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Autophagic punctum

Ufmylation bridges autophagy and ER homeostasis in plants

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Pages 2830-2831 | Received 30 Mar 2023, Accepted 11 Apr 2023, Published online: 01 May 2023
 

ABSTRACT

The autophagic machinery is highly conserved in eukaryotes. Plants, as sessile organisms, are more susceptible to environmental stresses than animals. Autophagy plays a pivotal role in plant stress responses, but the regulation of autophagic flux in plants remains enigmatic with few autophagic receptors identified. We recently characterized an E3 ligase, the ubiquitin-fold modifier 1 (Ufm1) ligase 1 (Ufl1), as well as its small modifier protein Ufm1, as interactors of the core autophagy-related (ATG) proteins. Mutants of these ufmylation system components are hypersensitive to salt stress and trigger the upregulation of endoplasmic reticulum (ER) stress-responsive genes, as well as the accumulation of ER sheets caused by a defect in reticulophagy. Increased expression of Ufl1, Ufm1 and Ufm1-conjugating enzyme 1 (Ufc1) are also triggered by salt stress in plants. This study identified and demonstrated the participation of ufmylation components in maintaining ER homeostasis by regulating reticulophagy under salt stress in plants.

Abbreviations: ATG, autophagy-related; ER, endoplasmic reticulum; LIR, LC3-interacting region; ROS, reactive oxygen species; CDK5RAP3/C53, CDK5 regulatory subunit-associated protein 3; Uba5, Ufm1-activating enzyme 5; Ufc1, Ufm1-conjugating enzyme 1; Ufl1, Ufm1 ligase 1; Ufm1, ubiquitin-fold modifier 1; UPR, unfolded protein response.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by grants from the National Natural Science Foundation of China (91854201), the Research Grants Council of Hong Kong (AoE/M-05/12, CUHK14101219, C4033-19E, C4002-20W, C4002-21EF, C2009-19 G, C2003-22WF, R4005-18 and Senior Research Fellow Scheme SRFS2122-4S01),The Chinese University of Hong Kong (CUHK) Research Committee, and CAS-Croucher Funding Scheme for Joint Laboratories to L.J.

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