Adaptive developmental plasticity: what is it,how can we recognize it and when can it evolve?

Developmental plasticity describes situations where a specific input during an individual''s development produces a lasting alteration in phenotype. Some instances of developmental plasticity may be adaptive, meaning that the tendency to produce the phenotype conditional on having experienced the developmental input has been under positive selection. We discuss the necessary assumptions and predictions of hypotheses concerning adaptive developmental plasticity (ADP) and develop guidelines for how to test empirically whether a particular example is adaptive. Central to our analysis is the distinction between two kinds of ADP: informational, where the developmental input provides information about the future environment, and somatic state-based, where the developmental input enduringly alters some aspect of the individual''s somatic state. Both types are likely to exist in nature, but evolve under different conditions. In all cases of ADP, the expected fitness of individuals who experience the input and develop the phenotype should be higher than that of those who experience the input and do not develop the phenotype, while the expected fitness of those who do not experience the input and do not develop the phenotype should be higher than those who do not experience the input and do develop the phenotype. We describe ancillary predictions that are specific to just one of the two types of ADP and thus distinguish between them.     

What is antibiotic resistance and how can we measure it?

Antibiotic resistance is being found with increasing frequency in both pathogenic and commensal bacteria of humans and animals. Quantifying resistance within and between bacterial and host populations presents scientists with complex challenges in terms of laboratory methodologies and sampling design. Here, we discuss, from an epidemiological perspective, how antibiotic resistance can be defined and measured and the limitations of current approaches.     

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.     

Litter decomposition: what controls it and how can we alter it to sequester more carbon in forest soils?

Key recent developments in litter decomposition research are reviewed. Long-term inter-site experiments indicate that temperature and moisture influence early rates of litter decomposition primarily by determining the plants present, suggesting that climate change effects will be small unless they alter the plant forms present. Thresholds may exist at which single factors control decay rate. Litter decomposes faster where the litter type naturally occurs. Elevated CO₂ concentrations have little effect on litter decomposition rates. Plant tissues are not decay-resistant; it is microbial and biochemical transformations of materials into novel recalcitrant compounds rather than selective preservation of recalcitrant compounds that creates stable organic matter. Altering single characteristics of litter will not substantially alter decomposition rates. Nitrogen addition frequently leads to greater stabilization into humus through a combination of chemical reactions and enzyme inhibition. To sequester more C in soil, we need to consider not how to slow decomposition, but rather how to divert more litter into humus through microbial and chemical reactions rather than allowing it to decompose. The optimal strategy is to have litter transformed into humic substances and then chemically or physically protected in mineral soil. Adding N through fertilization and N-fixing plants is a feasible means of stimulating humification.     

Sugarcane improvement: how far can we go?

In recent years, efforts to improve sugarcane have focused on the development of biotechnology for this crop. It has become clear that sugarcane lacks tools for the biotechnological route of improvement and that the initial efforts in sequencing ESTs had limited impact for breeding. Until recently, the models used by breeders in statistical genetics approaches have been developed for diploid organisms, which are not ideal for a polyploid genome such as that of sugarcane. Breeding programs are dealing with decreasing yield gains. The contribution of multiple alleles to complex traits such as yield is a basic question underlining the breeding efforts that could only be addressed by the development of specific tools for this grass. However, functional genomics has progressed and gene expression profiling is leading to the definition of gene networks. The sequencing of the sugarcane genome, which is underway, will greatly contribute to numerous aspects of research on grasses. We expect that both the transgenic and the marker-assisted route for sugarcane improvement will contribute to increased sugar, stress tolerance, and higher yield and that the industry for years to come will be able to rely on sugarcane as the most productive energy crop.     

Celiac disease: how complicated can it get?

In the small intestine of celiac disease patients, dietary wheat gluten and similar proteins in barley and rye trigger an inflammatory response. While strict adherence to a gluten-free diet induces full recovery in most patients, a small percentage of patients fail to recover. In a subset of these refractory celiac disease patients, an (aberrant) oligoclonal intraepithelial lymphocyte population develops into overt lymphoma. Celiac disease is strongly associated with HLA-DQ2 and/or HLA-DQ8, as both genotypes predispose for disease development. This association can be explained by the fact that gluten peptides can be presented in HLA-DQ2 and HLA-DQ8 molecules on antigen presenting cells. Gluten-specific CD4⁺ T cells in the lamina propria respond to these peptides, and this likely enhances cytotoxicity of intraepithelial lymphocytes against the intestinal epithelium. We propose a threshold model for the development of celiac disease, in which the efficiency of gluten presentation to CD4⁺ T cells determines the likelihood of developing celiac disease and its complications. Key factors that influence the efficiency of gluten presentation include: (1) the level of gluten intake, (2) the enzyme tissue transglutaminase 2 which modifies gluten into high affinity binding peptides for HLA-DQ2 and HLA-DQ8, (3) the HLA-DQ type, as HLA-DQ2 binds a wider range of gluten peptides than HLA-DQ8, (4) the gene dose of HLA-DQ2 and HLA-DQ8, and finally,(5) additional genetic polymorphisms that may influence T cell reactivity. This threshold model might also help to understand the development of refractory celiac disease and lymphoma.     

Remission in psoriatic arthritis: is it possible and how can it be predicted?

Introduction

Since remission is now possible in psoriatic arthritis (PsA) we wished to examine remission rates in PsA patients following anti tumour necrosis factor alpha (TNFα) therapy and to examine possible predictors of response.

