KNO1‐mediated autophagic degradation of the Bloom syndrome complex component RMI1 promotes homologous recombination

Abstract: Homologous recombination (HR) is a key DNA damage repair pathway that is tightly adjusted to the state of a cell. A central regulator of homologous recombination is the conserved helicase‐containing Bloom syndrome complex, renowned for its crucial role in maintaining genome integrity. Here, we show that in Arabidopsis thaliana, Bloom complex activity is controlled by selective autophagy. We find that the recently identified DNA damage regulator KNO1 facilitates K63‐linked ubiquitination of RMI1, a structural component of the complex, thereby triggering RMI1 autophagic degradation and resulting in increased homologous recombination. Conversely, reduced autophagic activity makes plants hypersensitive to DNA damage. KNO1 itself is also controlled at the level of proteolysis, in this case mediated by the ubiquitin–proteasome system, becoming stabilized upon DNA damage via two redundantly acting deubiquitinases, UBP12 and UBP13. These findings uncover a regulatory cascade of selective and interconnected protein degradation steps resulting in a fine‐tuned HR response upon DNA damage.

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch

Erschienen in
KNO1‐mediated autophagic degradation of the Bloom syndrome complex component RMI1 promotes homologous recombination ; day:27 ; month:03 ; year:2023 ; extent:21
The EMBO journal / European Molecular Biology Organization ; (27.03.2023) (gesamt 21)

Urheber
Chen, Poyu
De Winne, Nancy
De Jaeger, Geert
Ito, Masaki
Heese, Maren
Schnittger, Arp

DOI
10.15252/embj.2022111980
URN
urn:nbn:de:101:1-2023032715141771602815
Rechteinformation
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
14.08.2025, 10:50 MESZ

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Beteiligte

  • Chen, Poyu
  • De Winne, Nancy
  • De Jaeger, Geert
  • Ito, Masaki
  • Heese, Maren
  • Schnittger, Arp

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