DOI: 10.7763/IJBBB.2011.V1.56
The Cell Death in CMS Plants
Abstract—Reactive oxygen species (ROS)-mediated PCD was found to occur in CMS lines of many species. The excess production of ROS is probably caused by the decrease of the activity of ROS-scavenging enzymes in CMS plants at the abortion peak. Why antioxidant enzyme activities decline? Mostly, the ascorbate-glutathione cycle of mitochondria is blocked by the depletion of ATP and NADH which would result from mitochondrial dysfunction induced by the expression of mitochondrial chimeric open-reading frames (ORFs). Moreover, the interaction between ROS and some signaling molecules, such as ethylene, attenuated the induction of the cyanide-resistant respiration, which exacerbates the accumulation of the ROS. Under oxidative stress, cellular protein especially membrane protein and DNA damage occur, and thus lead to the cell death. The characteristic feature of the programmed cell death (PCD) in CMS plants may be that it can be blocked by a matching nuclear pathway that restores normal regulation. We will discuss the central role of the mitochondrion in the whole pathways of the cell death in CMS plants.
Index Terms—Cytoplasmic male sterility, Mitochondri-al, Programmed cell death.
L. Huang, C. Zhang, M. Fang, and H. Xu are with the Maize Research Institute of Sichuan Agricultural University/Key Laboratory of Crop Genetic Resource and Improvement, Ministry of Education, Ya’an 625014, Sichuan, China (e-mail: b1983429@126.com, 513657334@qq.com, 79145 0070@qq.com, 448553819@qq.com, respectively)
M. J. Cao (Corresponding author), is with the Maize Research Institute of Sichuan Agricultural University/Key Laboratory of Crop Genetic Resource and Improvement, Ministry of Education/ Key Laboratory of maize biology and Genetic Breeding on Southwest, Ministry of Agriculture, Ya`an 625014, Sichuan, China (e-mail:mojupp@163.com).
Cite: Ling Huang, Chen Zhang, Ming Fang, Hao Xu, and Moju Cao, "The Cell Death in CMS Plants," International Journal of Bioscience, Biochemistry and Bioinformatics vol. 1, no. 4, pp. 297-301, 2011.
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