Background: Rapeseed is the third largest oil seed crop in the world. The seeds of this plant store lipids in oil bodies, and oleosin is the most important structural protein in oil bodies. However, the function of oleosin in oil crops has received little attention. Results: In the present study, 48 oleosin sequences from the Brassica napus genome were identified and divided into four lineages (T, U, SH, SL). Synteny analysis revealed that most of the oleosin genes were conserved, and all of these genes experienced purifying selection during evolution. Three and four important oleosin genes from Arabidopsis and B. napus, respectively, were cloned and analyzed for function in Arabidopsis. Overexpression of these oleosin genes in Arabidopsis increased the seed oil content slightly, except for BnaOLE3. Further analysis revealed that the average oil body size of the transgenic seeds was slightly larger than that of the wild type (WT), except for BnaOLE1. The fatty acid profiles showed that the linoleic acid content (13.3% at most) increased and the peanut acid content (11% at most) decreased in the transgenic lines. In addition, the seed size and thousand-seed weight (TSW) also increased in the transgenic lines, which could lead to increased total lipid production. Conclusion: We identified oleosin genes in the B. napus genome, and overexpression of oleosin in Arabidopsis seeds increased the seed weight and linoleic acid content (13.3% at most).

Summary For decades, genetic engineering approaches to produce unusual fatty acids (UFAs) in crops has reached a bottleneck, including reduced seed oil production and seed vigor. Currently, plant models in the field of research are primarily used to investigate defects in oil production and seedling development, while the role of UFAs in embryonic developmental defects remains unknown. In this study, we developed a transgenic Arabidopsis plant model, in which the embryo exhibits severely wrinkled appearance owing to α‐linolenic acid (ALA) accumulation. RNA‐sequencing analysis in the defective embryo suggested that brassinosteroid synthesis, FA synthesis and photosynthesis were inhibited, while FA degradation, endoplasmic reticulum stress and oxidative stress were activated. Lipidomics analysis showed that ultra‐accumulated ALA is released from phosphatidylcholine as a free FA in cells, inducing severe endoplasmic reticulum and oxidative stress. Furthermore, we identified that overexpression of lysophosphatidic acid acyltransferase 2 rescued the defective phenotype. In the rescue line, the pool capacity of the Kennedy pathway was increased, and the esterification of ALA indirectly to triacylglycerol was enhanced to avoid stress. This study provides a plant model that aids in understanding the molecular mechanism of embryonic developmental defects and generates strategies to produce higher levels of UFAs.

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