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Demonstration of plant adaptation syndrome in plants and possible molecular mechanisms of its realization under conditions of anaerobic stress
Authors:B B Vartapetian  I P Generosova  N A Zakhmylova  A G Snkhchyan
Institution:(1) Timiryazev Institute of Plant Physiology, Russian Academy of Sciences, Botanicheskaya ul. 35, Moscow, 127276, Russia
Abstract:Electron-microscopic examination of mitochondrial membrane ultrastructure in detached leaves of four-day-old wheat (Triticum aestivum L.) seedlings incubated under conditions of strict anoxia in the presence of exogenous glucose and cycloheximide or in the absence of these compounds revealed a paradoxical phenomenon: in the absence of exogenous glucose and cycloheximide, even a short-term (15–30 min) anaerobiosis resulted in a pathological destruction of mitochondria (swelling and the loss of cristae); however, a longer uninterrupted anaerobiosis (3–4 h) did not induce further mitochondria degradation but, in contrast, resulted in the recovery of their initial ultrastructure. Irreversible mitochondria degradation was observed only during subsequent still longer leaf anaerobic treatment (24–48 h). When, under conditions of strict anoxia, leaves were fed with glucose to stimulate glycolysis and ethanolic fermentation, we did not observe any signs of early destruction of mitochondrial ultrastructure and their swelling. Blockage of anaerobic protein synthesis with cycloheximide resulted in early destruction and subsequent irreversible degradation of mitochondria without any indications of their structural recovery. Based on the results of the experiments, we concluded that cell energy metabolism controlled byboth the presence of utilizable carbohydrates and also by the induction of anaerobic protein synthesis played a key role during early mitochondria destruction under extreme conditions of anaerobic stress, their subsequent recovery, and irreversible degradation during continuous long-term strict anoxia.
Keywords:Triticum aestivum  seedlings  anaerobiosis  ultrastructure  mitochondria  glucose feeding  protein synthesis inhibition
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