Advanced search
1 file | 3.61 MB Add to list

Mitochondrial defects confer tolerance against cellulose deficiency

Zhubing Hu (UGent) , Rudy Vanderhaeghen (UGent) , Toon Cools (UGent) , Yan Wang, Inge De Clercq (UGent) , Olivier Leroux (UGent) , Long Nguyen (UGent) , Katharina Belt, A Harvey Millar, Dominique Audenaert (UGent) , et al.
(2016) PLANT CELL. 28(9). p.2276-2290
Author
Organization
Project
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.
Keywords
PENTATRICOPEPTIDE REPEAT PROTEIN, GENES-ENCODING MITOCHONDRIAL, OSMOTIC-STRESS TOLERANCE, NAC TRANSCRIPTION FACTOR, ARABIDOPSIS MUTANT CEV1, SYNTHASE COMPLEXES, RETROGRADE REGULATION, CYTOCHROME-C, ALTERNATIVE OXIDASE, ELECTRON-TRANSPORT

Downloads

  • (...).pdf
    • full text
    • |
    • UGent only
    • |
    • PDF
    • |
    • 3.61 MB

Citation

Please use this url to cite or link to this publication:

MLA
Hu, Zhubing, Rudy Vanderhaeghen, Toon Cools, et al. “Mitochondrial Defects Confer Tolerance Against Cellulose Deficiency.” PLANT CELL 28.9 (2016): 2276–2290. Print.
APA
Hu, Z., Vanderhaeghen, R., Cools, T., Wang, Y., De Clercq, I., Leroux, O., Nguyen, L., et al. (2016). Mitochondrial defects confer tolerance against cellulose deficiency. PLANT CELL, 28(9), 2276–2290.
Chicago author-date
Hu, Zhubing, Rudy Vanderhaeghen, Toon Cools, Yan Wang, Inge De Clercq, Olivier Leroux, Long Nguyen, et al. 2016. “Mitochondrial Defects Confer Tolerance Against Cellulose Deficiency.” Plant Cell 28 (9): 2276–2290.
Chicago author-date (all authors)
Hu, Zhubing, Rudy Vanderhaeghen, Toon Cools, Yan Wang, Inge De Clercq, Olivier Leroux, Long Nguyen, Katharina Belt, A Harvey Millar, Dominique Audenaert, Pierre Hilson, Ian Small, Grégory Mouille, Samantha Vernhettes, Frank Van Breusegem, James Whelan, Herman Höfte, and Lieven De Veylder. 2016. “Mitochondrial Defects Confer Tolerance Against Cellulose Deficiency.” Plant Cell 28 (9): 2276–2290.
Vancouver
1.
Hu Z, Vanderhaeghen R, Cools T, Wang Y, De Clercq I, Leroux O, et al. Mitochondrial defects confer tolerance against cellulose deficiency. PLANT CELL. 2016;28(9):2276–90.
IEEE
[1]
Z. Hu et al., “Mitochondrial defects confer tolerance against cellulose deficiency,” PLANT CELL, vol. 28, no. 9, pp. 2276–2290, 2016.
@article{8500074,
  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.}},
  author       = {{Hu, Zhubing and Vanderhaeghen, Rudy and Cools, Toon and Wang, Yan and De Clercq, Inge and Leroux, Olivier and Nguyen, Long and Belt, Katharina and Millar, A Harvey and Audenaert, Dominique and Hilson, Pierre and Small, Ian and Mouille, Grégory and Vernhettes, Samantha and Van Breusegem, Frank and Whelan, James and Höfte, Herman and De Veylder, Lieven}},
  issn         = {{1040-4651}},
  journal      = {{PLANT CELL}},
  keywords     = {{PENTATRICOPEPTIDE REPEAT PROTEIN,GENES-ENCODING MITOCHONDRIAL,OSMOTIC-STRESS TOLERANCE,NAC TRANSCRIPTION FACTOR,ARABIDOPSIS MUTANT CEV1,SYNTHASE COMPLEXES,RETROGRADE REGULATION,CYTOCHROME-C,ALTERNATIVE OXIDASE,ELECTRON-TRANSPORT}},
  language     = {{eng}},
  number       = {{9}},
  pages        = {{2276--2290}},
  title        = {{Mitochondrial defects confer tolerance against cellulose deficiency}},
  url          = {{http://dx.doi.org/10.1105/tpc.16.00540}},
  volume       = {{28}},
  year         = {{2016}},
}

Altmetric
View in Altmetric
Web of Science
Times cited: