Some aspects of salinity responses in peppermint (Mentha × piperita L.) to NaCl treatment.
Salinity is a major stress that adversely affects plant growth and crop production. Understanding the cellular responses and molecular mechanisms by which plants perceive and adopt salinity stress is of fundamental importance. In this work, some of the cellular signaling events including cell death, reactive oxygen species (ROS) generation, and the behaviors of organelles were analyzed in a salt-tolerant species (Keyuan-1) of peppermint (Mentha × piperita L.) under NaCl treatment. Our results showed that 200 mM NaCl treatment elicited a distinct progress of cell death with chromatin condensation and caspase-3-like activation and a dramatic burst of ROS which was required for the execution of cell death. The major ROS accumulation occurred in the mitochondria and chloroplasts, which were the sources of ROS production under NaCl stress. Moreover, mitochondrial activity and photosynthetic capacity also exhibited the obvious decrease in the ROS-dependent manner under 200 mM NaCl stress. Furthermore, the activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR), and dehydroascorbate reductase (DHAR) as well as the contents of ascorbate and glutathione changed in the concentration-dependent manner under NaCl stress. Altogether, our data showed the execution of programmed cell death (PCD), the ROS dynamics, and the behaviors of organelles especially mitochondria and chloroplasts in the cellular responses of peppermint to NaCl stress which can be used for the tolerance screening, and contributed to the understanding of the cellular responses and molecular mechanisms of peppermint to salinity stress, providing the theoretic basis for the further development and utilization of peppermint in saline areas.
Biotechnology Center of Shandong Academy of Sciences, Jinan, 250014, China, lizh@sdas.org.
Zhe
Z
Li
Hetong
H
Yang
Xiaoqing
X
Wu
Kai
K
Guo
Jishun
J
Li
D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002736:Chloroplasts / Q000187:drug effects / Q000378:metabolism; D002843:Chromatin / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008315:Malondialdehyde / Q000378:metabolism; D036142:Mentha piperita / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D010788:Photosynthesis / Q000187:drug effects; D011523:Protoplasts / Q000187:drug effects / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D054712:Salinity; D012965:Sodium Chloride / Q000494:pharmacology*; D013312:Stress, Physiological / Q000187:drug effects; D013347:Subcellular Fractions / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors
D000975:Antioxidants; D002843:Chromatin; D017382:Reactive Oxygen Species; D012965:Sodium Chloride; D008315:Malondialdehyde; D006861:Hydrogen Peroxide; D053148:Caspase 3