Male-Mediated Gene Flow in Patrilocal Primates

BACKGROUND: Many group-living species display strong sex biases in dispersal tendencies. However, gene flow mediated by apparently philopatric sex may still occur and potentially alters population structure. In our closest living evolutionary relatives, dispersal of adult males seems to be precluded by high levels of territoriality between males of different groups in chimpanzees, and has only been observed once in bonobos. Still, male-mediated gene flow might occur through rare events such as extra-group matings leading to extra-group paternity (EGP) and female secondary dispersal with offspring, but the extent of this gene flow has not yet been assessed. METHODOLOGY/PRINCIPAL FINDINGS: Using autosomal microsatellite genotyping of samples from multiple groups of wild western chimpanzees (Pan troglodytes verus) and bonobos (Pan paniscus), we found low genetic differentiation among groups for both males and females. Characterization of Y-chromosome microsatellites revealed levels of genetic differentiation between groups in bonobos almost as high as those reported previously in eastern chimpanzees, but lower levels of differentiation in western chimpanzees. By using simulations to evaluate the patterns of Y-chromosomal variation expected under realistic assumptions of group size, mutation rate and reproductive skew, we demonstrate that the observed presence of multiple and highly divergent Y-haplotypes within western chimpanzee and bonobo groups is best explained by successful male-mediated gene flow. CONCLUSIONS/SIGNIFICANCE: The similarity of inferred rates of male-mediated gene flow and published rates of EGP in western chimpanzees suggests this is the most likely mechanism of male-mediated gene flow in this subspecies. In bonobos more data are needed to refine the estimated rate of gene flow. Our findings suggest that dispersal patterns in these closely related species, and particularly for the chimpanzee subspecies, are more variable than previously appreciated. This is consistent with growing recognition of extensive behavioral variation in chimpanzees and bonobos

Smoking-related knowledge, attitudes, and behaviours among Alaska Native people: a population-based study

BACKGROUND: Several studies have shown that Alaska Native people have higher smoking prevalence than non-Natives. However, no population-based studies have explored whether smoking-related knowledge, attitudes, and behaviors also differ among Alaska Native people and non-Natives. OBJECTIVE: We compared current smoking prevalence and smoking-related knowledge, attitudes, and behavior of Alaska Native adults living in the state of Alaska with non-Natives. METHODS: We used Alaska Behavioral Risk Factor Surveillance System data for 1996 to 2010 to compare smoking prevalence, consumption, and cessation- and second-hand smoke-related knowledge, attitudes, and behaviors among self-identified Alaska Native people and non-Natives. RESULTS: Current smoking prevalence was 41% (95% CI: 37.9%–44.4%) among Alaska Native people compared with 17.1% (95% CI: 15.9%–18.4%) among non-Natives. Among current every day smokers, Alaska Natives were much more likely to smoke less than 10 cigarettes per day (OR=5.0, 95% CI: 2.6–9.6) than non-Natives. Compared with non-Native smokers, Alaska Native smokers were as likely to have made a past year quit attempt (OR=1.4, 95% CI: 0.9–2.1), but the attempt was less likely to be successful (OR=0.5, 95% CI: 0.2–0.9). Among current smokers, Alaska Natives were more likely to believe second-hand smoke (SHS) was very harmful (OR=4.5, 95% CI: 2.8–7.2), to believe that smoking should not be allowed in indoor work areas (OR=1.9, 95% CI: 1.1–3.1) or in restaurants (OR=4.2, 95% CI: 2.5–6.9), to have a home smoking ban (OR=2.5, 95% CI: 1.6–3.9), and to have no home exposure to SHS in the past 30 days (OR=2.3, 95% CI: 1.5–3.6) than non-Natives. CONCLUSION: Although a disparity in current smoking exists, Alaska Native people have smoking-related knowledge, attitudes, and behaviors that are encouraging for reducing the burden of smoking in this population. Programs should support efforts to promote cessation, prevent relapse, and establish smoke-free environments

Syndapin I is the phosphorylation-regulated dynamin I partner in synaptic vesicle endocytosis

Dynamin I is dephosphorylated at Ser-774 and Ser-778 during synaptic vesicle endocytosis (SVE) in nerve terminals. Phosphorylation was proposed to regulate the assembly of an endocytic protein complex with amphiphysin or endophilin. Instead, we found it recruits syndapin I for SVE and does not control amphiphysin or endophilin binding in rat synaptosomes. After depolarization, syndapin showed a calcineurin-mediated interaction with dynamin. A peptide mimicking the phosphorylation sites disrupted the dynamin-syndapin complex, not the dynamin-endophilin complex, arrested SVE and produced glutamate release fatigue after repetitive stimulation. Pseudophosphorylation of Ser-774 or Ser-778 inhibited syndapin binding without affecting amphiphysin recruitment. Site mutagenesis to alanine arrested SVE in cultured neurons. The effects of the sites were additive for syndapin I binding and SVE. Thus syndapin I is a central component of the endocytic protein complex for SVE via stimulus-dependent recruitment to dynamin I and has a key role in synaptic transmission

A Hip1R–cortactin complex negatively regulates actin assembly associated with endocytosis

Actin polymerization plays a critical role in clathrin-mediated endocytosis in many cell types, but how polymerization is regulated is not known. Hip1R may negatively regulate actin assembly during endocytosis because its depletion increases actin assembly at endocytic sites. Here, we show that the C-terminal proline-rich domain of Hip1R binds to the SH3 domain of cortactin, a protein that binds to dynamin, actin filaments and the Arp2/3 complex. We demonstrate that Hip1R deleted for the cortactin-binding site loses its ability to rescue fully the formation of abnormal actin structures at endocytic sites induced by Hip1R siRNA. To determine when this complex might function during endocytosis, we performed live cell imaging. The maximum in vivo recruitment of Hip1R, clathrin and cortactin to endocytic sites was coincident, and all three proteins disappeared together upon formation of a clathrin-coated vesicle. Finally, we showed that Hip1R inhibits actin assembly by forming a complex with cortactin that blocks actin filament barbed end elongation