The ecology of Bactrocera tryoni (Diptera: Tephritidae): what do we know to assist pest management?

The distribution, systematics and ecology of Bactrocera tryoni, the Queensland fruit fly, are reviewed. Bactrocera tryoni is a member of the B. tryoni complex of species, which currently includes four named species, viz. B. tryoni ssp., B. neohumeralis, B. melas and B. aquilonis. The species status of B. melas and B. aquilonis is unclear (they may be junior synonyms of B. tryoni) and their validity, or otherwise, needs to be confirmed as a matter of urgency. While Queensland fruit fly is regarded as a tropical species, it cannot be assumed that its distribution will spread further south under climate change scenarios. Increasing aridity and hot dry summers, as well as more complex, indirect interactions resulting from elevated CO₂, make predicting the future distribution and abundance of B. tryoni difficult. The ecology of B. tryoni is reviewed with respect to current control approaches (with the exception of sterile insect technique (SIT) which is covered in a companion paper). We conclude that there are major gaps in the knowledge required to implement most noninsecticide‐based management approaches. Priority areas for future research include host–plant interactions, protein and cue‐lure foraging and use, spatial dynamics, development of new monitoring tools, investigating the use of natural enemies and better integration of fruit flies into general horticultural IPM systems.     

Mechanisms of tolerance to herbivore damage:what do we know?

Identifying mechanisms of tolerance to herbivore damage will facilitate attempts to understand the role of tolerance in the evolutionary and ecological dynamics of plants and herbivores. Investigations of the physiological and morphological changes that occur in plants in response to herbivore damage have identified several potential mechanisms of tolerance. However, it is unlikely that all physiological changes that occur following damage are tolerance mechanisms. Few studies have made direct comparisons between the expression of tolerance and the relative expression of putative mechanisms. I briefly review empirical evidence for some of the better-studied potential mechanisms, including increased photosynthetic activity, compensatory growth, utilization of stored reserves, and phenological delays. For each of these mechanisms I discuss reasons why the relationship between tolerance and these characters may be more complicated than it first appears. I conclude by discussing several empirical approaches, including herbivore manipulations, quantitative trait loci (QTL) analysis, and selection experiments, that will further our understanding of tolerance mechanisms. This revised version was published online in July 2006 with corrections to the Cover Date.     

Skin and diabetes mellitus: what do we know?

Diabetes mellitus (DM) is becoming increasingly prevalent worldwide. Although major complications of this condition involve kidney, retina and peripheral nerves, the skin of diabetic patients is also frequently injured. Hence, interest is mounting in the definition of the structural and molecular profile of non-complicated diabetic skin, i.e., before injuries occur. Most of the available knowledge in this area has been obtained relatively recently and, in part, derives from various diabetic animal models. These include both insulin-dependent and insulin-resistant models. Structural work in human diabetic skin has also been carried out by means of tissue samples or of non-invasive methods. Indications have indeed been found for molecular/structural changes in diabetic skin. However, the overall picture that emerges is heterogeneous, incomplete and often contradictory and many questions remain unanswered. This review aims to detail, as much as possible, the various pieces of current knowledge in a systematic and synoptic manner. This should aid the identification of areas in which key questions are still open and more research is needed. A comprehensive understanding of this field could help in determining molecular targets for the prevention and treatment of skin injuries in DM and markers for the monitoring of cutaneous and systemic aspects of the disease. Additionally, with the increasing development of non-invasive optics-based deep-tissue-imaging diagnostic technologies, precise knowledge of cutaneous texture and molecular structure becomes an important pre-requisite for the use of such methods in diabetic patients.     

The role of stem cells in cutaneous wound healing: what do we really know?

Wound repair is a complex process involving the orchestrated interaction of multiple growth factors, cytokines, chemokines, and cell types. Dysregulation of this process leads to problems such as excessive healing in the form of keloids and hypertrophic scars and chronic, nonhealing wounds. These issues have broad global implications. Stem cells offer enormous potential for enhancing tissue repair and regeneration following injury. The rapidly developing fields of stem cell biology and skin tissue engineering create translational opportunities for the development of novel stem cell-based wound-healing therapies.     

The molecular biology of recombination in Mycobacteria: what do we know and how can we use it?

