The Rice Dynamin-Related Protein OsDRP1E Negatively Regulates Programmed Cell Death by Controlling the Release of Cytochrome c from Mitochondria.

Zhiqiang Li,Bo Ding,Guo-Liang Wang,Xueping Zhou,Yuanchao Wang

doi:10.1371/journal.ppat.1006157

Abstract

Programmed cell death (PCD) mediated by mitochondrial processes has emerged as an important mechanism for plant development and responses to abiotic and biotic stresses. However, the role of translocation of cytochrome c from the mitochondria to the cytosol during PCD remains unclear. Here, we demonstrate that the rice dynamin-related protein 1E (OsDRP1E) negatively regulates PCD by controlling mitochondrial structure and cytochrome c release. We used a map-based cloning strategy to isolate OsDRP1E from the lesion mimic mutant dj-lm and confirmed that the E409V mutation in OsDRP1E causes spontaneous cell death in rice. Pathogen inoculation showed that dj-lm significantly enhances resistance to fungal and bacterial pathogens. Functional analysis of the E409V mutation showed that the mutant protein impairs OsDRP1E self-association and formation of a higher-order complex; this in turn reduces the GTPase activity of OsDRP1E. Furthermore, confocal microscopy showed that the E409V mutation impairs localization of OsDRP1E to the mitochondria. The E409V mutation significantly affects the morphogenesis of cristae in mitochondria and causes the abnormal release of cytochrome c from mitochondria into cytoplasm. Taken together, our results demonstrate that the mitochondria-localized protein OsDRP1E functions as a negative regulator of cytochrome c release and PCD in plants.

Highlights

Programmed cell death (PCD) occurs in animals and plants, and the primary forms of PCD in mammals include apoptosis, autophagy, and necrosis [1]
Our results demonstrate that the mitochondria-localized protein OsDRP1E functions as a negative regulator of cytochrome c release and PCD in plants
Our results suggest that the E409V point mutation in the dynamin-related protein OsDRP1E affects the morphogenesis of mitochondrial cristae that leads to the cytochrome c release into cytoplasm

Summary

Introduction

Programmed cell death (PCD) occurs in animals and plants, and the primary forms of PCD in mammals include apoptosis, autophagy, and necrosis [1]. Some mutant plants exhibit spontaneous HR-like cell death even without pathogen invasion. Based on their cell death phenotypes, these mutants were designated lesion mimic or spotted leaf mutants [5]. More than 60 lesion mimic genes have been identified in plants [5] These genes encode proteins that play various regulatory roles in different pathways, such as sphingolipid and fatty acid biosynthesis [11], chloroplast activity and photosynthesis [12], transcriptional regulation [13], signal perception at the plasma membrane [14], Ca2+ signal transduction [15], and ubiquitination-mediated protein degradation [10]. Various pathways regulate the complex process of PCD in plants

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Conclusion