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In recent years, anthropogenic activities and climate change have significantly increased exposure of plants to environmental stresses (single or multiple) and pollutants, with negative consequences for the survival and productivity of vegetation. Plants may activate an armament of defenses against stresses. Isoprene, the most abundant biogenic volatile organic compound (BVOC) emitted by plants, is supposed to have a direct or indirect antioxidant role by quenching reactive oxygen species (ROS) or by reprogramming gene expression for antioxidant activation. On the other hand, isoprene is involved in the chemistry of troposphere, further contributing to a build up of pollutants when mixing with anthropogenic gases. In this review, we summarize present knowledge on the impact of air and soil pollutants on isoprene emission by plants, indicating possible feedback and feedforward mechanisms that may affect whole ecosystem functioning and evolution of plant species. 

Isoprene is emitted by some plants and is the most abundant biogenic hydrocarbon entering the atmosphere. Multiple studies have elucidated protective roles of isoprene against several environmental stresses, including high temperature, excessive ozone, and herbivory attack. However, isoprene emission adversely affects atmospheric chemistry by contributing to ozone production and aerosol formation. Thus, understanding the regulation of isoprene emission in response to varying environmental conditions, for example, elevated CO₂, is critical to comprehend how plants will respond to climate change. Isoprene emission decreases with increasing CO₂concentration; however, the underlying mechanism of this response is currently unknown. We demonstrated that high-CO₂-mediated suppression of isoprene emission is independent of photosynthesis and light intensity, but it is reduced with increasing temperature. Furthermore, we measured methylerythritol 4-phosphate (MEP) pathway metabolites in poplar leaves harvested at ambient and high CO₂to identify why isoprene emission is reduced under high CO₂. We found that hydroxymethylbutenyl diphosphate (HMBDP) was increased and dimethylallyl diphosphate (DMADP) decreased at high CO_2.This implies that high CO₂impeded the conversion of HMBDP to DMADP, possibly through the inhibition of HMBDP reductase activity, resulting in reduced isoprene emission. We further demonstrated that although this phenomenon appears similar to abscisic acid (ABA)-dependent stomatal regulation, it is unrelated as ABA treatment did not alter the effect of elevated CO₂on the suppression of isoprene emission. Thus, this study provides a comprehensive understanding of the regulation of the MEP pathway and isoprene emission in the face of increasing CO₂.

 

When isotopes of carbon are fed to photosynthesizing leaves, metabolites of the Calvin–Benson cycle (CBC) are rapidly labeled initially, but then the rate of labeling slows considerably, raising questions about the integration of the CBC within leaf metabolism. We have used 2-h time courses of labeling of Camelina sativa leaf metabolites to test models of 12 C washout when the CO 2 source is rapidly switched to 13 CO 2 . Fitting exponential functions to the time course of CBC metabolites, we found evidence for three temporally distinct processes contributing to the labeling but none for metabolically inactive pools. We next modeled the data of all metabolites by 13 C isotopically nonstationary metabolic flux analysis, testing a variety of flux networks. In the model that best explains measured data, three processes determine CBC metabolite labeling. First is fixation of incoming 13 CO 2 ; second is dilution by weakly labeled carbon in cytosolic glucose reentering the CBC following oxidative pentose phosphate pathway reactions, which forms a shunt bypassing much of the CBC. Third, very weakly labeled carbon from the vacuole further dilutes the labeling. This model predicts the shunt proceeds at about 5% of the rate of net CO 2 fixation and explains the three phases of labeling. In showing the interconnection of three compartments, we have drawn a more complete picture of how carbon moves through photosynthetic metabolism in a way that integrates the CBC, cytosolic sugar pools, glucose-6-phosphate shunt, and vacuolar sugars into a single system. 

Many plants, especially trees, emit isoprene in a highly light‐ and temperature‐dependent manner. The advantages for plants that emit, if any, have been difficult to determine. Direct effects on membranes have been disproven. New insights have been obtained by RNA sequencing, proteomic and metabolomic studies. We determined the responses of the phosphoproteome to exposure ofArabidopsisleaves to isoprene in the gas phase for either 1 or 5 h. Isoprene effects that were not apparent from RNA sequencing and other methods but were apparent in the phosphoproteome include effects on chloroplast movement proteins and membrane remodelling proteins. Several receptor kinases were found to have altered phosphorylation levels. To test whether potential isoprene receptors could be identified, we used molecular dynamics simulations to test for proteins that might have strong binding to isoprene and, therefore might act as receptors. Although manyArabidopsisproteins were found to have slightly higher binding affinities than a reference set ofHomo sapiensproteins, no specific receptor kinase was found to have a very high binding affinity. The changes in chloroplast movement, photosynthesis capacity and so forth, found in this work, are consistent with isoprene responses being especially useful in the upper canopy of trees.

