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Isolation of Arabidopsis ahg11, a weak ABA hypersensitive mutant defective in nad4 RNA editing

The phytohormone abscisic acid (ABA) plays pivotal roles in the regulation of developmental and environmental responses in plants. Identification of cytoplasmic ABA receptors enabled the elucidation of the main ABA signalling pathway, connecting ABA perception to either nuclear events or the action...

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Detalles Bibliográficos
Autores principales: Murayama, Maki, Hayashi, Shimpei, Nishimura, Noriyuki, Ishide, Mayumi, Kobayashi, Keiko, Yagi, 
Yusuke, Asami, Tadao, Nakamura, Takahiro, Shinozaki, Kazuo, Hirayama, Takashi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3430999/
https://www.ncbi.nlm.nih.gov/pubmed/22821940
http://dx.doi.org/10.1093/jxb/ers188
Descripción
Sumario:The phytohormone abscisic acid (ABA) plays pivotal roles in the regulation of developmental and environmental responses in plants. Identification of cytoplasmic ABA receptors enabled the elucidation of the main ABA signalling pathway, connecting ABA perception to either nuclear events or the action of several transporters. However, the physiological functions of ABA in cellular processes largely remain unknown. To obtain greater insight into the ABA response, genetic screening was performed to isolate ABA-related mutants of Arabidopsis and several novel ABA-hypersensitive mutants were isolated. One of those mutants—ahg11—was characterized further. Map-based cloning showed that AHG11 encodes a PPR type protein, which has potential roles in RNA editing. An AHG11-GFP fusion protein indicated that AHG11 mainly localized to the mitochondria. Consistent with this observation, the nad4 transcript, which normally undergoes RNA editing, lacks a single RNA editing event conferring a conversion of an amino acid residue in ahg11 mutants. The geminating ahg11 seeds have higher levels of reactive-oxygen-species-responsive genes. Presumably, partial impairment of mitochondrial function caused by an amino acid conversion in one of the complex I components induces redox imbalance which, in turn, confers an abnormal response to the plant hormone.