{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ling L"],"funding":["Guizhou Science and Technology Department","Science and Technology Program of Liupanshu","Scientific Research (Cultivation) Project of Liupanshui Normal University"],"pagination":["1169"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12467673"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(9)"],"pubmed_abstract":["<i>Diaporthe eres</i> is a harmful pathogen affecting Hongyang kiwifruit (<i>Actinidia chinensis</i>) after harvest, yet the antioxidant defense strategies are not well understood. This research thoroughly examines the dynamics of the antioxidant response during the infection process. Significant findings indicate an initial 3-day latent period (0-3 dpi) that allowed for pathogen establishment, followed by irreversible tissue breakdown characterized by water-soaked lesions at 4 dpi. The study identified a biphasic activation pattern of superoxide dismutase (SOD) with dual activity peaks (1 dpi and 4 dpi), orchestrated by mitochondrial hub gene <i>CEY00_Acc02790</i> that coordinates peroxidase (POD) networks, while peroxidase (POD) activity exhibited a synchronized but temporary increase, peaking at 4 dpi. Further bioinformatic analysis revealed the possible functional specialization of POD isoforms: α-helix-rich extracellular variants drove cell wall reinforcement through lignification, while random coil-dominant intracellular variants formed to mitigate cytoplasmic reactive oxygen species (ROS) damage, establishing dual physicochemical barriers. Malondialdehyde (MDA) levels rose significantly by 3 dpi, indicating permanent membrane damage. Collectively, these findings elucidate the mechanistic foundation of the <i>Actinidia</i>-<i>Diaporthe</i> pathosystem, identifying the bimodal SOD response and POD specialization as prime targets for developing resistant cultivars and precision postharvest interventions, ultimately reducing losses through biochemical interception of pathogenesis."],"journal":["Biology"],"pubmed_title":["Antioxidant Defense Strategies Against &lt;i&gt;Diaporthe eres&lt;/i&gt; Infection in Hongyang Kiwifruit."],"pmcid":["PMC12467673"],"funding_grant_id":["52020-2023-0-2-18","Qi-anKeHeJiChu-ZK[2022]530","LPSSY2023KJZDPY06"],"pubmed_authors":["Long X","Pan S","Ling L","Yang T","Zhang S"],"additional_accession":[]},"is_claimable":false,"name":"Antioxidant Defense Strategies Against &lt;i&gt;Diaporthe eres&lt;/i&gt; Infection in Hongyang Kiwifruit.","description":"<i>Diaporthe eres</i> is a harmful pathogen affecting Hongyang kiwifruit (<i>Actinidia chinensis</i>) after harvest, yet the antioxidant defense strategies are not well understood. This research thoroughly examines the dynamics of the antioxidant response during the infection process. Significant findings indicate an initial 3-day latent period (0-3 dpi) that allowed for pathogen establishment, followed by irreversible tissue breakdown characterized by water-soaked lesions at 4 dpi. The study identified a biphasic activation pattern of superoxide dismutase (SOD) with dual activity peaks (1 dpi and 4 dpi), orchestrated by mitochondrial hub gene <i>CEY00_Acc02790</i> that coordinates peroxidase (POD) networks, while peroxidase (POD) activity exhibited a synchronized but temporary increase, peaking at 4 dpi. Further bioinformatic analysis revealed the possible functional specialization of POD isoforms: α-helix-rich extracellular variants drove cell wall reinforcement through lignification, while random coil-dominant intracellular variants formed to mitigate cytoplasmic reactive oxygen species (ROS) damage, establishing dual physicochemical barriers. Malondialdehyde (MDA) levels rose significantly by 3 dpi, indicating permanent membrane damage. Collectively, these findings elucidate the mechanistic foundation of the <i>Actinidia</i>-<i>Diaporthe</i> pathosystem, identifying the bimodal SOD response and POD specialization as prime targets for developing resistant cultivars and precision postharvest interventions, ultimately reducing losses through biochemical interception of pathogenesis.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-05-02T03:09:42.539Z","creation":"2026-05-02T03:07:45.421Z"},"accession":"S-EPMC12467673","cross_references":{"pubmed":["41007314"],"doi":["10.3390/biology14091169"]}}