Abstract
Sweetpotato (Ipomoea batatas (L.) Lam.) is an important industrial and food crop. Both chilling and heat stress inhibits sweetpotato growth and development and then affects yield. However, the physiological and molecular mechanisms of sweetpotato response to chilling and heat stress is unclear. In this study, we investigated the effect of extreme temperature on sweetpotato physiological response, with a focus on oxidative stress and the potential microRNA (miRNA)-mediated molecular mechanism. Our results showed that both chilling and heat stress resulted in accumulation of reactive oxygen species (ROS), including H2O2 and O2–, and caused oxidative stress in sweetpotato. This further affected the activities of oxidative stress-related enzymes and products, including SOD, POD, and MDA. Both chilling and heat stress inhibited POD activities but induced the enzyme activities of SOD and MDA. This suggests that sweetpotato cells initiated its own defense mechanism to handle extreme temperature-caused oxidative damage. Oxidative damage and repair are one mechanism that sweetpotato plants respond to extreme temperatures. Another potential mechanism is miRNA-mediated gene response. Chilling and heat stress altered the expression of stress-responsive miRNAs in sweetpotato seedlings. These miRNAs regulate sweetpotato response to extreme stress through targeting individual protein-coding genes.
Highlights
Both chilling and heat stresses dysregulate active oxygen metabolism in plants, which leads to many cellular and physical changes, including oxidative stress, cell membrane lipid peroxidation, protein denaturation and nucleotide damage; the damage caused by the stress may cause cell death (Kuk et al, 2003)
Chilling and Heat Stress-Induced Oxidative Stress and the Related Biochemical Changes in Sweetpotato. We found both chilling and high temperature treatment resulted in H2O2 accumulation in sweetpotato leaves, evidenced by the leaves change color from green to brown and there are many brown spots on leaves
As a key enzyme in reactive oxygen species (ROS) scavenging system, superoxide dismutase (SOD) promotes the disproportionation of superoxide into oxygen and H2O2, it reduces the peroxidation of membrane lipids, maintains the stability of cell membrane, and removes it through different pathways (Bowler et al, 1992; Koca et al, 2006; Zhang F.-Q. et al, 2007; Zhang et al, 2011)
Summary
Both chilling and heat stresses dysregulate active oxygen metabolism in plants, which leads to many cellular and physical changes, including oxidative stress, cell membrane lipid peroxidation, protein denaturation and nucleotide damage; the damage caused by the stress may cause cell death (Kuk et al, 2003). With increase of heat stress, the plasma membrane permeability was increased in the leaves of four Lysimachia plants, and the activities of SOD and POD were first increased and Temperature-Induced Physiological Changes in Sweetpotato decreased, while the contents of chlorophyll, soluble protein, and proline were decreased (Xu and Zhang, 2009). Li et al (2015) observed that SOD, POD, catalase (CAT) activity and malondialdehyde (MDA) content were increased in the leaves of Atractylodes lancea with the prolongation of heat stress. Wang et al (2019) recently studied the antioxidative system in sweetpotato root under low temperature storage condition; their result showed that the activities of antioxidant enzymes were changed quickly during sweetpotato storage under chilling stress (Wang et al, 2019) Several studies over-expressed an individual gene to enhance the tolerance to low temperature stress in sweetpotato (Kim et al, 2011; Fan et al, 2012; Ji et al, 2017b; Jin et al, 2017). Wang et al (2019) recently studied the antioxidative system in sweetpotato root under low temperature storage condition; their result showed that the activities of antioxidant enzymes were changed quickly during sweetpotato storage under chilling stress (Wang et al, 2019)
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