Suitability of shrub establishment on Wyoming mined lands reclaimed for wildlife habitat

Restoring coal mined land to pre-mining shrub cover, density, height, community composition, and diversity to renew wildlife habitat quality is a priority for reclamation specialists. Long-term shrub reestablishment success on reclaimed mined land in Wyoming and suitability of these lands for wildlife habitat are unknown. Fourteen reclaimed study sites, 10 yr old or older, were selected on 8 mines in Wyoming to evaluate shrub reestablishment and wildlife habitat value for antelope ( Antilocapra americana ) and sage grouse ( Centrocercus urophasianus ). Five sites were categorized as fourwing saltbush ( Atriplex canescens ) sites and 9 as fourwing saltbush/big sagebrush ( A. canescens/Artemisia tridentata spp. wyomingensis ) sites. Published data describing antelope and sage grouse-preferred habitat requirements in sagebrush-grassland steppe ecosystems were used to evaluate shrub community value of sampled sites for wildlife habitat. Mean shrub canopy cover, density, and height for fourwing saltbush sites were 5.8%, 0.23 m -2 , and 41.6 cm, respectively, compared to 5.6%, 0.61 m -2 , and 31.1 cm for fourwing saltbush/big sagebrush sites. Two fourwing saltbush and 4 fourwing saltbush/big sagebrush sites provided sufficient cover for antelope, while 2 fourwing saltbush and 4 fourwing saltbush/big sagebrush sites were adequate for sage grouse. Only 1 fourwing saltbush/big sagebrush site provided high enough shrub densities for sage grouse. One fourwing saltbush and 7 fourwing saltbush/big sagebrush sites provided ample shrub heights for antelope, while 1 fourwing saltbush and 8 fourwing saltbush/big sagebrush sites were sufficient for sage grouse. One fourwing saltbush and 1 fourwing saltbush/big sagebrush site provided enough grass, forb, and shrub composition for antelope, while no site in either reclamation type was satisfactory for sage grouse. Shrub diversity was 3 times higher for fourwing saltbush/big sagebrush sites (0.984) than for fourwing saltbush sites (0.328). Individually, sites seeded with multiple shrub species had higher canopy cover, density, and diversity compared with single-species shrub seedings. Achieving premining shrub cover, density, height, community composition, and diversity within existing bond-release time frames is unrealistic, considering that some native shrublands require 30-60 yr to reach maturity.     

Comparison of the epiproct structure of two closely related species, Sweltsa fidelis (Banks) and S. revelstoka (Jewett) (Plecoptera: Chloroperlidae)

The male epiprocts of 2 closely related western Nearctic species, Sweltsa fidelis (Banks) and S. revelstoka (Jewett), were examined using SEM. The males of these 2 species have been historically distinguished by epiproct measurements. The ratio of the length of the base to greatest width versus total epiproct length ranges from 0.49 μm to 0.67 μm (￣ x = 0.56) in S. fidelis and 0.55 μm to 0.69 μm (￣ x = 0.60) in S. revelstoka . Similarities in measurement suggest that the location of the greatest epiproct width is not a reliable and consistent character for distinguishing males of these 2 species.     

Drosophila Piwi functions in Hsp90-mediated suppression of phenotypic variation

Canalization, also known as developmental robustness, describes an organism's ability to produce the same phenotype despite genotypic variations and environmental influences. In Drosophila, Hsp90, the trithorax-group proteins and transposon silencing have been previously implicated in canalization. Despite this, the molecular mechanism underlying canalization remains elusive. Here using a Drosophila eye-outgrowth assay sensitized by the dominant Kr(irregular facets-1)(Kr(If-1)) allele, we show that the Piwi-interacting RNA (piRNA) pathway, but not the short interfering RNA or micro RNA pathway, is involved in canalization. Furthermore, we isolated a protein complex composed of Hsp90, Piwi and Hop, the Hsp70/Hsp90 organizing protein homolog, and we demonstrated the function of this complex in canalization. Our data indicate that Hsp90 and Hop regulate the piRNA pathway through Piwi to mediate canalization. Moreover, they point to epigenetic silencing of the expression of existing genetic variants and the suppression of transposon-induced new genetic variation as two major mechanisms underlying piRNA pathway-mediated canalization.     

