Matching roots to their environment

Background

Plants form the base of the terrestrial food chain and provide medicines, fuel, fibre and industrial materials to humans. Vascular land plants rely on their roots to acquire the water and mineral elements necessary for their survival in nature or their yield and nutritional quality in agriculture. Major biogeochemical fluxes of all elements occur through plant roots, and the roots of agricultural crops have a significant role to play in soil sustainability, carbon sequestration, reducing emissions of greenhouse gasses, and in preventing the eutrophication of water bodies associated with the application of mineral fertilizers.

Scope

This article provides the context for a Special Issue of Annals of Botany on ‘Matching Roots to Their Environment’. It first examines how land plants and their roots evolved, describes how the ecology of roots and their rhizospheres contributes to the acquisition of soil resources, and discusses the influence of plant roots on biogeochemical cycles. It then describes the role of roots in overcoming the constraints to crop production imposed by hostile or infertile soils, illustrates root phenotypes that improve the acquisition of mineral elements and water, and discusses high-throughput methods to screen for these traits in the laboratory, glasshouse and field. Finally, it considers whether knowledge of adaptations improving the acquisition of resources in natural environments can be used to develop root systems for sustainable agriculture in the future.     

Ectomycorrhizal fungal diversity in Quercus ilex Mediterranean woodlands: variation among sites and over soil depth profiles in hyphal exploration types, species richness and community composition

Understanding the factors underlying the distribution of biodiversity is a challenging issue in ecology. Here, we examined the distribution patterns of ectomycorrhizal fungal diversity across the soil profile in three Quercus ilex forests. Contact exploration type strongly dominated at all sites, but was most prevalent in the upper, organic-rich soil layers. At each site, three quarters of the ectomycorrhizal tips and 59 % of taxa were restricted to the ten first centimeters of the soil profile. The relative abundance of the dominant family Russulaceae increased with increasing soil depth. Species composition varied significantly among sites, with most species being rare. Species that occurred in only one of the three sites accounted for 78.9 % of all species, and 57.3 % of species were represented by a single ECM root tip. Our results suggest that (i) rare species at both local and regional scales contribute to the highly diverse fungal assemblages in Mediterranean forests and (ii) multi-sites studies including the whole soil profile are needed to provide comprehensive overviews of the taxonomic and functional diversities of ectomycorrhizal communities.     

Assessment of systematic effects of methodological characteristics on candidate genetic associations

Candidate genetic association studies have been found to have a low replication rate in the past. Here, we aimed to assess whether aspects of reported methodological characteristics in genetic association studies may be related to the magnitude of effects observed. An observational, literature-based investigation of 511 case–control studies of genetic association studies indexed in 2007, was undertaken. Meta-regression analyses were used to assess the relationship between 23 reported methodological characteristics and the magnitude of genetic associations. The 511 studies had been conducted in 52 countries and were published in 220 journals (median impact factor 5.1). The multivariate meta-regression model of methodological characteristics plus disease category accounted for 17.2 % of the between-study variance in the magnitude of the reported genetic associations. Our findings are consistent with the view that better conducted and better reported genetic association research may lead to less inflated results.     

