<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ling L</submitter><funding>Guizhou Science and Technology Department</funding><funding>Science and Technology Program of Liupanshu</funding><funding>Scientific Research (Cultivation) Project of Liupanshui Normal University</funding><pagination>1169</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12467673</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(9)</volume><pubmed_abstract>&lt;i>Diaporthe eres&lt;/i> is a harmful pathogen affecting Hongyang kiwifruit (&lt;i>Actinidia chinensis&lt;/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 &lt;i>CEY00_Acc02790&lt;/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 &lt;i>Actinidia&lt;/i>-&lt;i>Diaporthe&lt;/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.</pubmed_abstract><journal>Biology</journal><pubmed_title>Antioxidant Defense Strategies Against &amp;lt;i&amp;gt;Diaporthe eres&amp;lt;/i&amp;gt; Infection in Hongyang Kiwifruit.</pubmed_title><pmcid>PMC12467673</pmcid><funding_grant_id>52020-2023-0-2-18</funding_grant_id><funding_grant_id>Qi-anKeHeJiChu-ZK[2022]530</funding_grant_id><funding_grant_id>LPSSY2023KJZDPY06</funding_grant_id><pubmed_authors>Long X</pubmed_authors><pubmed_authors>Pan S</pubmed_authors><pubmed_authors>Ling L</pubmed_authors><pubmed_authors>Yang T</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Antioxidant Defense Strategies Against &amp;lt;i&amp;gt;Diaporthe eres&amp;lt;/i&amp;gt; Infection in Hongyang Kiwifruit.</name><description>&lt;i>Diaporthe eres&lt;/i> is a harmful pathogen affecting Hongyang kiwifruit (&lt;i>Actinidia chinensis&lt;/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 &lt;i>CEY00_Acc02790&lt;/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 &lt;i>Actinidia&lt;/i>-&lt;i>Diaporthe&lt;/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.</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-05-02T03:09:42.539Z</modification><creation>2026-05-02T03:07:45.421Z</creation></dates><accession>S-EPMC12467673</accession><cross_references><pubmed>41007314</pubmed><doi>10.3390/biology14091169</doi></cross_references></HashMap>