Nonhost resistance: how much do we know?

Nonhost disease resistance is the most common form of disease resistance exhibited by plants against the majority of potentially pathogenic microorganisms. Recently, several components of nonhost disease resistance have been identified. Nonhost resistance exhibited against bacteria, fungi and oomycetes can be of two types. Type I nonhost resistance does not produce any visible symptoms whereas type II nonhost resistance results in a rapid hypersensitive response with cell death. Strong similarities exist between nonhost and gene-for-gene resistance responses but it is still not clear if the same mechanism is involved in producing these resistance responses.     

Identity of tendon stem cells – how much do we know?

Tendon stem cells are multi‐potent adult stem cells with broad differentiation plasticity that render them of great importance in cell‐based therapies for the repair of tendons. We called them tendon‐derived stem cells (TDSCs) to indicate the tissue origin from which the stem cells were isolated in vitro. Based on the work of other sources of MSCs and specific work on TDSCs, some properties of TDSCs have been characterized / implicated in vitro. Despite these findings, tendon stem cells remained controversial cells. This was because MSCs residing in different organs, although very similar, were not identical cells. There is evidence of differences in stem cell‐related properties and functions related to tissue origins. Similar to other stem cells, tendon stem cells were identified and characterized in vitro. Their in vivo identities, niche (both anatomical locations and regulators) and roles in tendons were less understood. This review aims to summarize the current evidence of the possible anatomical locations and niche signals regulating the functions of tendon stem cells in vivo. The possible roles of tendon stem cells in tendon healing and non‐healing are presented. Finally, the potential strategies for understanding the in vivo identity of tendon stem cells are discussed.     

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.     

Caspase-2: What do we know today?

Apoptosis (programmed cell death) is essential process in multicellular organisms. Apoptosis plays an important role in cell differentiation, damaged cell elimination, and immune system homeostasis. The review focuses on various mechanisms of signal transduction through caspase-2, which is thought to be one of the most enigmatic proteases involved in apoptosis. Caspase-2 is activated upon stimulation by various factors, including genotoxic stress, death receptor ligation, endoplasmic reticulum stress, metabolic changes, and a number of others. In addition, caspase-2 can act as a tumor suppressor and has been implicated in the cell response to oxidative stress and neurodegenerative progression during ischemic brain injury. Thus, the variety of pathways triggered by caspase-2 sets the enzyme apart from other members of the family and suggests a prominent role in apoptosis. The review analyzes the various functions of this unique caspase and discusses the possible applications of the available knowledge about it in modern oncology and medicine.     

Measures to reduce population fragmentation by roads: what has worked and how do we know?

Roads impede animal movement, which decreases habitat accessibility and reduces gene flow. Ecopassages have been built to mitigate this but there is little research with which to evaluate their effectiveness, owing to the difficulty in accessing results of existing research; the lack of scientific rigor in these studies; and the low priority of connectivity planning in road projects. In this article, we suggest that the imperative for improving studies of ecopassage effectiveness is that road ecology research should be included from the earliest stages of road projects onwards. This would enable before-after-control-impact (BACI) design research, producing useful information for the particular road project as well as rigorous results for use in future road mitigation. Well-designed studies on ecopassage effectiveness could help improve landscape connectivity even with the increasing number and use by traffic of roads.     

Ecological and evolutionary consequences of size‐selective harvesting: how much do we know?

Size-selective harvesting, where the large individuals of a particular species are preferentially taken, is common in both marine and terrestrial habitats. Preferential removal of larger individuals of a species has been shown to have a negative effect on its demography, life history and ecology, and empirical studies are increasingly documenting such impacts. But determining whether the observed changes represent evolutionary response or phenotypic plasticity remains a challenge. In addition, the problem is not recognized in most management plans for fish and marine invertebrates that still mandate a minimum size restriction. We use examples from both aquatic and terrestrial habitats to illustrate some of the biological consequences of size-selective harvesting and discuss possible future directions of research as well as changes in management policy needed to mitigate its negative biological impacts.     

Hypogeous sequestrate fungi in South America – how well do we know them?

Collecting and studying hypogeous sequestrate fungi and their particular fruiting biology has always been challenging and intriguing for scientists. However, knowledge of hypogeous taxa has for a long time been limited mainly to the Northern Hemisphere, and more recently, Australia. Nevertheless, cumulative information on sequestrate fungi for South America (SA) has increased considerably over the years, and constitutes by itself, the aim of this review. We have reviewed the available published literature, from 1880 until recent times, to extract information on records, ecology, and morphological characteristics of hypogeous sequestrate fungi from SA. Based on the 172 taxa cited in the available literature, a trend of increasing interest in the study of these fungi in the region is apparent, yet with an uneven distribution among countries, climate belts, and nature of forest habitats. Hypogeous truffle-like species in SA play a key role in regulating nutrient and carbon cycles and in all ecosystem multifunctionality. The symbiotic status is provided for most species listed, and mutualism, especially ectomycorrhizal, is predominant (82 %). The hypogeous sequestrate fungi in SA are an understudied group of fungi, with exceptional anatomical and biological features as well as in many cases intriguing phylogenetic relationships, requiring more attention and analysis from mycologists.     

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.     

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.     

Mitochondrial cAMP-PKA signaling: What do we really know?

Mitochondria are key organelles for cellular homeostasis. They generate the most part of ATP that is used by cells through oxidative phosphorylation. They also produce reactive oxygen species, neurotransmitters and other signaling molecules. They are important for calcium homeostasis and apoptosis. Considering the role of this organelle, it is not surprising that most mitochondrial dysfunctions are linked to the development of pathologies. Various mechanisms adjust mitochondrial activity according to physiological needs. The cAMP-PKA signaling emerged in recent years as a direct and powerful mean to regulate mitochondrial functions. Multiple evidence demonstrates that such pathway can be triggered from cytosol or directly within mitochondria. Notably, specific anchor proteins target PKA to mitochondria whereas enzymes necessary for generation and degradation of cAMP are found directly in these organelles. Mitochondrial PKA targets proteins localized in different compartments of mitochondria, and related to various functions. Alterations of mitochondrial cAMP-PKA signaling affect the development of several physiopathological conditions, including neurodegenerative diseases. It is however difficult to discriminate between the effects of cAMP-PKA signaling triggered from cytosol or directly in mitochondria. The specific roles of PKA localized in different mitochondrial compartments are also not completely understood. The aim of this work is to review the role of cAMP-PKA signaling in mitochondrial (patho)physiology.