Pathogens-induced disease development and ferroptosis of harvested blueberry fruit in association with membrane lipids metabolism

Abstract

Lipidomics offers comprehensive insights into the cell mechanisms underlying the postharvest disease of fruits and vegetables. This study aimed to elucidate the regulatory mechanism of membrane lipids metabolism in diseased blueberry fruit, with a particular focus on iron-dependent cell death. Results showed that infections by A. alternata and F. fujikuroi elevated total iron and ferrous ion levels, decreased glutathione (GSH) and increased hydrogen peroxide (H₂O₂)/malondialdehyde (MDA) levels in lesion and adjacent areas. Iron ions and GSH correlated highly with lesion diameters, which was consistent with ferroptosis characteristics. Fatty acids analysis indicated that the destruction of unsaturated fatty acids in phospholipids of infected fruit was more obvious than that in total lipids, and methoxy fatty acids were notably increased in phospholipids but absent in total lipids. Lipidomic analysis revealed that phosphatidic acid (PA), phosphatidylcholine (PC), methylphosphatidylcholine (MePC) and monolysocardiolipin (MLCL) showed significant correlations with iron ions, GSH, MDA, and H₂O₂, respectively. The more stable PC and the less stable PA were both decreased, and cardiolipin (CL) was undetectable. MLCL was abundant initially but decreased during disease progression, possibly due to the membrane destabilization caused by peroxidation. Across phospholipids, 66.7 % of MLCL, 60.6 % of PC, 50 % of MePC, 42.9 % of PA, 16.7 % phosphatidylethanolamine (PE), 8.7 % phosphatidylglycerol (PG), 9.1 % phosphatidylserine (PS) exhibited significant correlations with 1–4 ferroptosis indicators (iron, MDA, H₂O₂ and GSH). These combined findings suggest that lipid peroxidation induced by A. alternata and F. fujikuroi may be linked to increased iron/H₂O₂ and decreased GSH level in blueberry cells.