| Literature DB >> 30767893 |
Alexey Shapiguzov1,2,3, Julia P Vainonen1,2, Kerri Hunter1,2, Helena Tossavainen4,5, Arjun Tiwari6, Sari Järvi6, Maarit Hellman5, Fayezeh Aarabi7, Saleh Alseekh7,8, Brecht Wybouw9,10, Katrien Van Der Kelen9,10, Lauri Nikkanen6, Julia Krasensky-Wrzaczek1,2, Nina Sipari1,11, Markku Keinänen12, Esa Tyystjärvi6, Eevi Rintamäki6, Bert De Rybel9,10, Jarkko Salojärvi1,2, Frank Van Breusegem9,10, Alisdair R Fernie7,8, Mikael Brosché1,2,13, Perttu Permi4,5,14, Eva-Mari Aro6, Michael Wrzaczek1,2, Jaakko Kangasjärvi1,2.
Abstract
Reactive oxygen species (ROS)-dependent signaling pathways from chloroplasts and mitochondria merge at the nuclear protein RADICAL-INDUCED CELL DEATH1 (RCD1). RCD1 interacts in vivo and suppresses the activity of the transcription factors ANAC013 and ANAC017, which mediate a ROS-related retrograde signal originating from mitochondrial complex III. Inactivation of RCD1 leads to increased expression of mitochondrial dysfunction stimulon (MDS) genes regulated by ANAC013 and ANAC017. Accumulating MDS gene products, including alternative oxidases (AOXs), affect redox status of the chloroplasts, leading to changes in chloroplast ROS processing and increased protection of photosynthetic apparatus. ROS alter the abundance, thiol redox state and oligomerization of the RCD1 protein in vivo, providing feedback control on its function. RCD1-dependent regulation is linked to chloroplast signaling by 3'-phosphoadenosine 5'-phosphate (PAP). Thus, RCD1 integrates organellar signaling from chloroplasts and mitochondria to establish transcriptional control over the metabolic processes in both organelles.Entities:
Keywords: A. thaliana; plant biology; reactive oxygen species; redox signaling; retrograde signaling
Year: 2019 PMID: 30767893 PMCID: PMC6414205 DOI: 10.7554/eLife.43284
Source DB: PubMed Journal: Elife ISSN: 2050-084X Impact factor: 8.140