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Inactivation of Mitochondrial Complex I Induces the Expression of a Twin Cysteine Protein that Targets and Affects Cytosolic, Chloroplastidic and Mitochondrial Function
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Number of Authors: 17
2016 (English)In: Molecular Plant, ISSN 1674-2052, E-ISSN 1752-9867, Vol. 9, no 5, 696-710 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2016. Vol. 9, no 5, 696-710 p.
Keyword [en]
mitochondria, complex I, retrograde signaling, chloroplast, cytosol
National Category
Biological Sciences
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URN: urn:nbn:se:su:diva-131535DOI: 10.1016/j.molp.2016.01.009ISI: 000375958800007PubMedID: 26829715OAI: oai:DiVA.org:su-131535DiVA: diva2:945539
Available from: 2016-07-01 Created: 2016-06-21 Last updated: 2016-07-01Bibliographically approved

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Teixeira, Pedro F.Kmiec, BeataGlaser, Elzbieta
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