4.8 Article

Selective autophagy regulates heat stress memory inArabidopsisby NBR1-mediated targeting of HSP90 and ROF1

Journal

AUTOPHAGY
Volume 17, Issue 9, Pages 2184-2199

Publisher

TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2020.1820778

Keywords

Arabidopsis thaliana; heat stress; HSFA2; HSP90; 1; NBR1; ROF1; selective autophagy; stress memory; stress recovery

Categories

Funding

  1. Deutsche Forschungsgemeinschaft [SFB 973]

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Plants experience various stresses in their growth process, and autophagy plays an important role in regulating plant recovery and memory of heat stress. NBR1 functions as a receptor for selective autophagy during recovery from heat stress, interacting with HSP90.1 and ROF1 to mediate protein degradation and modulate the response to heat stress. Loss of NBR1 function results in a stronger memory phenotype for heat stress in plants.
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.

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