Strong phenotypic divergence in spite of low genetic structure in the endemic Mangrove Warbler subspecies (Setophaga petechia xanthotera) of Costa Rica

Despite the enormous advances in genetics, links between phenotypes and genotypes have been made for only a few nonmodel organisms. However, such links can be essential to understand mechanisms of ecological speciation. The Costa Rican endemic Mangrove Warbler subspecies provides an excellent subject to study differentiation with gene flow, as it is distributed along a strong precipitation gradient on the Pacific coast with no strong geographic barriers to isolate populations. Mangrove Warbler populations could be subject to divergent selection driven by precipitation, which influences soil salinity levels, which in turn influences forest structure and food resources. We used single nucleotide polymorphisms (SNPs) and morphological traits to examine the balance between neutral genetic and phenotypic divergence to determine whether selection has acted on traits and genes with functions related to specific environmental variables. We present evidence showing: (a) associations between environmental variables and SNPs, identifying candidate genes related to bill morphology (BMP) and osmoregulation, (b) absence of population genetic structure in neutrally evolving markers, (c) divergence in bill size across the precipitation gradient, and (d) strong phenotypic differentiation (P_ST) which largely exceeds neutral genetic differentiation (F_ST) in bill size. Our results indicate an important role for salinity, forest structure, and resource availability in maintaining phenotypic divergence of Mangrove Warblers through natural selection. Our findings add to the growing body of literature identifying the processes involved in phenotypic differentiation along environmental gradients in the face of gene flow.     

The relationship between isometric force-time curve characteristics and club head speed in recreational golfers

ABSTRACT: Leary, BK, Statler, J, Hopkins, B, Fitzwater, R, Kesling, T, Lyon, J, Phillips, B, Bryner, RW, Cormie, P, and Haff, GG. The relationship between isometric force-time curve characteristics and club head speed in recreational golfers. J Strength Cond Res 26(10): 2685-2697, 2012-The primary purpose of the present investigation was to examine the relationships between club head speed, isometric midthigh pull performance, and vertical jump performance in a cohort of recreational golfers. Twelve recreational golfers (age, 20.4 ± 1.0 years; weight, 77.0 ± 9.8 kg; height, 177.8 ± 6.3 cm; body fat, 17.1 ± 7.6%; handicap, 14.5 ± 7.3; experience, 8.9 ± 3.6 years) completed 3 testing sessions: (a) familiarization session and body composition measurements; (b) measurement of force-time curves in the isometric midthigh pull, countermovement, and static vertical jump (SJ); and (c) measurement of club head speed. During sessions 1 and 2, subjects performed 5 countermovement jumps, 5 SJ, and 2 isometric midthigh pulls. Isometric peak force was measured at 30, 50, 90, 100, 200, and 250 milliseconds. Rate of force development was measured among 0-30, 0-50, 0-90, 0-100, 0-200, and 0-250 milliseconds. Peak rate of force development was determined as the highest value in a 10-millisecond sampling windows. During session 3, subjects performed 10 maximal golf swings with a driver to measure club head speed; peak and average club head speed were analyzed across the 10 swings. Golf handicap was moderately correlated with average (r = -0.52, p = 0.04) and maximal club head speed (r = -0.45, p = 0.07). Force at 150 milliseconds during the isomeric midthigh pull test was moderately correlated with average (r = 0.46, p = 0.07) and maximal club head speed (r = 0.47, p = 0.06). Moderate correlations were also found between the rate of force development from 0 to 150 milliseconds and average (r = 0.38, p = 0.11) and maximal club head speed (r = 0.36, p = 0.12). The present findings suggest that the ability to exhibit high ground reaction forces in time frames <200 milliseconds are related to high club head speeds.     

Species loss and gain in communities under future climate change: consequences for functional diversity

It is anticipated that anthropogenic climate change will lead to substantial reassembly within communities in coming decades as individual species shift their ranges to track optimal conditions for growth and survival. As species are lost and gained in communities, what are the consequences for functional trait diversity? Functional traits are the characteristics of species that affect individual performance and provide the vital link between biodiversity at the species level and ecosystem function. We investigated how projected changes in species richness in plant communities under climate change scenarios for the decade 2050 will affect the distribution and diversity of five functional traits. We aggregated range change projections made in Maxent for the decade 2050 across all species in the regional pool of littoral rainforest vines in eastern Australia (n = 163 species). The effect of richness changes on trait diversity was assessed in nine rainforest reserves along the east coast of Australia. Although richness was predicted to significantly decline across all communities, functional diversity remained stable, indicating a decoupling in response to climate change at these two different levels of biological organization. A high degree of redundancy in trait composition in communities may buffer against the loss of function in these plant communities. Scaling‐up our understanding of the impact of climate change from the species level to communities is a critical step towards developing conservation strategies aimed at preserving ecosystem function.     

On the Role of the SP1 Domain in HIV-1 Particle Assembly: a Molecular Switch?

