Uncertainty and the role of information acquisition in the evolution of context-dependent emigration

There is increasing empirical evidence that individuals utilize social and environmental cues in making decisions as to whether or not to disperse. However, we lack theory exploring the influence of information acquisition and use on the evolution of dispersal strategies and metapopulation dynamics. We used an individual-based, spatially explicit simulation model to explore the evolution of emigration strategies under varying precision of information about the natal patch, cost of information acquisition, and environmental predictability. Our findings show an interesting interplay between information use and the evolved emigration propensity. Lack of information led to higher emigration probabilities in more unpredictable environments but to lower emigration probabilities in constant or highly predictable scenarios. Somewhat-informed dispersal strategies were selected for in most cases, even when the acquisition of information was associated with a moderate reproductive cost. Notably, selection rarely favored investment in acquisition of high-precision information, and the tendency to invest in information acquisition was greatest in predictable environments when the associated cost was low. Our results highlight that information use can affect dispersal in a complex manner and also emphasize that information-acquisition behaviors can themselves come under strong selection, resulting in evolutionary dynamics that are tightly coupled to those of context-dependent behaviors.     

Tissue loss (white syndrome) in the coral Montipora capitata is a dynamic disease with multiple host responses and potential causes

Tissue loss diseases or white syndromes (WS) are some of the most important coral diseases because they result in significant colony mortality and morbidity, threatening dominant Acroporidae in the Caribbean and Pacific. The causes of WS remain elusive in part because few have examined affected corals at the cellular level. We studied the cellular changes associated with WS over time in a dominant Hawaiian coral, Montipora capitata, and showed that: (i) WS has rapidly progressing (acute) phases mainly associated with ciliates or slowly progressing (chronic) phases mainly associated with helminths or chimeric parasites; (ii) these phases interchanged and waxed and waned; (iii) WS could be a systemic disease associated with chimeric parasitism or a localized disease associated with helminths or ciliates; (iv) corals responded to ciliates mainly with necrosis and to helminths or chimeric parasites with wound repair; (v) mixed infections were uncommon; and (vi) other than cyanobacteria, prokaryotes associated with cell death were not seen. Recognizing potential agents associated with disease at the cellular level and the host response to those agents offers a logical deductive rationale to further explore the role of such agents in the pathogenesis of WS in M. capitata and helps explain manifestation of gross lesions. This approach has broad applicability to the study of the pathogenesis of coral diseases in the field and under experimental settings.     

Complexes of Ag with mixed donor phenanthroline-containing macrocycles: spectrofluorimetric, spectrophotometric, conductometric and potentiometric studies

The reactions of Ag⁺ with five mixed donor phenanthroline-containing macrocycles (L¹-L⁵) having N₂S₃-, N₂S₂O-, N₂S₂-, N₃S₂-, and N₄S₂-donor sets, respectively, have been studied in MeCN by spectrofluorimetric, spectrophotometric, conductometric and potentiometric methods. All ligands form 1:1 [Ag(L)]⁺ complexes, and in the case of L⁴ and L⁵, formation of 1:2 [Ag(L)₂]⁺ species is also observed. The corresponding formation constants have been evaluated and their values allow a deeper insight into the role played by complexation process in the potentiometric selectivity for Ag⁺ of membrane electrodes (ISE), and in the selective transport of Ag⁺ through supported liquid membrane (SLM) systems based on these ligands. The X-ray crystal structure of the complex [Ag(L⁴)]BF₄ is also reported.     

Immunomodulation of polyamine biosynthesis in tobacco plants has a significant impact on polyamine levels and generates a dwarf phenotype

Ornithine decarboxylase (ODC) is a cytosolic enzyme that catalyses the direct decarboxylation of l-ornithine to putrescine, one of the rate-limiting steps of polyamine biosynthesis in plants. In the present study, an ODC-specific murine single-chain antibody fragment (scFvODC1) was generated by phage display technology. To evaluate the effect of the recombinant antibody fragment on ODC activity and polyamine levels, we produced transgenic tobacco plants that accumulated scFvODC1 in the cytosol. Expression levels of up to 4% total soluble protein (TSP) were achieved, resulting in the inhibition of up to 90% of endogenous ODC activity. A significant reduction in putrescine, spermidine and spermine levels was observed in transgenic lines producing high levels of scFvODC1. Furthermore, these lines showed developmental abnormalities and a dwarf phenotype. We show that the immunomodulation of enzyme activity is a powerful approach that can be used to alter complex and tightly controlled metabolic pathways, allowing specific steps in the pathway to be blocked and the resulting physiological effects to be investigated.     

Nonconsensus West Nile virus genomes arising during mosquito infection suppress pathogenesis and modulate virus fitness in vivo

West Nile virus (WNV) is similar to other RNA viruses in that it forms genetically complex populations within hosts. The virus is maintained in nature in mosquitoes and birds, with each host type exerting distinct influences on virus populations. We previously observed that prolonged replication in mosquitoes led to increases in WNV genetic diversity and diminished pathogenesis in mice without remarkable changes to the consensus genome sequence. We therefore sought to evaluate the relationships between individual and group phenotypes in WNV and to discover novel viral determinants of pathogenesis in mice and fitness in mosquitoes and birds. Individual plaque size variants were isolated from a genetically complex population, and mutations conferring a small-plaque and mouse-attenuated phenotype were localized to the RNA helicase domain of the NS3 protein by reverse genetics. The mutation, an Asp deletion, did not alter type I interferon production in the host but rendered mutant viruses more susceptible to interferon compared to wild type (WT) WNV. Finally, we used an in vivo fitness assay in Culex quinquefasciatus mosquitoes and chickens to determine whether the mutation in NS3 influenced fitness. The fitness of the NS3 mutant was dramatically lower in chickens and moderately lower in mosquitoes, indicating that RNA helicase is a major fitness determinant of WNV and that the effect on fitness is host specific. Overall, this work highlights the complex relationships that exist between individual and group phenotypes in RNA viruses and identifies RNA helicase as an attenuation and fitness determinant in WNV.     

