4.8 Article

The Transcription Factor MYB29 Is a Regulator of ALTERNATIVE OXIDASE1a1

期刊

PLANT PHYSIOLOGY
卷 173, 期 3, 页码 1824-1843

出版社

OXFORD UNIV PRESS INC
DOI: 10.1104/pp.16.01494

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资金

  1. Australian Research Council Centre of Excellence Program [CE140100008]
  2. Interuniversity Attraction Poles Program [IUAP P7/29]
  3. Ghent University Multidisciplinary Research Partnership Biotechnology for a Sustainable Economy [01MRB510W]
  4. Agency for Innovation by Science and Technology (IWT) in Flanders
  5. Australian Research Council [DP110102868]
  6. Ghent University Special Research Fund [01J11311]
  7. Research Foundation-Flanders [12N2415N, V450215N]

向作者/读者索取更多资源

Plants sense and integrate a variety of signals from the environment through different interacting signal transduction pathways that involve hormones and signaling molecules. Using ALTERNATIVE OXIDASE1a (AOX1a) gene expression as a model system of retrograde or stress signaling between mitochondria and the nucleus, MYB DOMAIN PROTEIN29 (MYB29) was identified as a negative regulator (regulator of alternative oxidase1a 7 [rao7] mutant) in a genetic screen of Arabidopsis (Arabidopsis thaliana). rao7/myb29 mutants have increased levels of AOX1a transcript and protein compared to wild type after induction with antimycin A. A variety of genes previously associated with the mitochondrial stress response also display enhanced transcript abundance, indicating that RAO7/MYB29 negatively regulates mitochondrial stress responses in general. Meta-analysis of hormone-responsive marker genes and identification of downstream transcription factor networks revealed that MYB29 functions in the complex interplay of ethylene, jasmonic acid, salicylic acid, and reactive oxygen species signaling by regulating the expression of various ETHYLENE RESPONSE FACTOR and WRKY transcription factors. Despite an enhanced induction of mitochondrial stress response genes, rao7/myb29 mutants displayed an increased sensitivity to combined moderate light and drought stress. These results uncover interactions between mitochondrial retrograde signaling and the regulation of glucosinolate biosynthesis, both regulated by RAO7/MYB29. This common regulator can explain why perturbation of the mitochondrial function leads to transcriptomic responses overlapping with responses to biotic stress.

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