Browsing by Author "Foyer, Christine H"

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    Nitric oxide, energy and redox-dependent responses to hypoxia
    (Oxford University Press, 2024) Samant, Sanjib Bal; Yadav, Nidhi; Swain, Jagannath; Joseph, Josepheena; Kumari, Aprajita; Praveen, Afsana; Sahoo, Ranjan Kumar; Manjunatha, Girigowda; Seth, Chandra Shekar; Singla-Pareek, Sneh Lata; Foyer, Christine H; Pareek, Ashwani; Gupta, Kapuganti Jagadis
    Hypoxia occurs when the oxygen levels fall below the levels required for mitochondria to support respiration. Regulated hypoxia is associated with quiescence, particularly in storage organs (seeds) and stem cell niches. In contrast, environmentally-induced hypoxia poses significant challenges for metabolically-active cells that are adapted to aerobic respiration. The perception of oxygen availability through cysteine oxidases, which function as oxygen-sensing enzymes in plants that control the N-degron pathway, and the regulation of hypoxia-responsive genes and processes is essential to survival. Functioning together with reactive oxygen species (ROS), particularly hydrogen peroxide and reactive nitrogen species (RNS), such as nitric oxide (•NO), nitrogen dioxide (•NO2), S‐nitrosothiols (SNOs), and peroxynitrite (ONOO−), hypoxia signaling pathways trigger anatomical adaptations such as formation of aerenchyma, mobilization of sugar reserves for anaerobic germination, formation of aerial adventitious roots and hyponastic response. NO and hydrogen peroxide (H2O2) participate in local and systemic signaling pathways that facilitate acclimation to changing energetic requirements, controlling glycolytic fermentation, the GABA shunt and amino acid synthesis. NO enhances antioxidant capacity and contributes to the recycling of redox equivalents energy metabolism through the phytoglobin (Pgb)-NO cycle. Here, we summarize current knowledge, highlighting the central role of NO and redox regulation in adaptive responses that prevent hypoxia-induced death in challenging conditions such as flooding.
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    Physiological implications of SWEETs in plants and their potential applications in improving source-sink relationships for enhanced yield
    (John Wiley & Sons, 2023) Singh, Jitender; Das, Shubhashis; Gupta, Kapuganti Jagadis; Ranjan, Aashish; Foyer, Christine H; Thakur, Jitendra K.
    The SWEET (SUGARS WILL EVENTUALLY BE EXPORTED TRANSPORTERS) family of transporters in plants is identified as a novel class of sugar carriers capable of transporting sugars, sugar alcohols, and hormones. Functioning in intercellular sugar transport, SWEETs influence a wide range of physiologically important processes. SWEETs regulate the development of sink organs by providing nutritional support from source leaves, responses to abiotic stresses by maintaining intracellular sugar concentrations, and host-pathogen interactions through the modulation of apoplastic sugar levels. Many bacterial and fungal pathogens activate the expression of SWEET genes in species such as rice and Arabidopsis to gain access to the nutrients that support virulence. The genetic manipulation of SWEETs has led to the generation of Bacterial Blight (BB) resistant rice varieties. Similarly, while the overexpression of the SWEETs involved in sucrose export from leaves and pathogenesis led to growth retardation and yield penalties, plants overexpressing SWEETs show improved disease resistance. Such findings demonstrate the complex functions of SWEETs in growth and stress tolerance. Here, we review the importance of SWEETs in plant-pathogen and source-sink interactions and abiotic stress resistance. We highlight the possible applications of SWEETs in crop improvement programs aimed at improving sink and source strengths important for enhancing the sustainability of yield. We discuss how the adverse effects of the overexpression of SWEETs on plant growth may be overcome.