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Foyer, C. H.

Publications and source records attributed to Foyer, C. H..

5 recordsLinked to original sources

Catalase 2-dependent regulation of autophagy in response to carbon starvation in Arabidopsis

Reactive oxygen species (ROS) are fundamental regulators of plant development and stress acclimation. However, their roles in carbon starvation tolerance remain largely unresolved. We therefore dissected the dynamics of redox regulation in carbon-starved Arabidopsis leaves. We present data showing the presence of an early ROS wave that activates autophagy, followed by a sustained, accumulation of hydrogen peroxide (H2O2) that leads to programmed cell death. We show that catalase 2 (CAT2) constitutively binds and sequesters the autophagy initiators ATG1a and ATG13a, a process that prevents the activation of autophagy under carbon-replete conditions. The accumulation of H2O2 in response to carbon starvation leads to oxidation of the Cys-370 and Cys-413 residues on the CAT2 protein and dissociation from ATG1a/13a, thereby allowing ATG1-kinase complex assembly and autophagosome formation. The expression of CAT2-C370S or CAT2-C413S variants in the cat2-1 mutant significantly enhanced carbon starvation tolerance, because both variants retain catalase activity but fail to bind ATG1a/13a. We conclude that CAT2 functions as a redox-sensitive regulator of autophagy.

plant biology↗

Investigating the Diuraphis noxia-Triticum aestivum interaction using transcriptomics

O_LIAphids often overcome host plant resistance by developing virulence. However, the underlying mechanisms and the precise modifications involved remain poorly understood. Additionally, the molecular response of resistant host plants during compatible (virulent aphid) and incompatible (avirulent aphid) interactions is another area requiring further investigation. C_LIO_LIHere, Diuraphis noxia (Russian wheat aphid) biotypes of varying virulence were transferred from susceptible Triticum aestivum to a near-isogenic line containing the Dn7 resistance gene. Transcriptomes of the D. noxia biotypes and the resistant host were sequenced before and after the host shift. C_LIO_LITranscriptomic analysis indicated that the D. noxia biotypes had unique responses which were involved in detoxification (e.g. L-xylulose reductase), membrane transport (e.g. Tert-1) and epigenetic regulation. In addition, many transposable elements were rapidly differentially regulated between biotypes and because of the host shift. In the host plant, all biotypes induced jasmonic acid signalling and terpenoid biosynthesis. However, the mono- and diterpenoid pathways were only upregulated following feeding by the biotypes avirulent to Dn7 and not SAMv2. C_LIO_LIRapid differential expression of transposons suggests a mechanism of adaptation for clonally reproducing aphids. Furthermore, SAMv2 may possess mechanisms to modulate the defence response of Dn7-containing T. aestivum. C_LI

genomics↗

Hydrogen Cyanamide Causes Reversible G2/M Cell Cycle Arrest Accompanied by Oxidation of the Nucleus and Cytosol in Arabidopsis thaliana Root Apical Meristem Cells

Hydrogen cyanamide (HC) is known to stimulate the production of reactive oxygen species (ROS) and also alter growth through modification of the cell cycle. However, the mechanisms by which HC alters cell proliferation and redox homeostasis are largely unknown. This study used roGFP2 expressing Arabidopsis seedlings to measure the oxidation states of the nuclei and cytosol in response to HC treatment. The Cytrap dual cell cycle phase marker system and flow cytometry were used to study associated changes in cell proliferation. HC (1.5mM) reversibly inhibited root growth during a 24h treatment. Higher concentrations were not reversible. HC did not synchronize the cell cycle. In contrast to hydroxyurea, HC caused a gradual accumulation of cells in the G2/M phase and decline of G1/S phase cells 16 to 24h post-treatment. This was accompanied by increased oxidation of both the nuclei and cytosol. Taken together, HC impairs proliferation of embryonic root meristem cells in a reversible manner through restriction of G2/M transition accompanied by increased oxidative poise.

plant biology↗

The seasonal dynamics of bud dormancy in grapevine suggest a regulated checkpoint prior to acclimation

Grapevine (Vitis vinifera L.) displays wide plasticity to climate and seasonality, ranging from strongly deciduous to evergreen. Understanding the physiology of decisions to grow or quiesce is critical for improved crop management, prediction, and the adaptability of production to alternative climate scenarios. The perenniating bud (N+2) is a major economic unit and focus of study. Here we investigated the physiology and transcriptome of cv. Merlot buds grown in a temperate maritime climate from summer to spring in two consecutive years. The changes in bud respiration, hydration and internal tissue oxygen data were consistent with the transcriptome data. ABA-responsive gene processes prevailed upon the transition to a deep metabolic and cellular quiescence in the bud during autumn. Light, together with hypoxia and redox signalling presided over the resumption of nuclear and cellular growth in the transition to spring. Comparisons with transcriptome data from bud burst studies revealed a number of regulatory candidates for the orderly resumption of growth in spring, including components that may integrate light and temperature signalling. Importantly however, the bud burst forcing data, which is widely used as a measure of bud dormancy, were not consistent with the physiological and transcription data. We hypothesise the existence of a physiological checkpoint following bud set in summer, which if not met results in extreme quiescence. Collectively this is the most integrated developmental dataset of the latent bud of cultivated grapevine, and establishes a platform for systems approaches to study seasonal plasticity. One sentence summaryPhysiology and transcriptome data provide strong evidence of a regulatory checkpoint prior to acclimation and dormancy in latent grapevine buds.

plant biology↗

On the move: Redox-dependent protein relocation

Compartmentation of proteins and processes is a defining feature of eukaryotic cells. The growth and development of organisms is critically dependent on the accurate sorting of proteins within cells. The mechanisms by which cytosol-synthesized proteins are delivered to the membranes and membrane compartments have been extensively characterised. However, the protein complement of any given compartment is not precisely fixed and some proteins can move between compartments in response to metabolic or environmental triggers. The mechanisms and processes that mediate such relocation events are largely uncharacterized. Many proteins can in addition perform multiple functions, catalyzing alternative reactions or performing structural, non-enzymatic functions. These alternative functions can be equally important functions in each cellular compartment. Such proteins are generally not dual targeted proteins in the classic sense of having targeting sequences that direct de novo synthesised proteins to specific cellular locations. Accumulating evidence suggests that redox post-translational modifications (PTMs) can control the compartmentation of many such proteins, including antioxidant and/or redox associated enzymes.

cell biology↗