 

Plant isoprene emissions are known to contribute to abiotic stress tolerance, especially during episodes of high temperature and drought, and during cellular oxidative stress. Recent studies have shown that genetic transformations to add or remove isoprene emissions cause a cascade of cellular modifications that include known signaling pathways, and interact to remodel adaptive growth-defense tradeoffs. The most compelling evidence for isoprene signaling is found in the shikimate and phenylpropanoid pathways, which produce salicylic acid, alkaloids, tannins, anthocyanins, flavonols and other flavonoids; all of which have roles in stress tolerance and plant defense. Isoprene also influences key gene expression patterns in the terpenoid biosynthetic pathways, and the jasmonic acid, gibberellic acid and cytokinin signaling networks that have important roles in controlling inducible defense responses and influencing plant growth and development, particularly following defoliation. In this synthesis paper, using past studies of transgenic poplar, tobacco and Arabidopsis, we present the evidence for isoprene acting as a metabolite that coordinates aspects of cellular signaling, resulting in enhanced chemical defense during periods of climate stress, while minimizing costs to growth. This perspective represents a major shift in our thinking away from direct effects of isoprene, for example, by changing membrane properties or quenching ROS, to indirect effects, through changes in gene expression and protein abundances. Recognition of isoprene’s role in the growth-defense tradeoff provides new perspectives on evolution of the trait, its contribution to plant adaptation and resilience, and the ecological niches in which it is most effective. 

Isoprene has recently been proposed to be a signaling molecule that can enhance tolerance of both biotic and abiotic stress. Not all plants make isoprene, but all plants tested to date respond to isoprene. We hypothesized that isoprene interacts with existing signaling pathways rather than requiring novel mechanisms for its effect on plants. We analyzed the cis‐regulatory elements (CREs) in promoters of isoprene‐responsive genes and the corresponding transcription factors binding these promoter elements to obtain clues about the transcription factors and other proteins involved in isoprene signaling. Promoter regions of isoprene‐responsive genes were characterized using the Arabidopsis cis‐regulatory element database. CREs bind ARR1, Dof, DPBF, bHLH112, GATA factors, GT‐1, MYB, and WRKY transcription factors, and light‐responsive elements were overrepresented in promoters of isoprene‐responsive genes; CBF‐, HSF‐, WUS‐binding motifs were underrepresented. Transcription factors corresponding to CREs overrepresented in promoters of isoprene‐responsive genes were mainly those important for stress responses: drought‐, salt/osmotic‐, oxidative‐, herbivory/wounding and pathogen‐stress. More than half of the isoprene‐responsive genes contained at least one binding site for TFs of the class IV (homeodomain leucine zipper) HD‐ZIP family, such as GL2, ATML1, PDF2, HDG11, ATHB17. While the HD‐zipper‐loop‐zipper (ZLZ) domain binds to the L1 box of the promoter region, a special domain called the steroidogenic acute regulatory protein‐related lipid transfer, or START domain, can bind ligands such as fatty acids (e.g., linolenic and linoleic acid). We tested whether isoprene might bind in such a START domain. Molecular simulations and modeling to test interactions between isoprene and a class IV HD‐ZIP family START‐domain‐containing protein were carried out. Without membrane penetration by the HDG11 START domain, isoprene within the lipid bilayer was inaccessible to this domain, preventing protein interactions with membrane bound isoprene. The cross‐talk between isoprene‐mediated signaling and other growth regulator and stress signaling pathways, in terms of common CREs and transcription factors could enhance the stability of the isoprene emission trait when it evolves in a plant but so far it has not been possible to say what how isoprene is sensed to initiate signaling responses.

 

Predicted increases in future global temperatures require us to better understand the dimensions of heat stress experienced by plants. Here we highlight four key areas for improving our approach towards understanding plant heat stress responses. First, although the term ‘heat stress’ is broadly used, that term encompasses heat shock, heat wave and warming experiments, which vary in the duration and magnitude of temperature increase imposed. A greater integration of results and tools across these approaches is needed to better understand how heat stress associated with global warming will affect plants. Secondly, there is a growing need to associate plant responses to tissue temperatures. We review how plant energy budgets determine tissue temperature and discuss the implications of using leaf versus air temperature for heat stress studies. Third, we need to better understand how heat stress affects reproduction, particularly understudied stages such as floral meristem initiation and development. Fourth, we emphasise the need to integrate heat stress recovery into breeding programs to complement recent progress in improving plant heat stress tolerance. Taken together, we provide insights into key research gaps in plant heat stress and provide suggestions on addressing these gaps to enhance heat stress resilience in plants.