Phylogenetic analysis reveals positive correlations between adaptations to diverse hosts in a group of pathogen‐like herbivores

A jack of all trades can be master of none—this intuitive idea underlies most theoretical models of host‐use evolution in plant‐feeding insects, yet empirical support for trade‐offs in performance on distinct host plants is weak. Trade‐offs may influence the long‐term evolution of host use while being difficult to detect in extant populations, but host‐use evolution may also be driven by adaptations for generalism. Here we used host‐use data from insect collection records to parameterize a phylogenetic model of host‐use evolution in armored scale insects, a large family of plant‐feeding insects with a simple, pathogen‐like life history. We found that a model incorporating positive correlations between evolutionary changes in host performance best fit the observed patterns of diaspidid presence and absence on nearly all focal host taxa, suggesting that adaptations to particular hosts also enhance performance on other hosts. In contrast to the widely invoked trade‐off model, we advocate a “toolbox” model of host‐use evolution in which armored scale insects accumulate a set of independent genetic tools, each of which is under selection for a single function but may be useful on multiple hosts.     

The basis of persistent bacterial infections

Selected bacterial pathogens, such as Helicobacter pylori and Mycobacterium tuberculosis, establish persistent infections in mammalian hosts despite activating inflammatory and antimicrobial responses. The strategies used to overcome host defense responses vary with the anatomical location of the infection but often rely on deliberate manipulations of the host cell responses. Phylogenetically unrelated bacteria can share similar strategies for the establishment of persistence and, in selected examples, one even can define homologous "persistence" genes. Such observations suggest that persistent infection is a specific phase in infection pathogenesis rather than a fortuitous imbalance in the host-pathogen interaction.     

Molecular systematics and evolution of the aphid family Lachnidae

The aphid family Lachnidae (c. 320 spp.)-sister-group to the economically devastating family Aphididae (c. 3300 spp.)-encompasses a diverse array of associations with hostplants and attendant hymenopterans and of life histories, including potentially long-term parthenogenesis. Most-parsimonious phylogenetic trees were inferred from partial (905-coding-bp) sequences of elongation factor 1alpha (EF-1alpha) and complete (675-bp) sequences of cytochrome oxidase 2 (CO2). The EF-1alpha, CO2, and combined analyses did not conflict with each other. Most tribes and infratribal relationships were robustly supported; intertribal relationships were mostly unresolved in the separate analysis and only weakly supported in the combined analysis. Both genes indicated a close relationship between the genera Nippolachnus and Tuberolachnus, both of which include species with the unusual habit of feeding along the midrib of leaves of Eriobotrya and which are here referred to the tribe Tuberolachnini Mamontova. A sister-group relationship between Tuberolachnini and the putatively ancient asexual tribe Tramini is supported. The combined analysis provides support (albeit weak) for the hypothesis that conifer-feeding is ancestral in Lachninae, which in turn implies that conifer-feeding may be a homologous and uninterrupted habit across disparate families of aphidoids (e.g., Adelgidae, Mindaridae, Drepanosiphidae, and Lachnidae).     

Small molecule inhibitors of the Yersinia type III secretion system impair the development of Chlamydia after entry into host cells

Background  

Chlamydiae are obligate intracellular pathogens that possess a type III secretion system to deliver proteins into the host cell during infection. Small molecule inhibitors of type III secretion in Yersinia, termed INPs (Innate Pharmaceuticals AB) were reported to strongly inhibit Chlamydia growth in epithelial cells. In this study we have analyzed the effect of these drugs on bacterial invasiveness.     

A large-scale survey of genetic copy number variations among Han Chinese residing in Taiwan

Background

Winter migration of immature brown trout (Salmo trutta) into freshwater rivers has been hypothesized to result from physiologically stressful combinations of high salinity and low temperature in the sea.

Results

We sampled brown trout from two Danish populations entering different saline conditions and quantified expression of the hsp70 and Na/K-ATPases α 1b genes following acclimation to freshwater and full-strength seawater at 2°C and 10°C. An interaction effect of low temperature and high salinity on expression of both hsp70 and Na/K-ATPase α 1b was found in trout from the river entering high saline conditions, while a temperature independent up-regulation of both genes in full-strength seawater was found for trout entering marine conditions with lower salinities.

Conclusion

Overall our results support the hypothesis that physiologically stressful conditions in the sea drive sea-run brown trout into freshwater rivers in winter. However, our results also demonstrate intra-specific differences in expression of important stress and osmoregulative genes most likely reflecting adaptive differences between trout populations on a regional scale, thus strongly suggesting local adaptations driven by the local marine environment.     

The rise and fall of bacterial clones: Streptococcus pneumoniae

Globally spreading bacterial strains belong to clonal types that have the capacity to colonize, spread and cause disease in the community. Recent comparative genomic analyses of well-defined clinical isolates have led to the identification of bacterial properties that are required for the successful spread of bacterial clones. In this Review, we discuss the evolution of bacterial clones, the importance of recombination versus mutations for evolution of clones, common methods used to study clonal relationships among bacteria, factors that may contribute to the clonal spread of bacteria and the potential relevance of bacterial clones to clinical disease. We focus on the common pathogen Streptococcus pneumoniae, although other bacteria are also briefly discussed, such as Helicobacter pylori, Staphylococcus aureus and Mycobacterium tuberculosis.     

Initiation of assembly and association of the structural elements of a bacterial pilus depend on two specialized tip proteins.

Uropathogenic Escherichia coli produce heteropolymeric surface fibers called P pili, which present an adhesin at their tip that specifically recognizes globoside receptors on the host uroepithelium. The initial attachment step is thought to be essential for pathogenesis. P pili are composite fibers consisting of a thin tip fibrillum joined end to end to a rigid helical rod. Here we show that the ordered assembly of these structures requires the activity of two proteins that are minor components of the tip fibrillum, PapF and PapK. PapF is required for the correct presentation of the adhesin at the distal end of the tip fibrillum. PapK regulates the length of the tip fibrillum and joins it to the pilus rod. We propose that these subunits function as adaptors, by providing complementary surfaces to different substructures of the pilus and promoting their proper associations. In addition, the conversion of chaperone-subunit complexes into pili depends on PapF and PapK since a papF- papK- double mutation abolishes piliation. We suggest that in addition to the adaptor functions of PapF and PapK, they are also required to initiate the formation of tip fibrillae and pilus rods.