Coupled land use and ecological models reveal emergence and feedbacks in socio‐ecological systems

Understanding the dynamics of socio‐ecological systems is crucial to the development of environmentally sustainable practices. Models of social or ecological sub‐systems have greatly enhanced such understanding, but at the risk of obscuring important feedbacks and emergent effects. Integrated modelling approaches have the potential to address this shortcoming by explicitly representing linked socio‐ecological dynamics. We developed a socio‐ecological system model by coupling an existing agent‐based model of land‐use dynamics and an individual‐based model of demography and dispersal. A hypothetical case‐study was established to simulate the interaction of crops and their pollinators in a changing agricultural landscape, initialised from a spatially random distribution of natural assets. The bi‐directional coupled model predicted larger changes in crop yield and pollinator populations than a unidirectional uncoupled version. The spatial properties of the system also differed, the coupled version revealing the emergence of spatial land‐use clusters that neither supported nor required pollinators. These findings suggest that important dynamics may be missed by uncoupled modelling approaches, but that these can be captured through the combination of currently‐available, compatible model frameworks. Such model integrations are required to further fundamental understanding of socio‐ecological dynamics and thus improve management of socio‐ecological systems.     

Resolving the conundrum of inbreeding depression but no inbreeding avoidance: Estimating sex‐specific selection on inbreeding by song sparrows (Melospiza melodia)

Inbreeding avoidance among interacting females and males is not always observed despite inbreeding depression in offspring fitness, creating an apparent “inbreeding paradox.” This paradox could be resolved if selection against inbreeding was in fact weak, despite inbreeding depression. However, the net magnitude and direction of selection on the degree to which females and males inbreed by pairing with relatives has not been explicitly estimated. We used long‐term pedigree data to estimate phenotypic selection gradients on the degree of inbreeding that female and male song sparrows (Melospiza melodia) expressed by forming socially persistent breeding pairs with relatives. Fitness was measured as the total numbers of offspring and grand offspring contributed to the population, and as corresponding expected numbers of identical‐by‐descent allele copies, thereby accounting for variation in offspring survival, reproduction, and relatedness associated with variation in parental inbreeding. Estimated selection gradients on the degree to which individuals paired with relatives were weakly positive in females, but negative in males that formed at least one socially persistent pairing. However, males that paired had higher mean fitness than males that remained socially unpaired. These analyses suggest that net selection against inbreeding may be weak in both sexes despite strong inbreeding depression, thereby resolving the “inbreeding paradox.”     

The Impact of Nitric Oxide Toxicity on the Evolution of the Glutathione Transferase Superfamily: A PROPOSAL FOR AN EVOLUTIONARY DRIVING FORCE*

Glutathione transferases (GSTs) are protection enzymes capable of conjugating glutathione (GSH) to toxic compounds. During evolution an important catalytic cysteine residue involved in GSH activation was replaced by serine or, more recently, by tyrosine. The utility of these replacements represents an enigma because they yield no improvements in the affinity toward GSH or in its reactivity. Here we show that these changes better protect the cell from nitric oxide (NO) insults. In fact the dinitrosyl·diglutathionyl·iron complex (DNDGIC), which is formed spontaneously when NO enters the cell, is highly toxic when free in solution but completely harmless when bound to GSTs. By examining 42 different GSTs we discovered that only the more recently evolved Tyr-based GSTs display enough affinity for DNDGIC (K_D < 10⁻⁹ m) to sequester the complex efficiently. Ser-based GSTs and Cys-based GSTs show affinities 10²–10⁴ times lower, not sufficient for this purpose. The NO sensitivity of bacteria that express only Cys-based GSTs could be related to the low or null affinity of their GSTs for DNDGIC. GSTs with the highest affinity (Tyr-based GSTs) are also over-represented in the perinuclear region of mammalian cells, possibly for nucleus protection. On the basis of these results we propose that GST evolution in higher organisms could be linked to the defense against NO.     

SR protein-mediated inhibition of CFTR exon 9 inclusion: molecular characterization of the intronic splicing silencer

The intronic splicing silencer (ISS) of CFTR exon 9 promotes exclusion of this exon from the mature mRNA. This negative influence has important consequences with regards to human pathologic events, as lack of exon 9 correlates well with the occurrence of monosymptomatic and full forms of CF disease. We have previously shown that the ISS element interacts with members of the SR protein family. In this work, we now provide the identification of SF2/ASF and SRp40 as the specific SR proteins binding to this element and map their precise binding sites in IVS9. We have also performed a functional analysis of the ISS element using a variety of unrelated SR-binding sequences and different splicing systems. Our results suggest that SR proteins mediate CFTR exon 9 exclusion by providing a ‘decoy’ sequence in the vicinity of its suboptimal donor site. The results of this study give an insight on intron ‘exonization’ mechanisms and provide useful indications for the development of novel therapeutic strategies aimed at the recovery of exon inclusion.