Bonelli's Eagle Hieraaetus fasciatus juvenile dispersal: hourly and daily movements tracked by GPS

Capsule Birds cover daily distances not normally exceeding 20 km during the initial phase of dispersal, with the daily peak of movement/activity in the afternoon.     

Axon targeting of the alpha 7 nicotinic receptor in developing hippocampal neurons by Gprin1 regulates growth

Cholinergic signaling plays an important role in regulating the growth and regeneration of axons in the nervous system. The α7 nicotinic receptor (α7) can drive synaptic development and plasticity in the hippocampus. Here, we show that activation of α7 significantly reduces axon growth in hippocampal neurons by coupling to G protein‐regulated inducer of neurite outgrowth 1 (Gprin1), which targets it to the growth cone. Knockdown of Gprin1 expression using RNAi is found sufficient to abolish the localization and calcium signaling of α7 at the growth cone. In addition, an α7/Gprin1 interaction appears intimately linked to a Gαo, growth‐associated protein 43, and CDC42 cytoskeletal regulatory pathway within the developing axon. These findings demonstrate that α7 regulates axon growth in hippocampal neurons, thereby likely contributing to synaptic formation in the developing brain.

     

Analysis of relatedness and determination of the source of founders in the captive bearded vulture, Gypaetus barbatus, population

Genetic relatedness among founders is a vitalparameter in the management of captivepopulations as kin structure can have asignificant effect on subsequent populationstructure. Methods for inferring relatednessfrom microsatellite markers have all beendeveloped for natural populations; theirapplicability to captive populations withunknown founder origins needs thereforetesting. We used information derived from 14microsatellites in 177 individuals and Quellerand Goodnight's approach, to estimaterelatedness in the captive bearded vulturepopulation and to test the assumption ofunrelated founders. Mean relatedness of knownparent–offspring, full-sib and half-sib pairswithin the captive population were in agreementwith theoretical distributions. Pairwiserelatedness values among the founders had amean of –0.051 (SE ± 0.007) and theirdistribution did only differ marginally fromthe one found in the natural Pyreneanpopulation. A maximum likelihood approach wasused to determine the likelihood of founderpairs to be as closely related as full-sibs orparent–offspring. These results were combinedwith data from 268 bp mitochondrial DNA controlregion sequences and studbook information. Wecould exclude a close relationship among themajority of the 36 successfully reproducingfounders. Our study therefore removesmanagement concerns about hidden problems ofinbreeding and inbreeding depression. Itdemonstrates the applicability of relatednessestimates based on microsatellite allelefrequency data even in captive populations.Furthermore, we verified studbook informationon the origin of two founders from thePyrenees, and show the value of assignmenttests based on microsatellites for deducingfounder origins and their important role infuture monitoring projects.     

Hepatitis C virus induces proteolytic cleavage of sterol regulatory element binding proteins and stimulates their phosphorylation via oxidative stress

Hepatic steatosis is a common histological feature of chronic hepatitis C. Hepatitis C virus (HCV) gene expression has been shown to alter host cell cholesterol/lipid metabolism and thus induce hepatic steatosis. Since sterol regulatory element binding proteins (SREBPs) are major regulators of lipid metabolism, we sought to determine whether genotype 2a-based HCV infection induces the expression and posttranslational activation of SREBPs. HCV infection stimulates the expression of genes related to lipogenesis. HCV induces the proteolytic cleavage of SREBPs. HCV core and NS4b derived from genotype 3a are also individually capable of inducing the proteolytic processing of SREBPs. Further, we demonstrate that HCV stimulates the phosphorylation of SREBPs. Our studies show that HCV-induced oxidative stress and subsequent activation of the phosphatidylinositol 3-kinase (PI3-K)-Akt pathway and inactivation (phosphorylation) of PTEN (phosphatase and tensin homologue) mediate the transactivation of SREBPs. HCV-induced SREBP-1 and -2 activities were sensitive to antioxidant (pyrrolidine dithiocarbamate), Ca(2+) chelator 1,2-bis(aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-tetra(acetoxymethyl) ester (BAPTA-AM), and PI3-K inhibitor (LY294002). Collectively, these studies provide insight into the mechanisms of hepatic steatosis associated with HCV infection.