Expression of a retroviral protein, Gag, in mammalian cells is sufficient for assembly of immature virus-like particles (VLPs). VLP assembly is mediated largely by interactions between the capsid (CA) domains of Gag molecules but is facilitated by binding of the nucleocapsid (NC) domain to nucleic acid. We have investigated the role of SP1, a spacer between CA and NC in HIV-1 Gag, in VLP assembly. Mutational analysis showed that even subtle changes in the first 4 residues of SP1 destroy the ability of Gag to assemble correctly, frequently leading to formation of tubes or other misassembled structures rather than proper VLPs. We also studied the conformation of the CA-SP1 junction region in solution, using both molecular dynamics simulations and circular dichroism. Consonant with nuclear magnetic resonance (NMR) studies from other laboratories, we found that SP1 is nearly unstructured in aqueous solution but undergoes a concerted change to an α-helical conformation when the polarity of the environment is reduced by addition of dimethyl sulfoxide (DMSO), trifluoroethanol, or ethanol. Remarkably, such a coil-to-helix transition is also recapitulated in an aqueous medium at high peptide concentrations. The exquisite sensitivity of SP1 to mutational changes and its ability to undergo a concentration-dependent structural transition raise the possibility that SP1 could act as a molecular switch to prime HIV-1 Gag for VLP assembly. We suggest that changes in the local environment of SP1 when Gag oligomerizes on nucleic acid might trigger this switch.     

Sprouty2 in the Dorsal Hippocampus Regulates Neurogenesis and Stress Responsiveness in Rats

Both the development and relief of stress-related psychiatric conditions such as major depression (MD) and post-traumatic stress disorder (PTSD) have been linked to neuroplastic changes in the brain. One such change involves the birth of new neurons (neurogenesis), which occurs throughout adulthood within discrete areas of the mammalian brain, including the dorsal hippocampus (HIP). Stress can trigger MD and PTSD in humans, and there is considerable evidence that it can decrease HIP neurogenesis in laboratory animals. In contrast, antidepressant treatments increase HIP neurogenesis, and their efficacy is eliminated by ablation of this process. These findings have led to the working hypothesis that HIP neurogenesis serves as a biomarker of neuroplasticity and stress resistance. Here we report that local alterations in the expression of Sprouty2 (SPRY2), an intracellular inhibitor of growth factor function, produces profound effects on both HIP neurogenesis and behaviors that reflect sensitivity to stressors. Viral vector-mediated disruption of endogenous Sprouty2 function (via a dominant negative construct) within the dorsal HIP of adult rats stimulates neurogenesis and produces signs of stress resilience including enhanced extinction of conditioned fear. Conversely, viral vector-mediated elevation of SPRY2 expression intensifies the behavioral consequences of stress. Studies of these manipulations in HIP primary cultures indicate that SPRY2 negatively regulates fibroblast growth factor-2 (FGF2), which has been previously shown to produce antidepressant- and anxiolytic-like effects via actions in the HIP. Our findings strengthen the relationship between HIP plasticity and stress responsiveness, and identify a specific intracellular pathway that could be targeted to study and treat stress-related disorders.     

Using Plasmodium knowlesi as a model for screening Plasmodium vivax blood-stage malaria vaccine targets reveals new candidates

Plasmodium vivax is responsible for the majority of malaria cases outside Africa. Unlike P. falciparum, the P. vivax life-cycle includes a dormant liver stage, the hypnozoite, which can cause infection in the absence of mosquito transmission. An effective vaccine against P. vivax blood stages would limit symptoms and pathology from such recurrent infections, and therefore could play a critical role in the control of this species. Vaccine development in P. vivax, however, lags considerably behind P. falciparum, which has many identified targets with several having transitioned to Phase II testing. By contrast only one P. vivax blood-stage vaccine candidate based on the Duffy Binding Protein (PvDBP), has reached Phase Ia, in large part because the lack of a continuous in vitro culture system for P. vivax limits systematic screening of new candidates. We used the close phylogenetic relationship between P. vivax and P. knowlesi, for which an in vitro culture system in human erythrocytes exists, to test the scalability of systematic reverse vaccinology to identify and prioritise P. vivax blood-stage targets. A panel of P. vivax proteins predicted to function in erythrocyte invasion were expressed as full-length recombinant ectodomains in a mammalian expression system. Eight of these antigens were used to generate polyclonal antibodies, which were screened for their ability to recognize orthologous proteins in P. knowlesi. These antibodies were then tested for inhibition of growth and invasion of both wild type P. knowlesi and chimeric P. knowlesi lines modified using CRISPR/Cas9 to exchange P. knowlesi genes with their P. vivax orthologues. Candidates that induced antibodies that inhibited invasion to a similar level as PvDBP were identified, confirming the utility of P. knowlesi as a model for P. vivax vaccine development and prioritizing antigens for further follow up.     

HIV capsid is a tractable target for small molecule therapeutic intervention

Despite a high current standard of care in antiretroviral therapy for HIV, multidrug-resistant strains continue to emerge, underscoring the need for additional novel mechanism inhibitors that will offer expanded therapeutic options in the clinic. We report a new class of small molecule antiretroviral compounds that directly target HIV-1 capsid (CA) via a novel mechanism of action. The compounds exhibit potent antiviral activity against HIV-1 laboratory strains, clinical isolates, and HIV-2, and inhibit both early and late events in the viral replication cycle. We present mechanistic studies indicating that these early and late activities result from the compound affecting viral uncoating and assembly, respectively. We show that amino acid substitutions in the N-terminal domain of HIV-1 CA are sufficient to confer resistance to this class of compounds, identifying CA as the target in infected cells. A high-resolution co-crystal structure of the compound bound to HIV-1 CA reveals a novel binding pocket in the N-terminal domain of the protein. Our data demonstrate that broad-spectrum antiviral activity can be achieved by targeting this new binding site and reveal HIV CA as a tractable drug target for HIV therapy.     

Floodplain ecosystem dynamics under extreme dry and wet phases in semi‐arid Australia

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