Phylogenetic and non-phylogenetic structure in trophic links between gall-forming herbivores and their parasitoid natural enemies.

Revealing processes that structure species interactions is central to understanding community assembly and dynamics. Species interact via their phenotypes, but identifying and quantifying the traits that structure species-specific interactions (links) can be challenging. Where these traits show phylogenetic signal, however, link properties are predictable using models that incorporate phylogenies in place of trait data. We analysed variation in link richness, frequency, and identity in a multi-site dataset of interactions between host oak cynipid galls and parasitoid natural enemies, using a Bayesian mixed modelling framework allowing concurrent fitting of terms for phylogenies of both trophic levels. In both link incidence (presence/absence) and link frequency datasets, we identified strong signatures of cophylogeny (related parasitoids attack related host galls) and patterns independent of either phylogeny. Our results are robust to simulations of substantially reduced sample completeness, and are consistent with the structuring of trophic interactions by a combination of phylogenetically conserved and convergently evolving traits at both trophic levels. We discuss our results in light of phenotypic traits thought to structure gall-parasitoid interactions and wider applications of this approach, including inference of underlying community assembly processes and prediction of economically important trophic interactions

Phylogenetic and non-phylogenetic structure in trophic links between gall-forming herbivores and their parasitoid natural enemies.

Revealing processes that structure species interactions is central to understanding community assembly and dynamics. Species interact via their phenotypes, but identifying and quantifying the traits that structure species-specific interactions (links) can be challenging. Where these traits show phylogenetic signal, however, link properties are predictable using models that incorporate phylogenies in place of trait data. We analysed variation in link richness, frequency, and identity in a multi-site dataset of interactions between host oak cynipid galls and parasitoid natural enemies, using a Bayesian mixed modelling framework allowing concurrent fitting of terms for phylogenies of both trophic levels. In both link incidence (presence/absence) and link frequency datasets, we identified strong signatures of cophylogeny (related parasitoids attack related host galls) and patterns independent of either phylogeny. Our results are robust to simulations of substantially reduced sample completeness, and are consistent with the structuring of trophic interactions by a combination of phylogenetically conserved and convergently evolving traits at both trophic levels. We discuss our results in light of phenotypic traits thought to structure gall-parasitoid interactions and wider applications of this approach, including inference of underlying community assembly processes and prediction of economically important trophic interactions

Central Nicotinic and Muscarinic Receptors in Health and Disease

Without acetylcholine (ACh) no skeletal muscle contraction, no preganglionic sympathetic or parasympathetic activity can be obtained. This can result in dysregulation of cardiac, respiratory, gastrointestinal, and renal functions as well as disruption of fluid secretion from various glands such as tears, saliva, digestive juices, sweat, and milk. Importantly, ACh deficiency in the brain can have severe cognitive consequences. The action of ACh is mediated by two distinct classes of receptors, namely the muscarinic (mAChRs), which are G-protein coupled (metabotropic) receptors and nicotinic receptors (nAChRs), which are ligand-gated ion channels (ionotropic receptors). The focus of this chapter is on interaction of these two distinct receptor classes and its implication in health and disease. Thus, following a brief description of ACh actions and its central circuitry, an update on mAChRs and nAChRs and how their interaction may impact neuropsychiatric/neurodegenerative diseases will be provided. Moreover, potential novel therapeutic intervention based on these interactions, particularly in relationship to Alzheimer’s and Parkinson’s diseases will be touched upon

Structure and composition of tritrophic communities associated with Fagaceae-feeding cynipid gallwasps in Sichuan, China

We provide the first description and analysis of species-rich communities of Fagaceae host plants, cynipid gall inducers and Hymenopteran parasitoids from two sites in western Sichuan, China. We use quantified interaction data to test the hypothesis that metabolically intimate cynipid-Fagaceae interactions are more specialised, resulting in more modular networks and stronger signatures of turnover than nestedness for beta diversity, than associations between parasitoids and Fagaceae. Rearing of nearly 27,000 cynipid gall specimens from 22 host plant species in Castanea, Castanopsis, Lithocarpus and Quercus (sections Cerris, Cyclobalanopsis, Ilex and Quercus) yielded 168 morphologically distinct cynipid gall morphotypes, and 3800 parasitoids in 67 morphospecies. The Sichuan parasitoid assemblage is similar in composition to cynipid-centred communities in the Western Palearctic and Nearctic. All of our predictions were confirmed. We discuss our findings in light of the processes thought to structure tritrophic interactions centred on gall inducing insect herbivores