It cuts two ways: microtubule loss during Alzheimer disease

EMBO J 32: 2920–2937 10.1038/emboj.2013.207; published online September242013Microtubule loss from axons and dendrites is a key contributor to nervous system degeneration during Alzheimer disease. Previous evidence suggested a simple pathway by which tau dissociation from microtubules in the axon allows excess severing of microtubules by katanin. Now, new evidence has emerged for a more complex pathway by which abnormal tau invasion into dendrites, triggered by Aβ oligomers, results in excess severing of microtubules by spastin.Alzheimer disease (AD) is a member of a category of neurodegenerative disorders called tauopathies (Wang and Liu, 2008). These are diseases of the nervous system in which tau becomes abnormally phosphorylated, and thereby detaches from microtubules. As the microtubules lose tau, they diminish in number and density, and this loss of microtubule mass negatively impacts the capacity of the neuron to maintain axonal transport and synaptic connections. Terms such as disintegrate or ‘fall apart'' are often used to describe the effect on the microtubules as they lose tau, but to date there has been very little information on how this happens. There is no mechanistic evidence to support the view that the microtubules become less stable and simply disassemble by their normal dynamic properties.One possibility is that tau normally protects microtubules from being destroyed by various proteins in the axon that would otherwise cut them into pieces or in some other way break them down. This presumably reflects a physiological mechanism wherein the regulation of tau dissociation from the microtubule via signalling pathways controls when and where microtubule breakage normally occurs. When a pathological condition causes tau to detach from microtubules, they become extremely sensitive to such factors. In addition, there is strong evidence that the abnormal tau, whether soluble or filamentous, can elicit toxic gain-of-function effects on the axon (Wang and Liu, 2008).To make matters even more complex, AD is not a pure tauopathy. Beta amyloid (Aβ) accumulates abnormally in the brain during AD, and this prompts tau to become hyperphosphorylated and lose association with microtubules. However, the Aβ can also elicit microtubule loss, independent of tau dissociation from the microtubules. In AD, there is also a loss of microtubules from dendrites, and this introduces an additional degree of complexity. Tau is normally less enriched in dendrites than axons. In AD, tau invades dendrites abnormally through deregulation of its normal sorting mechanism, and this somehow leads to microtubule loss from dendrites (Zempel et al, 2010).Microtubule loss is a common end point of multiple pathways, some involving loss of tau function, others involving gain-of-function effects of abnormal tau, and still others working through tau-dependent Aβ toxicity. All of this is not to say that the effects on microtubules are the only reason or even the principal explanation for axonal degeneration in AD, but the loss of microtubules is an important contributor to nervous system degeneration. Preventing or reversing the effects on microtubules could help stave off degeneration and hence provide patients with additional years of cognitive health and better quality of life.Microtubule assembly and disassembly occur from the ends of a microtubule, mainly (and often exclusively) at the plus end of the microtubule in living cells. Proteins that regulate microtubule stability affect the rate of these dynamics at microtubule ends. In recent years, a great deal of attention has focused on a category of proteins, termed microtubule-severing proteins. These proteins are enzymes that yank at the microtubule anywhere along its length to pull out a tubulin subunit, and thereby ‘cut'' the microtubule by causing it to break into pieces (Roll-Mecak and Vale, 2008). If the microtubule is sufficiently stable in the region of the break, the parent microtubule is cut into two shorter microtubules that persist, with minimal disassembly of either of the two pieces. If a microtubule is severed in its more labile region, the breakage could cause a great deal of disassembly. If the tubulin being yanked is situated at one of the ends of a microtubule, the result would be a shortening of the microtubule from that end; that is, disassembly. Thus, microtubule severing in the axon can certainly lead to microtubule loss, either by cutting the polymer all the way to subunits, inducing disassembly directly from microtubule ends or promoting disassembly as a secondary effect to the cutting.To date, the AAA enzymes katanin and spastin are the best studied of the microtubule-severing proteins (Yu et al, 2008). Spastin was originally identified as the product of the gene whose mutations are the chief cause of hereditary spastic paraplegia. Curiously, neurons express levels of spastin and katanin that are theoretically high enough to completely sever all of the microtubules in the neuron to subunits (Solowska et al, 2008), and yet this does not happen. Various regulatory mechanisms presumably keep the activities of the severing proteins in check. One of these mechanisms, in the case of katanin, is microtubule-bound tau, which protects the microtubule from being accessed by katanin (Qiang et al, 2006).Could microtubule loss in AD be due, at least in part, to excess microtubule severing due to deregulation of microtubule-severing proteins? We have posited that heightened severing of the microtubules by katanin, as the microtubules lose association with tau, is a contributing factor to the degradation of microtubules in the axons of AD patients (Sudo and Baas, 2011). A role for spastin in this pathway is questionable, because tau does not appear to protect microtubules against spastin as effectively as it does against katanin (Qiang et al, 2006). However, we now know that spastin is far from irrelevant to AD, as an exciting new article from the Mandelkow and Dawson laboratories implicates spastin in an entirely different pathway for microtubule loss in AD (Zempel et al, 2013). Whereas the katanin pathway is more relevant to axons, this new spastin pathway is more relevant to dendrites.In this new work, Zempel et al (2013) exposed mature primary neurons to oligomers of Aβ and observed microtubule breakdown in dendrites that had been invaded by tau. They found that the missorting of tau leads to an elevation of TTLL6 (Tubulin-Tyrosine-Ligase-Like-6) in dendrites, and this results in a marked increase in the polyglutamylation status of the microtubules. Because spastin has a strong preference for polyglutamylated microtubules, the microtubules become more sensitive to spastin-induced severing. Exactly why katanin is not a factor remains unclear, as polyglutamylation renders microtubules more sensitive to both of the severing proteins, not just spastin (Lacroix et al, 2010). Perhaps some of the tau that invades the dendrite is able to bind to microtubules and protect them from katanin, or perhaps katanin is less potent in dendrites because their microtubules are poorly acetylated, as katanin prefers acetylated microtubules to unacetylated ones (Sudo and Baas, 2011). Whatever the case, these new studies suggest that spastin, a protein whose mutations cause an entirely different neurodegenerative disease, is also a major factor in AD.What are the implications of these findings for AD treatment? In recent years, there have been encouraging results on rodent models for AD, in which behavioural improvement and enhanced neuronal vitality were observed when the animals were treated with drugs that stabilize microtubules against disassembly (Zhang et al, 2012). Such drugs are currently in clinical trials for AD (Barten et al, 2012). This strategy is based on the presumption that the microtubule loss that occurs in AD is due to destabilization of the microtubules. However, the results discussed here suggest that the primary cause of the microtubule loss could be something quite different, namely excess severing of microtubules. In this regard, it is relevant that both katanin and spastin seem to have a preference for severing stable microtubules (Lacroix et al, 2010; Sudo and Baas, 2011). Therefore, while treatment with a microtubule-stabilizing drug would mitigate disassembly that occurs as an aftereffect of microtubule severing, the severing events themselves would likely be increased (Figure 1). Heightened microtubule severing in axons and dendrites, even if the total levels of microtubule mass are preserved, could result in a gradual shift from a normal distribution of long and short microtubules to a predominance of microtubules too short to support sustained excursions of organelle transport. Long microtubules are also necessary as compression-bearing struts that prevent axons and dendrites from collapsing on themselves. We suspect that appropriate treatment regimes can be devised to prevent such dire consequences from happening, but we would advocate for the development of new drugs that inhibit microtubule-severing proteins. Such drugs may prove to be a better approach (on their own or in combination with a stabilizing drug) for preserving the fidelity of axonal and dendritic microtubules in AD patients. Given that the structure of the severing proteins is known, it may be straightforward to develop inhibitors, especially to their ATPase domains.Open in a separate windowFigure 1Microtubules in axons and dendrites consist of a stable region towards the minus end of the microtubule and a labile region towards the plus end, as well as a pool of free tubulin subunits. Microtubule severing is a normal event in the neuron, when tightly regulated. Abnormal (deregulated) microtubule severing is posited to account for microtubule loss in AD. Severing in the stable region of the microtubule would create two new microtubules, with fairly minimal disassembly of either one. Severing in the labile region of the microtubule would result in notably more disassembly. Severing at the end of the microtubule would result in disassembly. Because known microtubule-severing proteins favour the stable region of the microtubule, treatment of AD with a microtubule-stabilizing drug may mitigate disassembly that occurs as an aftereffect of the severing, but the severing events themselves would likely increase.     

