The N-degron pathway governs autophagy to promote thermotolerance in Arabidopsis
Seu Ha Kim,
Jun Seok Park,
Myoung-Hoon Lee,
Joongyu Seo,
Jaekwan Kim,
Woo Seok Yang,
Jihye Park,
Kwangmin Yoo,
Jungmin Choi,
Jong-Bok Seo,
Hyun Kyu Song and
Ohkmae K. Park ()
Additional contact information
Seu Ha Kim: Korea University
Jun Seok Park: Korea University
Myoung-Hoon Lee: Korea University
Joongyu Seo: Korea University College of Medicine
Jaekwan Kim: Seoul Center
Woo Seok Yang: Korea University
Jihye Park: Korea University
Kwangmin Yoo: Korea University College of Medicine
Jungmin Choi: Korea University College of Medicine
Jong-Bok Seo: Seoul Center
Hyun Kyu Song: Korea University
Ohkmae K. Park: Korea University
Nature Communications, 2025, vol. 16, issue 1, 1-20
Abstract:
Abstract Autophagy is a vital process that enables plants to adapt to various environmental changes. During heat stress (HS), misfolded and denatured proteins accumulate in cells, necessitating autophagy for their removal. Here, we show that a core autophagy component ATG8a is targeted for degradation via the Arg/N-degron pathway. ATG8a is expressed as two alternatively spliced transcripts encoding ATG8a isoforms, namely ATG8a(S) and ATG8a(L), with distinct N-termini. While ATG8a(S) remains stable, ATG8a(L) is N-terminally processed to expose the Arg/N-degron, leading to its degradation. Ubiquitin protein ligase E3 component N-recognin 7 (UBR7), identified as an N-recognin, is responsible for ubiquitination and proteasomal degradation of ATG8a(L). Notably, ATG8a(S) and ATG8a(L) show dynamic expression patterns, fluctuating ATG8a levels during the HS and recovery periods. Our findings highlight the crucial role of ATG8a turnover in conferring thermotolerance, which is governed by Arg/N-degron-mediated regulation. Understanding the molecular basis of ATG8a stability will provide valuable insights into plant resilience to HS under changing climatic conditions.
Date: 2025
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-61191-5
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DOI: 10.1038/s41467-025-61191-5
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