Selective autophagy regulates heat stress memory in Arabidopsis by NBR1-mediated targeting of HSP90 and ROF1

Autor: Thirumalaikumar, V.P., Gorka, M., Schulz, K., Masclaux-Daubresse, C., Sampathkumar, A., Skirycz, A., Vierstra, R.D., Balazadeh, S.
Přispěvatelé: Max Planck Institute of Molecular Plant Physiology (MPI-MP), Max-Planck-Gesellschaft, Institute of Biochemistry and Biology, University of Potsdam, Department of Biology, Washington University in Saint Louis (WUSTL), Institut Jean-Pierre Bourgin (IJPB), AgroParisTech-Université Paris-Saclay-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Institute of Biology, Leiden University, Universiteit Leiden [Leiden], German Research Foundation (DFG)SFB 973
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: Autophagy
Autophagy, 17(9), 2184-2199
Autophagy, Taylor & Francis, 2020, pp.1-16. ⟨10.1080/15548627.2020.1820778⟩
ISSN: 1554-8627
1554-8635
DOI: 10.1080/15548627.2020.1820778
Popis: International audience; In nature, plants are constantly exposed to many transient, but recurring, stresses. Thus, to complete their life cycles, plants require a dynamic balance between capacities to recover following cessation of stress and maintenance of stress memory. Recently, we uncovered a new functional role for macroautophagy/autophagy in regulating recovery from heat stress (HS) and resetting cellular memory of HS inArabidopsis thaliana. Here, we demonstrated that NBR1 (next to BRCA1 gene 1) plays a crucial role as a receptor for selective autophagy during recovery from HS. Immunoblot analysis and confocal microscopy revealed that levels of the NBR1 protein, NBR1-labeled puncta, and NBR1 activity are all higher during the HS recovery phase than before. Co-immunoprecipitation analysis of proteins interacting with NBR1 and comparative proteomic analysis of annbr1-null mutant and wild-type plants identified 58 proteins as potential novel targets of NBR1. Cellular, biochemical and functional genetic studies confirmed that NBR1 interacts with HSP90.1 (heat shock protein 90.1) and ROF1 (rotamase FKBP 1), a member of the FKBP family, and mediates their degradation by autophagy, which represses the response to HS by attenuating the expression ofHSPgenes regulated by the HSFA2 transcription factor. Accordingly, loss-of-function mutation ofNBR1resulted in a stronger HS memory phenotype. Together, our results provide new insights into the mechanistic principles by which autophagy regulates plant response to recurrent HS.
Databáze: OpenAIRE