Abstract
Mitochondrial involvement has not been identified in the programmed cell death (PCD) of leaf senescence which suggests that processes such as those involving reactive oxygen species (ROS) are controlled by chloroplasts. We report that transgenic tobacco (ΔndhF), with the plastid ndhF gene knocked-out, shows low levels of the plastid Ndh complex, homologous to mitochondrial complex I, and more than a 30-day-delay in leaf senescence with respect to wt. The comparison of activities and protein levels and analyses of genetic and phenotypic traits of wtxΔndhF crosses indicate that regulatory roles of mitochondria in animal PCD are assumed by chloroplasts in leaf senescence. The Ndh complex would increase the reduction level of electron transporters and the generation of ROS. Chloroplastic control of leaf senescence provides a nonclassical model of PCD and reveals an unexpected role of the plastid ndh genes that are present in most higher plants. © 2005 Nature Publishing Group. All rights reserved.
Author supplied keywords
Cite
CITATION STYLE
Zapata, J. M., Guéra, A., Esteban-Carrasco, A., Martín, M., & Sabater, B. (2005). Chloroplasts regulate leaf senescence: Delayed senescence in transgenic ndhF-defective tobacco. Cell Death and Differentiation, 12(10), 1277–1284. https://doi.org/10.1038/sj.cdd.4401657
Register to see more suggestions
Mendeley helps you to discover research relevant for your work.