Evolution of host-plant associations and biogeographic patterns on a global scale within the oak gall wasps

Co-evolutionary interactions between insect herbivores and their host plants underlie much contemporary biodiversity and are vital to assembly of natural ecosystems. Assemblages of galls on oaks induced by Cynipini wasps (Hymenoptera: Cynipidae) occur across much of the Northern Hemisphere, their diversity peaking in the Nearctic and on white oaks (Quercus section Quercus). However, the evolutionary history of the clade has been debated with respect to geographic origins, direction and timings of dispersal events, and shifts in host plant associations. We examined these questions using a global-scale, 6-gene phylogeny of 430 Cynipini species and a dataset of their associated host plants encompassing all eight sections within Quercus plus five Fagaceae genera. Likelihood-based ancestral state reconstructions demonstrate a Nearctic origin of the Cynipini followed by repeated colonisations of the Palearctic via both westwards and eastwards dispersal. These inferences are robust to bias in taxon sampling across continents and the inclusion of Protobalandricus as the sister lineage to Cynipini sensu stricto. Likewise, the association with white oaks is probably ancestral and has been retained by many Cynipini lineages. However, host shifts to other sections within Quercus and related Fagaceae genera are widely distributed across the cynipid phylogeny. They are associated with both global-scale range shifts and within-bioregion exploitation of alternative hosts, and their frequency typically correlates with host-plant relatedness. These findings highlight the evolutionary success of cynipids on white oak hosts and the connectedness of continental assemblages of gall wasps over evolutionary time

Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome

Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder characterized by features reminiscent of marked premature ageing(1,2). Here, we present evidence of mutations in lamin A (LMNA) as the cause of this disorder. The HGPS gene was initially localized to chromosome 1q by observing two cases of uniparental isodisomy of 1q - the inheritance of both copies of this material from one parent - and one case with a 6-megabase paternal interstitial deletion. Sequencing of LMNA, located in this interval and previously implicated in several other heritable disorders(3,4), revealed that 18 out of 20 classical cases of HGPS harboured an identical de novo ( that is, newly arisen and not inherited) single-base substitution, G608G( GGC > GGT), within exon 11. One additional case was identified with a different substitution within the same codon. Both of these mutations result in activation of a cryptic splice site within exon 11, resulting in production of a protein product that deletes 50 amino acids near the carboxy terminus. Immunofluorescence of HGPS fibroblasts with antibodies directed against lamin A revealed that many cells show visible abnormalities of the nuclear membrane. The discovery of the molecular basis of this disease may shed light on the general phenomenon of human ageing.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62684/1/nature01629.pd

Methylthioadenosine reprograms macrophage activation through adenosine receptor stimulation

Regulation of inflammation is necessary to balance sufficient pathogen clearance with excessive tissue damage. Central to regulating inflammation is the switch from a pro-inflammatory pathway to an anti-inflammatory pathway. Macrophages are well-positioned to initiate this switch, and as such are the target of multiple therapeutics. One such potential therapeutic is methylthioadenosine (MTA), which inhibits TNFα production following LPS stimulation. We found that MTA could block TNFα production by multiple TLR ligands. Further, it prevented surface expression of CD69 and CD86 and reduced NF-KB signaling. We then determined that the mechanism of this action by MTA is signaling through adenosine A2 receptors. A2 receptors and TLR receptors synergized to promote an anti-inflammatory phenotype, as MTA enhanced LPS tolerance. In contrast, IL-1β production and processing was not affected by MTA exposure. Taken together, these data demonstrate that MTA reprograms TLR activation pathways via adenosine receptors to promote resolution of inflammation. © 2014 Keyel et al