Coevolution of Genome Architecture and Social Behavior.

Although social behavior can have a strong genetic component, it can also result in selection on genome structure and function, thereby influencing the evolution of the genome itself. Here we explore the bidirectional links between social behavior and genome architecture by considering variation in social and/or mating behavior among populations (social polymorphisms) and across closely related species. We propose that social behavior can influence genome architecture via associated demographic changes due to social living. We establish guidelines to exploit emerging whole-genome sequences using analytical approaches that examine genome structure and function at different levels (regulatory vs structural variation) from the perspective of both molecular biology and population genetics in an ecological context

Host-Microbe Battles over Iron

Hosts and pathogens are locked in an endless battle to gain selective advantages over one another. Host-pathogen interactions therefore provide valuable systems for studying evolutionary genetics, natural selection, microbiology and infectious disease. The sequestration of essential iron has emerged as a crucial innate defense system termed nutritional immunity, leading pathogens to evolve mechanisms of 'iron piracy' to scavenge this essential metal from host proteins. This battle for iron carries numerous consequences not only for host-pathogen evolution but also microbial community interactions. The Elde lab demonstrated that the iron carrier protein transferrin has evolved to allow hosts to escape bacterial "iron piracy". For example, one transferrin polymorphism allows hosts to evade iron piracy by the pathogenic bacterium, Haemophilus influenzae, revealing a functional basis for standing genetic variation in the human population. These findings identify a central role for nutritional immunity in the persistent evolutionary conflicts between primates and bacterial pathogens

Regulation of Innate Immune Pathways

Cells must regulate their innate immune pathways so that they can respond rapidly to pathogens, yet avoid aberrant activation that can lead to inflammation. The evolution of these regulatory mechanisms remain to be understood, however. Elde, Feschotte and colleagues demonstrated that endogenous retroviruses, and the promoters that they introduce into the genome, have been co-opted by cells to play key roles in regulating the innate immune system. Although these regulatory sequences likely arose in ancient viruses, they now constitute a dynamic reservoir of interferon-inducible enhancers that fuel genetic innovation in mammalian immune defenses. Thus, we have turned the tables, and ancient viral DNA has now become important for mounting a proper defense against today's viral infections

Adaptive duplication and genetic diversification of protein kinase R contribute to the specificity of bat-virus interactions

Several bat species act as asymptomatic reservoirs for many viruses that are highly pathogenic in other mammals. Here, we have characterized the functional diversification of the protein kinase R (PKR), a major antiviral innate defense system. Our data indicate that PKR has evolved under positive selection and has undergone repeated genomic duplications in bats in contrast to all studied mammals that have a single copy of the gene. Functional testing of the relationship between PKR and poxvirus antagonists revealed how an evolutionary conflict with ancient pathogenic poxviruses has shaped a specific bat host-virus interface. We determined that duplicated PKRs of the Myotis species have undergone genetic diversification, allowing them to collectively escape from and enhance the control of DNA and RNA viruses. These findings suggest that viral-driven adaptations in PKR contribute to modern virus-bat interactions and may account for bat-specific immunity.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Static Clathrin Assemblies at the Peripheral Vacuole—Plasma Membrane Interface of the Parasitic Protozoan Giardia lamblia

Giardia lamblia is a parasitic protozoan that infects a wide range of vertebrate hosts including humans. Trophozoites are non-invasive but associate tightly with the enterocyte surface of the small intestine. This narrow ecological specialization entailed extensive morphological and functional adaptations during host-parasite co-evolution, including a distinctly polarized array of endocytic organelles termed peripheral vacuoles (PVs), which are confined to the dorsal cortical region exposed to the gut lumen and are in close proximity to the plasma membrane (PM). Here, we investigated the molecular consequences of these adaptations on the Giardia endocytic machinery and membrane coat complexes. Despite the absence of canonical clathrin coated vesicles in electron microscopy, Giardia possesses conserved PV-associated clathrin heavy chain (GlCHC), dynamin-related protein (GlDRP), and assembly polypeptide complex 2 (AP2) subunits, suggesting a novel function for GlCHC and its adaptors. We found that, in contrast to GFP-tagged AP2 subunits and DRP, CHC::GFP reporters have no detectable turnover in living cells, indicating fundamental differences in recruitment to the membrane and disassembly compared to previously characterized clathrin coats. Histochemical localization in electron tomography showed that these long-lived GlCHC assemblies localized at distinctive approximations between the plasma and PV membrane. A detailed protein interactome of GlCHC revealed all of the conserved factors in addition to novel or highly diverged proteins, including a putative clathrin light chain and lipid-binding proteins. Taken together, our data provide strong evidence for giardial CHC as a component of highly stable assemblies at PV-PM junctions that likely have a central role in organizing continuities between the PM and PV membranes for controlled sampling of the fluid environment. This suggests a novel function for CHC in Giardia and the extent of molecular remodeling of endocytosis in this species