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Published on June 20, 2008; 10.1104/pp.108.121384


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Received April 17, 2008
Accepted June 11, 2008

Identification of regulatory pathways controlling gene expression of stress responsive mitochondrial proteins in Arabidopsis

Lois HM Ho , Estelle Giraud , Vindya Uggalla , Ryan Lister , Rachel Clifton , Angela Glen , Dave Thirkettle-Watts , Olivier Van Aken , and James Whelan *

ARC Centre of Excellence in Plant Energy Biology, MCS Building M316 University of Western Australia, 35 Stirling Highway, Crawley 6009, Western Australia, Australia

* Corresponding author; email: seamus{at}cyllene.uwa.edu.au.

In this study we analysed transcript abundance and promoters of genes encoding mitochondrial proteins to identify signalling pathways that regulate stress-induced gene expression. We used Arabidopsis alternative oxidase AOX1a, external NAD(P)H-dehydrogenase NDB2 and two additional highly stress-responsive genes, At2g21640 and BCS1. As a starting point, the promoter region of AOX1a was analysed and functional analysis identified ten cis-acting regulatory elements (CAREs), which played a role in response to treatment with H2O2, rotenone or both. Six of these elements were also functional in the NDB2 promoter. The promoter region of At2g21640, previously defined as a hallmark of oxidative stress, shared two functional CAREs with AOX1a and was responsive to treatment with H2O2 but not rotenone. Microarray analysis further supported that signalling pathways induced by H2O2 and rotenone are not identical. The promoter of BCS1 was not responsive to H2O2 or rotenone, but highly responsive to salicylic acid (SA), while the promoters of AOX1a and NDB2 were unresponsive to SA. Analysis of transcript abundance of these genes in a variety of defence signalling mutants confirmed that BCS1 expression is regulated in a different manner compared to AOX1a, NDB2 and At2g21640. These mutants also revealed a pathway, associated with programmed cell death, that regulated AOX1a in a manner distinct from the other genes. Thus at least three distinctive pathways regulate mitochondrial stress response at a transcriptional level, an SA dependent pathway represented by BCS1, a second pathway that represents a convergence point for signals generated by H2O2 and rotenone on multiple CAREs, some of which are shared between responsive genes, and a third pathway that acts via EDS1 and PAD4 regulating only AOX1a. Furthermore, post-transcriptional regulation accounts for changes in transcript abundance by SA treatment for some genes.




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