Effects of Prairie Dogs and Cattle on Vegetation Disappearance on Prairie Dog Towns in Mixed-Grass Prairie

Quantitative data is lacking on competition between prairie dogs and cattle for forage on mixed-grass prairie pastures. The objective of this study was to determine the disappearance of vegetation attributable to cattle and prairie dogs on pastures with prairie dog towns. During the summers of 2002 and 2003, biomass estimates were made periodically on three mixed-grass prairie pastures in south central South Dakota that had varying degrees of prairie dog town coverage (percent of pasture area). Two types of grazing exclosures were established. Cattle exclosures allowed grazing by prairie dogs only. Cattle/prairie dog exclosures excluded both herbivores. Permanent plots outside cages were established that allowed grazing by both species. Biomass estimates on individual vegetation species were obtained both inside the exclosures and on permanent plots outside the exclosures two times in 2002 and 2003. Forage removed was estimated and compared for cattle alone, prairie dogs alone, and cattle and prairie dogs together in each year. Forage removed by prairie dogs on the on-town sites was nearly three times as great as forage removed by cattle on the on-town sites for the June and July sampling periods. Cattle removed two times more forage on off-town sites than on on-town sites. Total forage removed on on-town sites (cattle + prairie dogs) was almost two times greater than on off-town sites. Livestock forage was significantly reduced on prairie dog towns compared to unoccupied sites. Classic carrying capacity calculations overestimate forage availability when prairie dog towns are present. Stocking rates on pastures with prairie dog towns should be adjusted to account for forage disappearance due to prairie dogs

Large-scale exome sequencing study implicates both developmental and functional changes in the neurobiology of autism

Summary We present the largest exome sequencing study of autism spectrum disorder (ASD) to date (n=35,584 total samples, 11,986 with ASD). Using an enhanced Bayesian framework to integrate de novo and case-control rare variation, we identify 102 risk genes at a false discovery rate ≤ 0.1. Of these genes, 49 show higher frequencies of disruptive de novo variants in individuals ascertained for severe neurodevelopmental delay, while 53 show higher frequencies in individuals ascertained for ASD; comparing ASD cases with mutations in these groups reveals phenotypic differences. Expressed early in brain development, most of the risk genes have roles in regulation of gene expression or neuronal communication (i.e., mutations effect neurodevelopmental and neurophysiological changes), and 13 fall within loci recurrently hit by copy number variants. In human cortex single-cell gene expression data, expression of risk genes is enriched in both excitatory and inhibitory neuronal lineages, consistent with multiple paths to an excitatory/inhibitory imbalance underlying ASD

Large-scale exome sequencing study implicates both developmental and functional changes in the neurobiology of autism

We present the largest exome sequencing study of autism spectrum disorder (ASD) to date (n = 35,584 total samples, 11,986 with ASD). Using an enhanced analytical framework to integrate de novo and case-control rare variation, we identify 102 risk genes at a false discovery rate of 0.1 or less. Of these genes, 49 show higher frequencies of disruptive de novo variants in individuals ascertained to have severe neuro-developmental delay, whereas 53 show higher frequencies in individuals ascertained to have ASD; comparing ASD cases with mutations in these groups reveals phenotypic differences. Expressed early in brain development, most risk genes have roles in regulation of gene expression or neuronal communication (i.e., mutations effect neurodevelopmental and neurophysiological changes), and 13 fall within loci recurrently hit by copy number variants. In cells from the human cortex, expression of risk genes is enriched in excitatory and inhibitory neuronal lineages, consistent with multiple paths to an excitatory-inhibitory imbalance underlying ASD