Inactivation of Mitochondrial Complex I Induces the Expression of a Twin Cysteine Protein that Targets and Affects Cytosolic, Chloroplastidic and Mitochondrial Function
(2016) In Molecular Plant 9(5). p.696-710- Abstract
At12Cys-1 (At5g64400) and At12Cys-2 (At5g09570) are two closely related isogenes that encode small, twin cysteine proteins, typically located in mitochondria. At12Cys-2 transcript is induced in a variety of mutants with disrupted mitochondrial proteins, but an increase in At12Cys protein is only detected in mutants with reduced mitochondrial complex I abundance. Induction of At12Cys protein in mutants that lack mitochondrial complex I is accompanied by At12Cys protein located in mitochondria, chloroplasts, and the cytosol. Biochemical analyses revealed that even single gene deletions, i.e., At12cys-1 or At12cys-2, have an effect on mitochondrial and chloroplast functions. However, only double mutants, i.e., At12cys-1:At12cys-2, affect... (More)
At12Cys-1 (At5g64400) and At12Cys-2 (At5g09570) are two closely related isogenes that encode small, twin cysteine proteins, typically located in mitochondria. At12Cys-2 transcript is induced in a variety of mutants with disrupted mitochondrial proteins, but an increase in At12Cys protein is only detected in mutants with reduced mitochondrial complex I abundance. Induction of At12Cys protein in mutants that lack mitochondrial complex I is accompanied by At12Cys protein located in mitochondria, chloroplasts, and the cytosol. Biochemical analyses revealed that even single gene deletions, i.e., At12cys-1 or At12cys-2, have an effect on mitochondrial and chloroplast functions. However, only double mutants, i.e., At12cys-1:At12cys-2, affect the abundance of protein and mRNA transcripts encoding translation elongation factors as well as rRNA abundance. Blue native PAGE showed that At12Cys co-migrated with mitochondrial supercomplex I + III. Likewise, deletion of both At12cys-1 and At12cys-2 genes, but not single gene deletions, results in enhanced tolerance to drought and light stress and increased anti-oxidant capacity. The induction and multiple localization of At12Cys upon a reduction in complex I abundance provides a mechanism to specifically signal mitochondrial dysfunction to the cytosol and then beyond to other organelles in the cell.
(Less)
- author
- publishing date
- 2016-05-02
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- mitochondria, complex I, retrograde signaling, chloroplast, cytosol
- in
- Molecular Plant
- volume
- 9
- issue
- 5
- pages
- 15 pages
- publisher
- Oxford University Press
- external identifiers
-
- pmid:26829715
- scopus:84966662480
- ISSN
- 1752-9867
- DOI
- 10.1016/j.molp.2016.01.009
- language
- English
- LU publication?
- no
- id
- 499aa330-9fbf-4d8d-8976-a49be06db98d
- date added to LUP
- 2017-05-08 10:46:11
- date last changed
- 2024-09-16 00:46:13
@article{499aa330-9fbf-4d8d-8976-a49be06db98d, abstract = {{<p>At12Cys-1 (At5g64400) and At12Cys-2 (At5g09570) are two closely related isogenes that encode small, twin cysteine proteins, typically located in mitochondria. At12Cys-2 transcript is induced in a variety of mutants with disrupted mitochondrial proteins, but an increase in At12Cys protein is only detected in mutants with reduced mitochondrial complex I abundance. Induction of At12Cys protein in mutants that lack mitochondrial complex I is accompanied by At12Cys protein located in mitochondria, chloroplasts, and the cytosol. Biochemical analyses revealed that even single gene deletions, i.e., At12cys-1 or At12cys-2, have an effect on mitochondrial and chloroplast functions. However, only double mutants, i.e., At12cys-1:At12cys-2, affect the abundance of protein and mRNA transcripts encoding translation elongation factors as well as rRNA abundance. Blue native PAGE showed that At12Cys co-migrated with mitochondrial supercomplex I + III. Likewise, deletion of both At12cys-1 and At12cys-2 genes, but not single gene deletions, results in enhanced tolerance to drought and light stress and increased anti-oxidant capacity. The induction and multiple localization of At12Cys upon a reduction in complex I abundance provides a mechanism to specifically signal mitochondrial dysfunction to the cytosol and then beyond to other organelles in the cell.</p>}}, author = {{Wang, Yan and Lyu, Wenhui and Berkowitz, Oliver and Radomiljac, Jordan D and Law, Simon R and Murcha, Monika W and Carrie, Chris and Teixeira, Pedro F and Kmiec, Beata and Duncan, Owen and Van Aken, Olivier and Narsai, Reena and Glaser, Elzbieta and Huang, Shaobai and Roessner, Ute and Millar, A. Harvey and Whelan, James}}, issn = {{1752-9867}}, keywords = {{mitochondria; complex I; retrograde signaling; chloroplast; cytosol}}, language = {{eng}}, month = {{05}}, number = {{5}}, pages = {{696--710}}, publisher = {{Oxford University Press}}, series = {{Molecular Plant}}, title = {{Inactivation of Mitochondrial Complex I Induces the Expression of a Twin Cysteine Protein that Targets and Affects Cytosolic, Chloroplastidic and Mitochondrial Function}}, url = {{http://dx.doi.org/10.1016/j.molp.2016.01.009}}, doi = {{10.1016/j.molp.2016.01.009}}, volume = {{9}}, year = {{2016}}, }