Further insights into how low-light signaling delays leaf senescence in soybean under high-temperature

Abstract

Plants go through several physiological modifications in their life cycle. Leaf senescence (LS) occurs at the later stage of plant development but can also be initiated by high temperature (HT) stress. LS involves the breakdown of certain key developmental processes in plants, which affect leaf greenness, thereby decreasing plant photosynthetic performance. Light signaling pathway modulates plant growth processes under high-temperature stress, suggesting that light and temperature signaling pathways are linked. However, our knowledge of how light signaling pathways delay LS in soybean under HT remains incomplete. Therefore, this study aimed to investigate how low light signaling pathway delays LS in soybean under HT stress. The results showed that low light signaling delayed LS in soybean under high-temperature stress. Our gas exchange analysis showed that low light signaling improved soybean photosynthetic process and chlorophyll contents under HT stress. Further analysis indicated that low light treatment improved soybean soluble sugar, starch, and free amino acids of plants exposed to HT stress. The phytohormones analysis suggested that under low light, plants accumulated endogenous jasmonic acid (JA) and salicylic acid (SA) when exposed to HT stress. The transcriptional analysis suggested that soybean STAY-GREEN genes (GmSGR1and GmSGR2), sucrose phosphate synthase genes (GmSPS1 and GmSPS2), and starch synthase genes (GmAGP1 and GmUGP1−1) were upregulated in the high-temperature and low light treatment. Again, the JA defense pathway genes GmPDF1.2, GmJAR1.1 GmFAD3.1, and GmPR4.2 expression levels were significantly upregulated in the high-temperature and low light treatment as compared to SA defense pathway genes GmSID2, GmEDS5, GmNPR1, and GmPR1. The regulation mechanisms involving how low light signaling delays leaf senescence in soybean under high temperature through improved photosynthetic rate and JA defense signaling activation are discussed.