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Mitochondrial retrograde regulation in plants

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MITOCHONDRION
卷 7, 期 3, 页码 177-194

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ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2007.01.002

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mitochondria; retrograde regulation; retrograde signaling; inter-organellar communication; mitochondria-to-nucleus signaling

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Plant cells must react to a variety of adverse environmental conditions that they may experience on a regular basis. Part of this response centers around (1) ROS as damaging molecules and signaling molecules; (2) redox status, which can be influenced by ROS production; and (3) availability of metabolites. All of these are also likely to interface with changes in hormone levels [Desikan, R., Hancock, J., Neill, S., 2005. Reactive oxygen species as signalling molecules. In: Smirnoff, N. led.), Antioxidants and reactive oxygen species in plants. Blackwell Pub. Ltd., Oxford, pp. 169-196; Kwak, J.M., Nguyen, V., Schroeder, J.I., 2006. The role of reactive oxygen species in hormonal responses. Plant Physiol. 141, 323-329]. Each of these areas can be strongly influenced by changes in mitochondrial function. Such changes trigger altered nuclear gene expression by a poorly understood process of mitochondrial retrograde regulation (MRR), which is likely composed of several distinct signaling pathways. Much of what is known about plant MRR centers around the response to a dysfunctional mtETC and subsequent induction of genes encoding proteins involved in recovery of mitochondrial functions, such as AOX and alternative NAD(P)H dehydrogenases, and genes encoding enzymes aimed at regaining ROS level/redox homeostasis, such as glutathione transferases, catalases, ascorbate peroxidases and superoxide dismutases. However, as evidence of new and interesting targets of MRR emerge, this picture is likely to change and the complexity and importance of MRR in plant responses to stresses and the decision for cells to either recover or switch into programmed cell death mode is likely to become more apparent. (c) 2007 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

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