolerant native species have been eliminated from areas that are continually and heavily grazed, whereas transient, light grazing increases richness of both exotics and natives. The results support the observation that the processes and scales at which they operate differ between coevolved ungulate—grassland systems and those in transition due to recent invasion of herbivores and associated plant species.     

Geographic Tools for Eradication Programs of Insular Non-native Mammals

Non-native mammals are major drivers of ecosystem change and biodiversity loss; this is especially apparent on islands. However, techniques exist to remove non-native mammals, providing a powerful conservation tool. Conservation practitioners are now targeting larger islands for restoration. Leveraging existing and developing new techniques and technologies will prove critical to successful eradications on large islands. Using the removal of introduced goats (Capra hircus) from Santiago Island, Galápagos as a case study, we present a suite of Geographic Information System (GIS) tools that aid island conservation actions. GIS tools were incorporated into the three phases of the eradication campaign: planning, hunting, and monitoring. Further, these tools were adopted for three eradication techniques: ground-based hunting, aerial hunting by helicopter, and Judas goats. These geographic approaches provide a foundation for statistical, spatial, and economic analyses that should increase the capability and efficiency of removal campaigns. Given limited conservation funds and the dire status of many insular species, efficiently removing non-native mammals from islands is of paramount global conservation importance.     

High Fat Diet Increases [3H] Flunitrazepam Binding in the Mouse Brain that is Dependent on the Expression of the Dopamine D2 Gene

Neurochemical Research - Dopamine is an important neuromodulator in the brain that binds to dopamine D1-like receptors (D1, D5) as well as dopamine D2-like receptors (D2, D3, D4). The D2 receptor...     

CHARMM-GUI HMMM Builder for Membrane Simulations with the Highly Mobile Membrane-Mimetic Model

Slow diffusion of the lipids in conventional all-atom simulations of membrane systems makes it difficult to sample large rearrangements of lipids and protein-lipid interactions. Recently, Tajkhorshid and co-workers developed the highly mobile membrane-mimetic (HMMM) model with accelerated lipid motion by replacing the lipid tails with small organic molecules. The HMMM model provides accelerated lipid diffusion by one to two orders of magnitude, and is particularly useful in studying membrane-protein associations. However, building an HMMM simulation system is not easy, as it requires sophisticated treatment of the lipid tails. In this study, we have developed CHARMM-GUI HMMM Builder (http://www.charmm-gui.org/input/hmmm) to provide users with ready-to-go input files for simulating HMMM membrane systems with/without proteins. Various lipid-only and protein-lipid systems are simulated to validate the qualities of the systems generated by HMMM Builder with focus on the basic properties and advantages of the HMMM model. HMMM Builder supports all lipid types available in CHARMM-GUI and also provides a module to convert back and forth between an HMMM membrane and a full-length membrane. We expect HMMM Builder to be a useful tool in studying membrane systems with enhanced lipid diffusion.     

cGMP/Protein Kinase G Signaling Suppresses Inositol 1,4,5-Trisphosphate Receptor Phosphorylation and Promotes Endoplasmic Reticulum Stress in Photoreceptors of Cyclic Nucleotide-gated Channel-deficient Mice

Photoreceptor cyclic nucleotide-gated (CNG) channels play a pivotal role in phototransduction. Mutations in the cone CNG channel subunits CNGA3 and CNGB3 are associated with achromatopsia and cone dystrophies. We have shown endoplasmic reticulum (ER) stress-associated apoptotic cone death and increased phosphorylation of the ER Ca²⁺ channel inositol 1,4,5-trisphosphate receptor 1 (IP₃R1) in CNG channel-deficient mice. We also presented a remarkable elevation of cGMP and an increased activity of the cGMP-dependent protein kinase (protein kinase G, PKG) in CNG channel deficiency. This work investigated whether cGMP/PKG signaling regulates ER stress and IP₃R1 phosphorylation in CNG channel-deficient cones. Treatment with PKG inhibitor and deletion of guanylate cyclase-1 (GC1), the enzyme producing cGMP in cones, were used to suppress cGMP/PKG signaling in cone-dominant Cnga3^−/−/Nrl^−/− mice. We found that treatment with PKG inhibitor or deletion of GC1 effectively reduced apoptotic cone death, increased expression levels of cone proteins, and decreased activation of Müller glial cells. Furthermore, we observed significantly increased phosphorylation of IP₃R1 and reduced ER stress. Our findings demonstrate a role of cGMP/PKG signaling in ER stress and ER Ca²⁺ channel regulation and provide insights into the mechanism of cone degeneration in CNG channel deficiency.     

