Broccoli (Brassica oleracea L. var. italica) is prone to rapid yellowing when stored at ambient temperature after harvest due to membrane damage. Here, freshly harvested broccoli florets were stored in a static magnetic field (5 mT) at 20 °C. The current results demonstrated that a static magnetic field lowered postharvest yellowing (chlorophyll breakdown), water loss, and oxidative stress. An integrated transcriptome and metabolome analysis suggested that static magnetic field-mediated alleviation of postharvest yellowing and senescence of broccoli florets involved the following factors: (1) downregulating the expression of genes related to organ senescence; (2) delaying the breakdown of chlorophylls through preventing the upregulation of chlorophyll degradation-related genes and the increase in oxidative stress; (3) alleviating cellular energy imbalance by upregulated fatty acid oxidation (as indicated by decreased free fatty acids) to reduce water loss and oxidative stress and to maintain membrane integrity; (4) increasing the abundances of lysophospholipids and sphingolipids and preventing the decrease in phosphatidylcholine abundance to lower water loss and oxidative stress, inhibit ethylene production, delay chlorophyll degradation, and keep membrane integrity; (5) reducing water loss via increasing cutin, suberin, and wax biosynthesis and stomatal closure brought about by upregulated expression of phospholipase D genes; and (6) preventing the increase in malondialdehyde (MDA) content, electrolyte leakage, and weight loss rate. To conclude, this work provided some novel data elucidating the underlying mechanism by which a static magnetic field delayed postharvest yellowing and senescence of broccoli florets. A static magnetic field could retard postharvest deterioration of broccoli florets, thereby providing a clean and non-thermal method for their green preservation.

Pepper (Capsicum annuum), a widely cultivated vegetable of significant economic importance globally, is frequently subjected to attacks from pathogens such as Ralstonia solanacearum, as well as high-temperature stress. However, the mechanisms by which pepper combats these stresses remain poorly understood. Herein, we reported that the expression of the leucine-rich repeat protein CaLRR13, which lacks a nucleotide-binding site (NBS), kinase domains, and a transmembrane region, was transcriptionally activated by both R. solanacearum inoculation and high-temperature stress. Through transient overexpression in the epidermal cells of Nicotiana benthamiana leaves, we found that CaLRR13 localized in both the cytoplasm and the nuclei. Reducing the expression of CaLRR13 via virus-induced gene silencing (VIGS) increased the sensitivity of pepper to R. solanacearum infection and high-temperature exposure, accompanied by reduced expression of immunity- and thermotolerance-related genes, including CaWRKY40, CaPR1, CaNPR1, CaDEF1, and CaHSP24. In contrast, transient overexpression of CaLRR13 in pepper leaves induced a like-hypersensitive response (HR) and enhanced the expression of the aforementioned immunity- and thermotolerance-related genes. Thus, we conclude that CaLRR13 plays a positive role in pepper immunity against R. solanacearum and thermotolerance, providing a new perspective on the crosstalk and management of plant responses to these two stresses.