Recombination is a ubiquitous genetic process which results in the exchange of DNA between two substrates. Homologous recombination occurs between DNA species with identical sequence whereas illegitimate recombination can occur between DNA with very little or no homology. Site-specific recombination is often used by temperate phages to stably integrate into bacterial chromosomes. Characterisation of the mechanisms of recombination in mycobacteria has mainly focussed on RecA-dependent homologous recombination and phage-directed site-specific recombination. In contrast the high frequency of illegitimate recombination in slow-growing mycobacteria has not been explained. The role of DNA repair in dormancy and infection have not yet been fully established, but early work suggests that RecA-mediated pathways are not required for virulence. All three recombination mechanisms have been utilised in developing genetic techniques for the analysis of the biology and pathogenesis of mycobacteria. A recently developed method for studying essential genes will generate further insights into the biology of these important organisms.     

UV radiation: what we know and do we protect ourselves adequately?

Chronic sun exposure causes degenerative changes in the skin that are recognized as photoaging, immunosuppression and photocarcinogenesis. Sun is necessary for life, so total sun avoidance is impossible. Sun exposure during the first 15 years of life and blistering sunburns before age 20 have been linked to an increased risk of melanoma. Individuals who have outdoor lifestyles, live in sunny climates, and are lightly pigmented will experience the greatest degree of photoaging. In our study, performed four years ago, we have shown the knowledge of more than 4000 people about the effects of UV rays on the skin. The results show us that sun exposure is still exaggerated and uncontrolled due to the lack of knowledge about this topic. Encouraging photoprotection and improving the awareness of the general public about the harmful effects of too much sun exposure must be the leading preventative health strategy.     

Host cell invasion by apicomplexans: what do we know?

Apicomplexan zoites enter host cells by forming and actively moving through a tight junction (TJ) formed between the parasite and host cell surfaces. Although the TJ was first described decades ago, its molecular characterization has proved difficult mainly because of its transient existence during an internalization process that lasts only seconds. In the past 7 years, work has led to a model of the TJ in which the association between AMA1 and RON proteins structures the TJ and bridges the cytoskeletons of the two cells. However, more recent work questions this view. Here, we critically discuss the current model and speculate on alternative models of the AMA1-RON association and of the apicomplexan TJ.     

Neuroendocrine control of life histories: what do we need to know to understand the evolution of phenotypic plasticity?

Almost all life histories are phenotypically plastic: that is, life-history traits such as timing of breeding, family size or the investment in individual offspring vary with some aspect of the environment, such as temperature or food availability. One approach to understanding this phenotypic plasticity from an evolutionary point of view is to extend the optimality approach to the range of environments experienced by the organism. This approach attempts to understand the value of particular traits in terms of the selection pressures that act on them either directly or owing to trade-offs due to resource allocation and other factors such as predation risk. Because these selection pressures will between environments, the predicted optimal phenotype will too. The relationship expressing the optimal phenotype for different environments is the optimal reaction norm and describes the optimal phenotypic plasticity. However, this view of phenotypic plasticity ignores the fact that the reaction norm must be underlain by some sort of control system: cues about the environment must be collected by sense organs, integrated into a decision about the appropriate life history, and a message sent to the relevant organs to implement that decision. In multicellular animals, this control mechanism is the neuroendocrine system. The central question that this paper addresses is whether the control system affects the reaction norm that evolves. This might happen in two different ways: first, the control system will create constraints on the evolution of reaction norms if it cannot be configured to produce the optimal reaction norm and second, the control system will create additional selection pressures on reaction norms if the neuroendocrine system is costly. If either of these happens, a full understanding of the way in which selection shapes reaction norms must include details of the neuroendocrine control system. This paper presents the conceptual framework needed to explain what is meant by a constraint or cost being created by the neuroendocrine system and discusses the extent to which this occurs and some possible examples. The purpose of doing this is to encourage endocrinologists to take a fresh look at neuroendocrine mechanisms and help identify the properties of the system and situations in which these generate constraints and costs that impinge on the evolution of phenotypic plasticity.     

Dying with dementia: what do we know about it?