Methods

Analysis of a prospective patient cohort attending a biologic clinic, between November 2004 and March 2008, was performed prior to commencing therapy and at regular intervals. Baseline clinical characteristics including demographics, previous disease-modifying antirheumatic drug (DMARD) response, tender and swollen joint counts, early morning stiffness, pain visual analogue score, patient global assessment, C reactive protein (CRP) and health assessment questionnaire (HAQ) were collected.

Results

A total of 473 patients (152 PsA; 321 rheumatoid arthritis (RA)) were analyzed. At 12 months remission, defined according to the disease activity score using 28 joint count and CRP (DAS28-CRP), was achieved in 58% of PsA patients compared to 44% of RA patients, significant improvement in outcome measures were noted in both groups (P < 0.05). Analysis of a subgroup of PsA and RA patients matched for DAS28-CRP at baseline also showed higher numbers of PsA patients achieving remission. Linear regression analysis identified the HAQ at baseline as the best predictor of remission in PsA patients (P < 0.001).

Conclusions

DAS28 remission is possible in PsA patients at one year following anti-TNF therapy, at higher rates than in RA patients and is predicted by baseline HAQ.     

Environmental auditing: what is it and how can it contribute to environmental education?

The concept of environmental auditing and its use by industry and commerce are explained. A questionnaire-based method is described which can be used to introduce students to the techniques of environmental auditing, as well as developing problem-solving and communication skills and possibly even resulting in positive benefit to the educational institution.     

Stem cell ageing: does it happen and can we intervene?

Adult stem cells have become the focus of intense research in recent years as a result of their role in the maintenance and repair of tissues. They exert this function through their extensive expansion (self-renewal) and multipotent differentiation capacity. Understanding whether adult stem cells retain this capacity throughout the lifespan of the individual, or undergo a process of ageing resulting in a decreased stem cell pool, is an important area of investigation. Progress in this area has been hampered by lack of suitable models and of appropriate markers and assays to identify stem cells. However, recent data suggest that an understanding of the mechanisms governing stem cell ageing can give insight into the mechanism of tissue ageing and, most importantly, advance our ability to use stem cells in cell and gene therapy strategies.     

Estrogen and memory in women: how can we reconcile the findings?

Although several randomized controlled trials (RCTS) of surgically menopausal women have provided evidence that estrogen protects aspects of memory, many cross-sectional and longitudinal studies, including those from the RCT, the Women's Health Initiative Memory Study (WHIMS), have reported inconsistent information with regard to the relationship between estrogen and aspects of cognitive function. Although numerous reasons could be offered to explain these discrepancies in research findings, recent evidence from rodent, nonhuman primate, and human studies consistently suggests that one possibility may be critical to our understanding of the estrogenic effect on memory. Results of these animal and human studies indicate that the initiation of estrogen treatment at the time of menopause, or soon after ovariectomy (OVX), provides a window of opportunity for the preservation of memory in females whereas the administration of the hormone following a considerable delay in time after OVX has little or no beneficial effect on cognition. Considering the evidence that, in several organ systems, heightened disease risks accrue to a longer duration of estrogen deprivation in women, it would seem important to determine whether this is also true for brain structure and function in order to protect the quality of life for the considerable number of women who undergo a surgical menopause before their natural menopause had occurred.     

What is speciation and how should we study it?

To understand speciation, we first need to know what species are. Yet debates over species concepts have seemed endless, with little obvious relevance to the study of speciation. Recently, there has been progress in resolving these debates, favoring a lineage-based, evolutionary species concept. This progress calls for reconsideration of the study of speciation. Traditional speciation research based on the biological species concept has led to great advances in understanding how nonallopatric speciation occurs and how species diverge and remain separate from each other. However, this research has neglected the question of how new species arise in the first place for the most common geographic mode (allopatric). A new and very different research program is needed to understand the ecological and evolutionary processes that split an ancestral species into new allopatric lineages. This research program will connect speciation to many other fundamental questions in evolutionary biology, ecology, biogeography, and conservation biology.     

Nuclear architecture: Is it important for genome function and can we prove it?

Gene regulation in higher eukaryotes has been shown to involve regulatory sites, such as promoters and enhancers which act at the level of individual genes, and mechanisms which control the functional state of gene clusters. A fundamental question is whether additional levels of genome control exist. Nuclear organization and large-scale chromatin structure may constitute such a level and play an important role in the cell-type specific orchestration of the expression of thousands of genes in eukaryotic cells. Numerous observations indicate a tight correlation between genome activity and nuclear and large-scale chromatin structure. However, causal relationships are rare. Here we explore how these might be uncovered.     

When does selective hunting select,how can we tell,and what should we do about it?

Potential evolutionary consequences of selective hunting of mammals are controversial because of limited evidence and important socio‐economic impacts. Several ecological and management variables facilitate evolutionary responses to selection for horn, tusk or antler size, including strong selective hunting pressure; harvest of males with large horns, tusks or antlers before they can breed; unavailable or ineffective sources of unselected immigrants; and age‐dependent relationships between horn, tusk or antler size and male mating success. Plastic responses of male horns, tusks and antlers to environment are probably more common than evolutionary changes. Evidence for evolutionary effects of selective hunting is strong for large mammals where biological characteristics and hunting regulations combine to favour them.