It is important to detect population bottlenecks in threatened and managed species because bottlenecks can increase the risk of population extinction. Early detection is critical and can be facilitated by statistically powerful monitoring programs for detecting bottleneck-induced genetic change. We used Monte Carlo computer simulations to evaluate the power of the following tests for detecting genetic changes caused by a severe reduction in a population's effective size (Ne): a test for loss of heterozygosity, two tests for loss of alleles, two tests for change in the distribution of allele frequencies, and a test for small Ne based on variance in allele frequencies (the 'variance test'). The variance test was most powerful; it provided an 85% probability of detecting a bottleneck of size Ne = 10 when monitoring five microsatellite loci and sampling 30 individuals both before and one generation after the bottleneck. The variance test was almost 10-times more powerful than a commonly used test for loss of heterozygosity, and it allowed for detection of bottlenecks before 5% of a population's heterozygosity had been lost. The second most powerful tests were generally the tests for loss of alleles. However, these tests had reduced power for detecting genetic bottlenecks caused by skewed sex ratios. We provide guidelines for the number of loci and individuals needed to achieve high-power tests when monitoring via the variance test. We also illustrate how the variance test performs when monitoring loci that have widely different allele frequency distributions as observed in five wild populations of mountain sheep (Ovis canadensis).

Fire can cause profound changes in the composition and abundance of plant and animal species, but logistics, unpredictability of weather, and inherent danger make it nearly impossible to study high‐severity fire effects experimentally. We took advantage of a unique opportunity to use a before–after/control–impact (BACI) approach to analyze changes in bird assemblages after the severe fires of 2000 in the Bitterroot Valley, Montana. Observers surveyed birds using 10‐minute point counts and collected vegetation data from 13 burned and 13 unburned transects for five years before fire and three years after fire. We compared changes in vegetation variables and relative bird abundance from before to after fire between the set of points that burned and the set of points that did not burn. The magnitude of change in vegetation variables from before to after fire increased with fire severity. The relative abundances of nine bird species showed significantly greater changes from before to after fire at burned points compared with unburned points. Moreover, when burned points were separated by whether they burned at low, moderate, or high severity, an additional 10 species showed significant changes in relative abundance from before to after fire at one or more severities. Overall, almost twice as many bird species increased as decreased significantly in response to fire. We also found changes in abundance between one year after and two years after fire for most species that responded to fire. Thus, species that have been termed “mixed responders” in the literature appear to be responding differently to different fire severities or different time periods since fire, rather than responding variably to the same fire conditions. These findings underscore the importance of fire severity and time since fire and imply that both factors must be considered to understand the complexities of fire effects on biological communities. Because different bird species responded positively to different fire severities, our results suggest a need to manage public lands for the maintenance of all kinds of fires, not just the low‐severity, understory burns that dominate most discussions revolving around the use of fire in forest restoration.

Natural populations worldwide are increasingly fragmented by habitat loss. Isolation at small population size is thought to reduce individual and population fitness via inbreeding depression. However, little is known about the time-scale over which adverse genetic effects may develop in natural populations or the number and types of traits likely to be affected. The benefits of restoring gene flow to isolates are therefore also largely unknown. In contrast, the potential costs of migration (e.g. disease spread) are readily apparent. Management for ecological connectivity has therefore been controversial and sometimes avoided. Using pedigree and life-history data collected during 25 years of study, we evaluated genetic decline and rescue in a population of bighorn sheep founded by 12 individuals in 1922 and isolated at an average size of 42 animals for 10-12 generations. Immigration was restored experimentally, beginning in 1985. We detected marked improvements in reproduction, survival and five fitness-related traits among descendants of the 15 recent migrants. Trait values were increased by 23-257% in maximally outbred individuals. This is the first demonstration, to our knowledge, of increased male and female fitness attributable to outbreeding realized in a fully competitive natural setting. Our findings suggest that genetic principles deserve broader recognition as practical management tools with near-term consequences for large-mammal conservation.

