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Plant Cell. 2016 Sep;28(9):2276-2290. doi: 10.1105/tpc.16.00540. Epub 2016 Aug 19.

Mitochondrial Defects Confer Tolerance against Cellulose Deficiency.

Author information

1
Department of Plant Systems Biology, VIB, B-9052 Gent, Belgium.
2
Department of Plant Biotechnology and Bioinformatics, Ghent University, B-9052 Gent, Belgium.
3
College of Life Sciences, Nanjing Agricultural University, 210095 Nanjing, People's Republic of China.
4
Department of Botany, ARC Centre of Excellence in Plant Energy Biology, School of Life Science, La Trobe University, Bundoora 3086, Victoria, Australia.
5
Department of Biology, Ghent University, B-9000 Gent, Belgium.
6
Compound Screening Facility, VIB, B-9052 Gent, Belgium.
7
Australian Research Council Centre of Excellence in Plant Energy Biology, University of Western Australia, Crawley 6009, Australia.
8
Institut Jean-Pierre Bourgin, INRA, Centre National pour la Recherche Scientifique, AgroParisTech, Université Paris-Saclay, 78026 Versailles Cedex, France.
9
Department of Plant Systems Biology, VIB, B-9052 Gent, Belgium lieven.deveylder@psb.vib-ugent.be.

Abstract

Because the plant cell wall provides the first line of defense against biotic and abiotic assaults, its functional integrity needs to be maintained under stress conditions. Through a phenotype-based compound screening approach, we identified a novel cellulose synthase inhibitor, designated C17. C17 administration depletes cellulose synthase complexes from the plasma membrane in Arabidopsis thaliana, resulting in anisotropic cell elongation and a weak cell wall. Surprisingly, in addition to mutations in CELLULOSE SYNTHASE1 (CESA1) and CESA3, a forward genetic screen identified two independent defective genes encoding pentatricopeptide repeat (PPR)-like proteins (CELL WALL MAINTAINER1 [CWM1] and CWM2) as conferring tolerance to C17. Functional analysis revealed that mutations in these PPR proteins resulted in defective cytochrome c maturation and activation of mitochondrial retrograde signaling, as evidenced by the induction of an alternative oxidase. These mitochondrial perturbations increased tolerance to cell wall damage induced by cellulose deficiency. Likewise, administration of antimycin A, an inhibitor of mitochondrial complex III, resulted in tolerance toward C17. The C17 tolerance of cwm2 was partially lost upon depletion of the mitochondrial retrograde regulator ANAC017, demonstrating that ANAC017 links mitochondrial dysfunction with the cell wall. In view of mitochondria being a major target of a variety of stresses, our data indicate that plant cells might modulate mitochondrial activity to maintain a functional cell wall when subjected to stresses.

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