Attenuation of insulin signalling contributes to FSN‐1‐mediated regulation of synapse development

A neuronal F‐box protein FSN‐1 regulates Caenorhabditis elegans neuromuscular junction development by negatively regulating DLK‐mediated MAPK signalling. In the present study, we show that attenuation of insulin/IGF signalling also contributes to FSN‐1‐dependent synaptic development and function. The aberrant synapse morphology and synaptic transmission in fsn‐1 mutants are partially and specifically rescued by reducing insulin/IGF‐signalling activity in postsynaptic muscles, as well as by reducing the activity of EGL‐3, a prohormone convertase that processes agonistic insulin/IGF ligands INS‐4 and INS‐6, in neurons. FSN‐1 interacts with, and potentiates the ubiquitination of EGL‐3 in vitro, and reduces the EGL‐3 level in vivo. We propose that FSN‐1 may negatively regulate insulin/IGF signalling, in part, through EGL‐3‐dependent insulin‐like ligand processing.     

CREB3L1 Is a Metastasis Suppressor That Represses Expression of Genes Regulating Metastasis,Invasion, and Angiogenesis

The unfolded protein response (UPR) is activated in response to hypoxia-induced stress such as in the tumor microenvironment. This study examined the role of CREB3L1 (cyclic AMP [cAMP]-responsive element-binding protein 3-like protein 1), a member of the UPR, in breast cancer development and metastasis. Initial experiments identified the loss of CREB3L1 expression in metastatic breast cancer cell lines compared to low-metastasis or nonmetastatic cell lines. When metastatic cells were transfected with CREB3L1, they demonstrated reduced invasion and migration in vitro, as well as a significantly decreased ability to survive under nonadherent or hypoxic conditions. Interestingly, in an in vivo rat mammary tumor model, not only did CREB3L1-expressing cells fail to form metastases compared to CREB3L1 null cells but regression of the primary tumors was seen in 70% of the animals as a result of impaired angiogenesis. Microarray and chromatin immunoprecipitation with microarray technology (ChIP on Chip) analyses identified changes in the expression of many genes involved in cancer development and metastasis, including a decrease in those involved in angiogenesis. These data suggest that CREB3L1 plays an important role in suppressing tumorigenesis and that loss of expression is required for the development of a metastatic phenotype.     

