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Isoprene synthase converts dimethylallyl diphosphate to isoprene and appears to be necessary and sufficient to allow plants to emit isoprene at significant rates. Isoprene can protect plants from abiotic stress but is not produced naturally by all plants; for example, Arabidopsis (Arabidopsis thaliana) and tobacco (Nicotiana tabacum) do not produce isoprene. It is typically present at very low concentrations, suggesting a role as a signaling molecule; however, its exact physiological role and mechanism of action are not fully understood. We transformed Arabidopsis with a Eucalyptus globulus isoprene synthase. The regulatory mechanisms of photosynthesis and isoprene emission were similar to those of native emitters, indicating that regulation of isoprene emission is not specific to isoprene-emitting species. Leaf chlorophyll and carotenoid contents were enhanced by isoprene, which also had a marked positive effect on hypocotyl, cotyledon, leaf, and inflorescence growth in Arabidopsis. By contrast, leaf and stem growth was reduced in tobacco engineered to emit isoprene. Expression of genes belonging to signaling networks or associated with specific growth regulators (e.g. gibberellic acid that promotes growth and jasmonic acid that promotes defense) and genes that lead to stress tolerance was altered by isoprene emission. Isoprene likely executes its effects on growth and stress tolerance through direct regulation of gene expression. Enhancement of jasmonic acid-mediated defense signaling by isoprene may trigger a growth-defense tradeoff leading to variations in the growth response. Our data support a role for isoprene as a signaling molecule.

Isoprene, the most abundant endogenous hydrocarbon in human breath, is a promising biomarker for metabolic and cardiovascular diseases. In this paper, we present the detection of isoprene in exhaled breath using the off-beam Quartz-Enhanced Photoacoustic Spectroscopy (QEPAS) method. The sensor employs a homemade quantum cascade laser emitting at 11.03 μm. We use numerical simulations to evaluate the impact of interfering gases (CO2 and H2O) and optimize the laser modulation parameters. The limit of detection reached for 1 s acquisition time is close to 220 parts per billion in volume (ppbv) with a normalized noise equivalent absorption (NNEA) of 1.1×10−8cm−1·W·Hz−1/2. Breath measurements conducted on healthy volunteers reveal a significant increase in isoprene concentration from resting levels (~250–350 ppbv) to elevated levels (~450–650 ppbv) after moderate physical exercise.

BACKGROUND: Some, but not all, plants emit isoprene. Emission of the related monoterpenes is more universal among plants, but the amount of isoprene emitted from plants dominates the biosphere-atmosphere hydrocarbon exchange. SCOPE: The emission of isoprene from plants affects atmospheric chemistry. Isoprene reacts very rapidly with hydroxyl radicals in the atmosphere making hydroperoxides that can enhance ozone formation. Aerosol formation in the atmosphere may also be influenced by biogenic isoprene. Plants that emit isoprene are better able to tolerate sunlight-induced rapid heating of leaves (heat flecks). They also tolerate ozone and other reactive oxygen species better than non-emitting plants. Expression of the isoprene synthase gene can account for control of isoprene emission capacity as leaves expand. The emission capacity of fully expanded leaves varies through the season but the biochemical control of capacity of mature leaves appears to be at several different points in isoprene metabolism. CONCLUSIONS: The capacity for isoprene emission evolved many times in plants, probably as a mechanism for coping with heat flecks. It also confers tolerance of reactive oxygen species. It is an example of isoprenoids enhancing membrane function, although the mechanism is likely to be different from that of sterols. Understanding the regulation of isoprene emission is advancing rapidly now that the pathway that provides the substrate is known.

Isoprene is the dominant non-methane organic compound emitted to the atmosphere 1 – 3 . It drives ozone and aerosol production, modulates atmospheric oxidation and interacts with the global nitrogen cycle 4 – 8 . Isoprene emissions are highly uncertain 1 , 9 , as is the nonlinear chemistry coupling isoprene and the hydroxyl radical, OH—its primary sink 10 – 13 . Here we present global isoprene measurements taken from space using the Cross-track Infrared Sounder. Together with observations of formaldehyde, an isoprene oxidation product, these measurements provide constraints on isoprene emissions and atmospheric oxidation. We find that the isoprene–formaldehyde relationships measured from space are broadly consistent with the current understanding of isoprene–OH chemistry, with no indication of missing OH recycling at low nitrogen oxide concentrations. We analyse these datasets over four global isoprene hotspots in relation to model predictions, and present a quantification of isoprene emissions based directly on satellite measurements of isoprene itself. A major discrepancy emerges over Amazonia, where current underestimates of natural nitrogen oxide emissions bias modelled OH and hence isoprene. Over southern Africa, we find that a prominent isoprene hotspot is missing from bottom-up predictions. A multi-year analysis sheds light on interannual isoprene variability, and suggests the influence of the El Niño/Southern Oscillation. Direct satellite measurements of atmospheric isoprene are compared with model predictions, showing broad agreement but highlighting spatial and temporal biases in modelled isoprene and nitrogen oxide emissions.