Systematic documentation and analysis of human genetic variation in hemoglobinopathies using the microattribution approach

We developed a series of interrelated locus-specific databases to store all published and unpublished genetic variation related to hemoglobinopathies and thalassemia and implemented microattribution to encourage submission of unpublished observations of genetic variation to these public repositories. A total of 1,941 unique genetic variants in 37 genes, encoding globins and other erythroid proteins, are currently documented in these databases, with reciprocal attribution of microcitations to data contributors. Our project provides the first example of implementing microattribution to incentivise submission of all known genetic variation in a defined system. It has demonstrably increased the reporting of human variants, leading to a comprehensive online resource for systematically describing human genetic variation in the globin genes and other genes contributing to hemoglobinopathies and thalassemias. The principles established here will serve as a model for other systems and for the analysis of other common and/or complex human genetic diseases.     

Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease

The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3). Both joint analysis and meta-analysis approaches were used. We obtained genome-wide significant results at MS4A4A (rs4938933; stages 1 and 2, meta-analysis P (P(M)) = 1.7 × 10(-9), joint analysis P (P(J)) = 1.7 × 10(-9); stages 1, 2 and 3, P(M) = 8.2 × 10(-12)), CD2AP (rs9349407; stages 1, 2 and 3, P(M) = 8.6 × 10(-9)), EPHA1 (rs11767557; stages 1, 2 and 3, P(M) = 6.0 × 10(-10)) and CD33 (rs3865444; stages 1, 2 and 3, P(M) = 1.6 × 10(-9)). We also replicated previous associations at CR1 (rs6701713; P(M) = 4.6 × 10(-10), P(J) = 5.2 × 10(-11)), CLU (rs1532278; P(M) = 8.3 × 10(-8), P(J) = 1.9 × 10(-8)), BIN1 (rs7561528; P(M) = 4.0 × 10(-14), P(J) = 5.2 × 10(-14)) and PICALM (rs561655; P(M) = 7.0 × 10(-11), P(J) = 1.0 × 10(-10)), but not at EXOC3L2, to late-onset Alzheimer's disease susceptibility.     

Genome-wide association study identifies susceptibility loci for open angle glaucoma at TMCO1 and CDKN2B-AS1

We report a genome-wide association study for open-angle glaucoma (OAG) blindness using a discovery cohort of 590 individuals with severe visual field loss (cases) and 3,956 controls. We identified associated loci at TMCO1 (rs4656461[G] odds ratio (OR) = 1.68, P = 6.1 × 10(-10)) and CDKN2B-AS1 (rs4977756[A] OR = 1.50, P = 4.7 × 10(-9)). We replicated these associations in an independent cohort of cases with advanced OAG (rs4656461 P = 0.010; rs4977756 P = 0.042) and two additional cohorts of less severe OAG (rs4656461 combined discovery and replication P = 6.00 × 10(-14), OR = 1.51, 95% CI 1.35-1.68; rs4977756 combined P = 1.35 × 10(-14), OR = 1.39, 95% CI 1.28-1.51). We show retinal expression of genes at both loci in human ocular tissues. We also show that CDKN2A and CDKN2B are upregulated in the retina of a rat model of glaucoma.     

Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes

Cardiomyocytes use glucose as well as fatty acids for ATP production. These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. Others, however, have different roles in either GLUT4 or CD36 translocation. These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy.     

MicroRNA-128 downregulates Bax and induces apoptosis in human embryonic kidney cells

MicroRNAs (miRNAs) are short ~21-nt non-coding RNA molecules that have been shown to regulate a number of biological processes. Previous reports have shown that overexpression of miR-128 in glioma cells inhibited cell proliferation. Literature also suggests that miR-128 negatively regulates prostate cancer cell invasion. Here, we show that overexpression of hsa-miR-128, a brain-enriched microRNA, induces apoptosis in HEK293T cells as elucidated by apoptosis assay, cell cycle changes, loss of mitochondrial membrane potential and multicaspase assay. By in silico analysis, we identified a putative target site within the 3′ untranslated region (UTR) of Bax, a proapoptotic member of the apoptosis pathway. We found that ectopic expression of hsa-miR-128 suppressed a luciferase reporter containing the Bax-3′ UTR and reduced the levels of Bax in HEK293T cells. Taken together, our study demonstrates that overexpression of hsa-miR-128 not only induces apoptosis in HEK293T cells but also is an endogenous regulator of Bax protein.