Agonist binding to the GluK5 subunit is sufficient for functional surface expression of heteromeric GluK2/GluK5 kainate receptors

Trafficking of ionotropic glutamate receptors to the plasma membrane commonly requires occupation of the agonist binding sites. This quality control check does not typically involve receptor activation, as binding by competitive antagonists or to non-functional channels may also permit surface expression. The tetrameric kainate receptors can be assembled from five different subunits (GluK1–GluK5). While the “low-affinity” GluK1-3 subunits are able to produce functional homomeric receptors, the “high-affinity” GluK4 and GluK5 subunits require co-assembly with GluK1, 2, or 3 for surface expression. These two different types of subunits have distinct functional roles in the receptor. Therefore, we examined the relative importance of occupancy of the agonist site of the GluK2 or GluK5 subunit for surface expression of heteromeric receptors. We created subunits with a mutation within the S2 ligand-binding domain which decreased agonist affinity. Mutations at this site reduced functional surface expression of homomeric GluK2 receptors, but surface expression of these receptors could be increased with either a competitive antagonist or co-assembly with wild-type GluK5. In contrast, mutations in the GluK5 subunit reduced the production of functional heteromeric receptors at the membrane, and could not be rescued with either an antagonist or wild-type GluK2. These findings indicate that ligand binding to only the GluK5 subunit is both necessary and sufficient to allow trafficking of recombinant GluK2/K5 heteromers to the cell membrane, but that occupancy of the GluK2 site alone is not. Our results suggest a distinct role for the GluK5 subunit in regulating surface expression of heteromeric kainate receptors.     

Protection against peroxynitrite-induced DNA damage by mesalamine: implications for anti-inflammation and anti-cancer activity

Mesalamine (5-aminosalicylic acid, 5-ASA) is known to be the first-line medication for treatment of patients with ulcerative colitis. Studies have demonstrated that ulcerative colitis patients treated with 5-ASA have an overall decrease in the risk of developing colorectal carcinoma. However, the mechanisms underlying 5-ASA-mediated anti-inflammatory and anti-cancer effects are yet to be elucidated. Because peroxynitrite has been critically involved in inflammatory stress and carcinogenesis, this study was undertaken to investigate the effects of 5-ASA in peroxynitrite-induced DNA strand breaks, an important event leading to peroxynitrite-elicited cytotoxicity. Incubation of φX-174 plasmid DNA with the peroxynitrite generator 3-morpholinosydnonimine (SIN-1) led to the formation of both single- and double-stranded DNA breaks in a concentration-dependent manner. The presence of 5-ASA at 0.1 and 1.0 mM was found to significantly inhibit SIN-1-induced DNA strand breaks in a concentration-dependent manner. The consumption of oxygen induced by SIN-1 was found to not be affected by 5-ASA at 0.1–50 mM, indicating that 5-ASA at these concentrations is not involved in the auto-oxidation of SIN-1 to form peroxynitrite. It is observed that 5-ASA at 0.1–1 mM showed considerable inhibition of peroxynitrite-mediated luminol chemiluminescence in a dose-dependent fashion, suggesting that 5-ASA is able to directly scavenge the peroxynitrite. Electron paramagnetic resonance (EPR) spectroscopy in combination with spin-trapping experiments, using 5,5-dimethylpyrroline-N-oxide (DMPO) as spin trap resulting in the formation of DMPO-hydroxyl radical adduct from peroxynitrite, and 5-ASA only at higher concentration (1 mM) inhibited the hydroxyl radical adduct while shifting EPR spectra, indicating that 5-ASA at higher concentrations may generate a more stable free radical species rather than acting purely as a hydroxyl radical scavenger. Taken together, these studies demonstrate for the first time that 5-ASA can potently inhibit peroxynitrite-mediated DNA strand breakage, scavenge peroxynitrite, and affect peroxynitrite-mediated radical formation, which may be responsible, at least partially, for its anti-inflammatory and anti-cancer effects.     

Integrating multiple data sources to assess the distribution and abundance of bottlenose dolphins Tursiops truncatus in Scottish waters

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