Atmospheric chemistry: forest isoprene clears the air Terrestrial vegetation releases vast amounts of volatile organic compounds (VOCs) into the atmosphere, mainly isoprene and derivatives such as monoterpenes and sesquiterpenes, some familiar as the aroma of pine trees. It has been suggested that these compounds are involved in the formation of organic aerosols, which act as 'seeds' for cloud formation and hence as cooling agents via an effect on radiative forcing. Experiments in a plant chamber simulating forest conditions show that isoprene can significantly inhibit new particle formation owing to its high hydroxyl radical reactivity. This surprising result may explain the observed seasonality in the frequency of aerosol nucleation events, as terpene emissions peak in summer, when there are fewer nucleation events than in autumn and spring. This work suggests that an increase in the isoprene content of VOCs in response to climate or land use change might reduce the potential for the formation of new aerosol particles, introducing a previously unrecognized element of climate warming. Volatile organic compounds, such as isoprene and monoterpenes, are emitted by terrestrial vegetation and have been suggested to be involved in organic aerosol formation, which in turn affects radiative forcing and climate. Simulation experiments conducted in a plant chamber now reveal that isoprene can significantly inhibit new particle formation; this may explain the observed seasonality in the frequency of aerosol nucleation events. It has been suggested that volatile organic compounds (VOCs) are involved in organic aerosol formation, which in turn affects radiative forcing and climate 1 . The most abundant VOCs emitted by terrestrial vegetation are isoprene and its derivatives, such as monoterpenes and sesquiterpenes 2 . New particle formation in boreal regions is related to monoterpene emissions 3 and causes an estimated negative radiative forcing 4 of about -0.2 to -0.9 W m -2 . The annual variation in aerosol growth rates during particle nucleation events correlates with the seasonality of monoterpene emissions of the local vegetation, with a maximum during summer 5 . The frequency of nucleation events peaks, however, in spring and autumn 5 . Here we present evidence from simulation experiments conducted in a plant chamber that isoprene can significantly inhibit new particle formation. The process leading to the observed decrease in particle number concentration is linked to the high reactivity of isoprene with the hydroxyl radical (OH). The suppression is stronger with higher concentrations of isoprene, but with little dependence on the specific VOC mixture emitted by trees. A parameterization of the observed suppression factor as a function of isoprene concentration suggests that the number of new particles produced depends on the OH concentration and VOCs involved in the production of new particles undergo three to four steps of oxidation by OH. Our measurements simulate conditions that are typical for forested regions and may explain the observed seasonality in the frequency of aerosol nucleation events, with a lower number of nucleation events during summer compared to autumn and spring 5 . Biogenic emissions of isoprene are controlled by temperature and light 2 , and if the relative isoprene abundance of biogenic VOC emissions increases in response to climate change or land use change, the new particle formation potential may decrease, thus damping the aerosol negative radiative forcing effect.

Ground-level ozone is adverse to human and vegetation health. High ground-level ozone concentrations usually occur over the United States in the summer, often referred to as the ozone season. However, observed monthly mean ozone concentrations in the southeastern United States were higher in October than July in 2010. The October ozone average in 2010 reached that of July in the past three decades (1980–2010). Our analysis shows that this extreme October ozone in 2010 over the Southeast is due in part to a dry and warm weather condition, which enhances photochemical production, air stagnation, and fire emissions. Observational evidence and modeling analysis also indicate that another significant contributor is enhanced emissions of biogenic isoprene, a major ozone precursor, from water-stressed plants under a dry and warm condition. The latter finding is corroborated by recent laboratory and field studies. This climate-induced biogenic control also explains the puzzling fact that the two extremes of high October ozone both occurred in the 2000s when anthropogenic emissions were lower than the 1980s and 1990s, in contrast to the observed decreasing trend of July ozone in the region. The occurrences of a drying and warming fall, projected by climate models, will likely lead to more active photochemistry, enhanced biogenic isoprene and fire emissions, an extension of the ozone season from summer to fall, and an increase of secondary organic aerosols in the Southeast, posing challenges to regional air quality management.