DNA loops generate intracentromere tension in mitosis

The centromere is the DNA locus that dictates kinetochore formation and is visibly apparent as heterochromatin that bridges sister kinetochores in metaphase. Sister centromeres are compacted and held together by cohesin, condensin, and topoisomerase-mediated entanglements until all sister chromosomes bi-orient along the spindle apparatus. The establishment of tension between sister chromatids is essential for quenching a checkpoint kinase signal generated from kinetochores lacking microtubule attachment or tension. How the centromere chromatin spring is organized and functions as a tensiometer is largely unexplored. We have discovered that centromere chromatin loops generate an extensional/poleward force sufficient to release nucleosomes proximal to the spindle axis. This study describes how the physical consequences of DNA looping directly underlie the biological mechanism for sister centromere separation and the spring-like properties of the centromere in mitosis.     

Changes in growth and maturation parameters of Pacific sardine Sardinops sagax collected off California during a period of stock recovery from 1994 to 2010

Whether fluctuation in density influenced the growth and maturation variables of three aggregated cohorts (fish born during the 1986–1993, 1996–2003 and 2004–2008 periods) of Pacific sardine Sardinops sagax caeruleus collected off the Californian coast from 2004 to 2010 was investigated. Using a von Bertalanffy mixed‐effects model with aggregated cohorts as covariates, estimated growth rate significantly covaried with aggregated cohorts. Growth rate (K) was modelled as a fixed effect and estimated to be 0·264 ± 0·015 (±s.e ). Statistical contrasts among aggregated cohorts showed that the 1996–2003 cohorts had a significantly lower growth rate than the other two aggregated cohorts. The theoretical age at length zero (t₀) and the standard length at infinity (L_S∞) were modelled as random effects, and were estimated to be ?2·885 ± 0·259 (±s.e ) and 273·13 ± 6·533 mm (±s.e ). The relation of ovary‐free mass at length was significantly different among the three aggregated cohorts, with the allometric coefficient estimated to be 2·850 ± 0·013 (±s.e ) for the S. sagax population. The age‐at‐length trajectory of S. sagax born between 1986 and 2008 showed strong density dependence effects on somatic growth rates. In contrast to the density‐dependent nature of growth, the probability to be mature at‐size or at‐age was not significantly affected by aggregated cohort density. The size and the age‐at‐50% maturity were estimated to be 150·92 mm and 0·56 years, respectively. Stock migration, natural fluctuations in biomass and removal of older and larger S. sagax by fishing might have been interplaying factors controlling growth parameters during 1986–2010.     

Loss of Core 1-derived O-Glycans Decreases Breast Cancer Development in Mice

Mucin-type core 1-derived O-glycans, one of the major types of O-glycans, are highly expressed in mammary gland epithelium. Abnormal O-glycans such as Tn antigen are found in over 90% of breast cancers; however, the in vivo role of these aberrant O-glycans in the etiology of breast cancer is unclear. We generated mice with mammary epithelial specific deletion of core 1-derived O-glycans. By crossing with two spontaneous mouse breast cancer models, we determined that loss of core 1-derived O-glycans delays the onset and progression of breast cancer development. Deficiency of core 1 O-glycosylation impaired the localization of Muc1, a major O-glycoprotein, on the apical surfaces of mammary epithelium. Signaling mediated by Muc1, which is critical for breast cancer development, was also defective in the absence of core 1 O-glycans. This study reveals an unexpected role of core 1-derived O-glycans in breast cancer development in mice.