Death with dementia is increasingly common, yet research on end of life with dementia and end-of-life care for such patients has been sparse. This article reviews recent studies in this area, most of which were done in US nursing homes. Research focused on five domains: prognosis, decision making, treatment, patient's health and suffering, and family's circumstances and satisfaction with care. Prognostication focused on developing risk scores for mortality within 6 months or a year, and while decision making was usually studied qualitatively, the other three domains were largely covered by a series of small, retrospective studies. Future direction in research is discussed, including the ongoing CASCADE project in Boston and the Dutch End of Life with Dementia Study (DEOLD). Both of these prospective studies in nursing home residents assess decision making, as well as factors associated with family's satisfaction and patient suffering. These studies will provide insight into interventions that are most likely to improve end of life care of patients with dementia in the respective countries and elsewhere.     

Modifications of symbionts during ectomycorrhiza formation what do we know and where do we go?

Abstract

Ectomycorrhizas are subterranean organs resulting from the alteration in root structure by soil-inhabiting symbiotic fungi. Hyphae of the mycobiont have to contact the root surface, become attached to the root, and subsequently enter the root by growing between epidermal cells (and in some species, cortical cells) to form the Hartig net. A chemotropic stimulus might be involved in early hypha-root contact and recognition-adhesion may involve a polysaccharide-lectin interaction, but further research is needed to confirm this. Fungal hyphae adhering to the root surface change their mode of growth from apical, extension growth to a loss of this pattern resulting in a multi-branched mycelium. A similar change in pattern of branching occurs as hyphae form the Hartig net. In both cases, a change in the cytoskeleton might precede the change in branching. The ingress of hyphae between epidermal cells in angiosperm roots triggers radial rather than axial elongation of these cells; a reorientation of the cytoskeleton and subsequently the cellulose microfibrils is hypothesized to be involved in this process. Wall changes in root cells contiguous to Hartig net hyphae also occur, and these might facilitate nutrient exchange between the symbionts.     

Microplastics and freshwater microalgae: what do we know so far?

The constant entry of microplastics in several environmental matrices has been of great concern to the scientific community and to society in general, mainly due to the mysteries that surround the implications of this pollutant in the environment. Freshwater ecosystems are resources especially susceptible to variations in environmental quality, and the lack of data on the impacts caused by plastic fragments exacerbates the vulnerability of this environment. Considering the results of other studies, which demonstrate the increasing entry of polymeric fragments in the aquatic environment can lead to algae growth inhibition, an investigation was carried out to determine the current state of research on the interaction between microplastics and freshwater microalgae. In total, 20 scientific articles were analyzed. Different species were subjected to toxicological tests under controlled conditions in the laboratory with small microplastics (size range between 0.1 and 1000 µm), primary and secondary microplastics of different types of polymer. Four toxicity class of indicators were chosen to assess the microalgae response to exposure to microplastic in the selected studies: growth inhibition; photosynthetic activity; pigment analysis; and enzymatic activity and oxidative stress. In this review, a critical analysis is made on the effects of the shape, size, concentration, and duration of exposure to microplastics and research gaps are identified to guide future research priorities in this area of study.

     

The sylvatic cycle of Neospora caninum: where do we go from here?

Bovine abortions due to Neospora caninum infection are a major cattle-production problem worldwide. The parasite is readily maintained in cattle populations by vertical transmission. The domestic dog excretes oocysts in its feces and, after sporulation, these oocysts are infectious to cattle. Current control measures are aimed at culling infected cows and limiting the access of cattle to infective oocysts. The recent revelations that coyotes (Canis latrans) can excrete N. caninum oocysts in their feces and that white-tailed deer (Odocoileus virginianus) are natural intermediate hosts of the parasite demonstrate the existence of a sylvatic cycle of neosporosis in North America. This complicates parasite-prevention programs but opens many new and exciting avenues of research. Similar canid-ruminant sylvatic cycles might exist in other countries and, if so, need to be investigated.     

Sexual selection and environmental change:what do we know and what comes next?

Anthropogenic environmental change is the most significant threat to biodiversity in the 21st century.Animal populations are experi-encing rapid changes in thei...     

The molecular ecology of biological invasions: what do we know about non-additive genotypic effects and invasion success?

Recent research suggests that non-additive genotypic effects may play an important role in the establishment success of invasive species. However, most empirical data for these inferences come from greenhouse experiments. Only recently has researchers tested non-additive genotypic effects and establishment success of invasive alien species under field conditions. Here we give a brief overview of this research and also carefully consider data from the first publication, to our knowledge, to report on non-additive genotypic effects on invasion success under field conditions. We identify some shortcomings in this important study and make suggestions for future research aimed at better understanding the contributions of non-additive genotypic effects to establishment success and invasion.