Natural rubber is a unique biopolymer of strategic importance that, in many of its most significant applications, cannot be replaced by synthetic alternatives. The rubber tree Hevea brasiliensis is the almost exclusive commercial source of natural rubber currently and alternative crops should be developed for several reasons, including: a disease risk to the rubber tree that could potentially decimate current production, a predicted shortage of natural rubber supply, increasing allergic reactions to rubber obtained from the Brazilian rubber tree and a general shift towards renewables. This review summarizes our knowledge of plants that can serve as alternative sources of natural rubber, of rubber biosynthesis and the scientific gaps that must be filled to bring the alternative crops into production.

Apicomplexan parasites possess a plastid organelle called the apicoplast. Inhibitors that selectively target apicoplast housekeeping functions, including DNA replication and protein translation, are lethal for the parasite, and several (doxycycline, clindamycin, and azithromycin) are in clinical use as antimalarials. A major limitation of such drugs is that treated parasites only arrest one intraerythrocytic development cycle (approximately 48 hours) after treatment commences, a phenotype known as the 'delayed death' effect. The molecular basis of delayed death is a long-standing mystery in parasitology, and establishing the mechanism would aid rational clinical implementation of apicoplast-targeted drugs. Parasites undergoing delayed death transmit defective apicoplasts to their daughter cells and cannot produce the sole, blood-stage essential metabolic product of the apicoplast: the isoprenoid precursor isopentenyl-pyrophosphate. How the isoprenoid precursor depletion kills the parasite remains unknown. We investigated the requirements for the range of isoprenoids in the human malaria parasite Plasmodium falciparum and characterised the molecular and morphological phenotype of parasites experiencing delayed death. Metabolomic profiling reveals disruption of digestive vacuole function in the absence of apicoplast derived isoprenoids. Three-dimensional electron microscopy reveals digestive vacuole fragmentation and the accumulation of cytostomal invaginations, characteristics common in digestive vacuole disruption. We show that digestive vacuole disruption results from a defect in the trafficking of vesicles to the digestive vacuole. The loss of prenylation of vesicular trafficking proteins abrogates their membrane attachment and function and prevents the parasite from feeding. Our data show that the proximate cause of delayed death is an interruption of protein prenylation and consequent cellular trafficking defects.

Isoprene is a substantial contributor to the global secondary organic aerosol (SOA) burden, with implications for public health and the climate system. The mechanism by which isoprene-derived SOA is formed and the influence of environmental conditions, however, remain unclear. We present evidence from controlled smog chamber experiments and field measurements that in the presence of high levels of nitrogen oxides (NO ₓ = NO + NO ₂) typical of urban atmospheres, 2-methyloxirane-2-carboxylic acid (methacrylic acid epoxide, MAE) is a precursor to known isoprene-derived SOA tracers, and ultimately to SOA. We propose that MAE arises from decomposition of the OH adduct of methacryloylperoxynitrate (MPAN). This hypothesis is supported by the similarity of SOA constituents derived from MAE to those from photooxidation of isoprene, methacrolein, and MPAN under high-NO ₓ conditions. Strong support is further derived from computational chemistry calculations and Community Multiscale Air Quality model simulations, yielding predictions consistent with field observations. Field measurements taken in Chapel Hill, North Carolina, considered along with the modeling results indicate the atmospheric significance and relevance of MAE chemistry across the United States, especially in urban areas heavily impacted by isoprene emissions. Identification of MAE implies a major role of atmospheric epoxides in forming SOA from isoprene photooxidation. Updating current atmospheric modeling frameworks with MAE chemistry could improve the way that SOA has been attributed to isoprene based on ambient tracer measurements, and lead to SOA parameterizations that better capture the dependency of yield on NO ₓ.

The complexity inherent in biological systems challenges efforts to rationally engineer novel phenotypes, especially those not amenable to high-throughput screens and selections. In nature, increased mutation rates generate diversity in a population that can lead to the evolution of new phenotypes. Here we construct an adaptive control system that increases the mutation rate in order to generate diversity in the population, and decreases the mutation rate as the concentration of a target metabolite increases. This system is called feedback-regulated evolution of phenotype (FREP), and is implemented with a sensor to gauge the concentration of a metabolite and an actuator to alter the mutation rate. To evolve certain novel traits that have no known natural sensors, we develop a framework to assemble synthetic transcription factors using metabolic enzymes and construct four different sensors that recognize isopentenyl diphosphate in bacteria and yeast. We verify FREP by evolving increased tyrosine and isoprenoid production. Cells can adapt rapidly to survive and efficiently exploit constantly changing environments by varying their mutation rate. Here the authors construct an in silico system to modulate mutation rate, and demonstrate that this method can be used in the laboratory to create specific phenotypes.