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Relationship between loss of desiccation tolerance and programmed cell death (PCD) in mung bean (Vigna radiata) seeds.
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- المؤلفون: Tian, Xiangrong1,2,3; Li, Sidi1; Zeng, Qing4; Huang, Wei1; Liu, Xuanming3 ; Song, Songquan2,5
- المصدر:
PLoS ONE. 7/2/2019, Vol. 14 Issue 7, p1-19. 19p.
- الموضوع:
- معلومة اضافية
- نبذة مختصرة :
Mung bean (Vigna radiata), an important legume crop, has the property of desiccation tolerance (DT), which is lost in the final stage of germination (preimbibition, 18 h-24 h). We compared parameters related to the programmed cell death (PCD) of mung bean seeds before and after dehydration at different imbibition stages through various detection methods. The results of Evans blue and TTC staining methods showed that the dehydration process could lead to cell death. The results of optical and subcellular morphology showed that PCD occurred after dehydration. The destruction of DNA integrity and the activity changes in caspase and total nuclease in mung bean seeds after dehydration treatment indicated that the loss of desiccation tolerance was related to PCD. Dehydration resulted in the destruction of the mitochondrial structure, reversal of the membrane potential, and the entrance of cytochrome C into the cytoplasm. These processes all indicate that the mitochondrial apoptosis pathway was the main form of dehydration-induced PCD. The results of cytoplasmic Ca2+ concentration showed that Ca2+ signaling also played a role in inducing PCD, with the upstream signal being dehydration-induced changes in water potential and the downstream signal being the ROS and mitochondrial PT channel, according to the order in which these signals happened. The mitochondrial apoptosis pathway can be considered the main mechanism of dehydration-induced PCD based on our analysis of the sequence of major events in PCD. The main processes include dehydration induction, changes in Ca2+ and mitochondrial respiratory electron transport, the reversal of mitochondrial membrane potential induced by ROS and Ca2+, and the transmission and execution of PCD downstream signals induced by cytochrome C release. [ABSTRACT FROM AUTHOR]
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