Summary Background Microparticles (MPs), small vesicles shed from stimulated cells, permit cross-talk between cells within a particular environment. Their composition is thought to reflect their cell of origin, and differs according to whether they are produced by stimulation or by apoptosis. Whether MP properties vary according to stimulus is not yet known. Methods We studied the characteristics of MPs produced from monocytic THP-1 cells upon stimulation with lipopolysaccharide or a soluble P-selectin chimera, using proteomics, flow cytometry, western blotting, and electron microscopy. Results Utilizing a novel criterion of calcein-AM staining to define MPs, we found that MP populations were similar with respect to size, presence and organization of cytoskeleton, and expression of certain antigens. The MPs shared the same level of procoagulant activity. We found that MPs also have distinct characteristics, depending on stimuli. These include differences in phosphatidylserine expression and expression of proteins from specific subcellular locations such as the mitochondria, and of unique antigens such as leukocyte-associated immunoglobin-like-receptor (LAIR)-1, which was found only upon stimulation with the soluble P-selectin chimera. Conclusion We found that the properties of MPs depend on the stimulus that produced them. This supports the concept that monocytic MPs differentially modulate thrombosis, inflammation and immune regulation according to stimulus.

Wnts regulate important intracellular signaling events, and dysregulation of the Wnt pathway has been linked to human disease. Here, we uncover numerous Wnt canonical effectors in human platelets where Wnts, their receptors, and downstream signaling components have not been previously described. We demonstrate that the Wnt3a ligand inhibits platelet adhesion, activation, dense granule secretion, and aggregation. Wnt3a also altered platelet shape change and inhibited the activation of the small GTPase RhoA. In addition, we found the Wnt-␤-catenin signaling pathway to be functional in platelets. Finally, disruption of the Wnt Frizzled 6 receptor in the mouse resulted in a hyperactivatory platelet phenotype and a reduced sensitivity to Wnt3a. Taken together our studies reveal a novel functional role for Wnt signaling in regulating anucleate platelet function and may provide a tractable target for future antiplatelet therapy.Wnt-␤-catenin pathway ͉ integrin ␣IIb␤3 ͉ frizzled 6 knockout mice A nucleate platelets are the principle effectors of haemostasis and are found circulating in a nonadhesive, quiescent state. At sites of vascular damage, platelets adhere to various exposed subendothelial matrix proteins and are activated, converting from a resting, discoid shape into larger, flattened structures with extended pseudopodia (1). Such activated platelets secrete and synthesize further agonists, inflammatory mediators, and vasoactive substances and through conformational changes in their major integrin receptor, ␣IIb␤3, aggregate to other platelets via fibrinogen (Fb) to form a haemostatic plug (2). Aberrant platelet activation can cause pathological thrombus formation, leading to thrombosis and ultimately vessel occlusion and tissue ischemia, the processes underlying myocardial infarction and stroke. Understanding the regulation of platelet activity is thus fundamental to comprehending thrombotic disorders and developing therapeutic strategies.The mammalian Wnt gene family is comprised of 19 secreted Wnt glycoproteins, which play essential roles in cell proliferation, cell-fate determination, and cell-fate differentiation during embryonic development and adult homeostasis (3, 4). These Wnt ligands activate a number of different signaling pathways via distinct receptors and downstream effectors to mediate effects on gene transcription and cell adhesion/migration (5, 6). For the Wnt-␤-catenin (␤-cat) signaling pathway (Fig. 1A), traditionally referred to as the ''canonical'' pathway, Wnts bind to a surface receptor complex comprised of a Frizzled (Fzd) receptor and the Lipoprotein Receptor-related Protein 5/6 (LRP5/6) coreceptor (5, 7). The signal is then transduced to the cytoplasmic protein Dishevelled (Dvl) where downstream pathways regulate the stability of ␤-cat (5, 7). In the absence of Wnt, ␤-cat is phosphorylated by a destruction complex containing Casein Kinase 1 (CK1), Glycogen Synthase Kinase 3␤ (GSK3␤), Axin-1, FRAT-1, and Adenomatous Polyposis Coli (APC), which targets ␤-cat for degradation via ubiquitina...