Abstract
Cold stress restricts peanut (Arachis hypogaea L.) growth, development, and yield. However, the specific mechanism of cold tolerance in peanut remains unknown. Here, the comparative physiological, transcriptomic, and lipidomic analyses of cold tolerant variety NH5 and cold sensitive variety FH18 at different time points of cold stress were conducted to fill this gap. Transcriptomic analysis revealed lipid metabolism including membrane lipid and fatty acid metabolism may be a significant contributor in peanut cold tolerance, and 59 cold-tolerant genes involved in lipid metabolism were identified. Lipidomic data corroborated the importance of membrane lipid remodeling and fatty acid unsaturation. It indicated that photosynthetic damage, resulted from the alteration in fluidity and integrity of photosynthetic membranes under cold stress, were mainly caused by markedly decreased monogalactosyldiacylglycerol (MGDG) levels and could be relieved by increased digalactosyldiacylglycerol (DGDG) and sulfoquinovosyldiacylglycerol (SQDG) levels. The upregulation of phosphatidate phosphatase (PAP1) and phosphatidate cytidylyltransferase (CDS1) inhibited the excessive accumulation of PA, thus may prevent the peroxidation of membrane lipids. In addition, fatty acid elongation and fatty acid β-oxidation were also worth further studied in peanut cold tolerance. Finally, we constructed a metabolic model for the regulatory mechanism of peanut cold tolerance, in which the advanced lipid metabolism system plays a central role. This study lays the foundation for deeply analyzing the molecular mechanism and realizing the genetic improvement of peanut cold tolerance.