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

Poyu Chen, Nancy De Winne (UGent) , Geert De Jaeger (UGent) , Masaki Ito, Maren Heese and Arp Schnittger
(2023) EMBO JOURNAL. 42.
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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.
Keywords
General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, Molecular Biology, General Neuroscience, autophagy, DNA damage response, homologous recombination, proteasome, ubiquitination, TOPOISOMERASE-III-ALPHA, CROSS-LINK REPAIR, DNA-DAMAGE, SYNDROME PROTEIN, UBIQUITIN, PATHWAY, KINASE, FAMILY, PHOSPHORYLATION, REPLICATION

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MLA
Chen, Poyu, et al. “KNO1‐mediated Autophagic Degradation of the Bloom Syndrome Complex Component RMI1 Promotes Homologous Recombination.” EMBO JOURNAL, vol. 42, 2023, doi:10.15252/embj.2022111980.
APA
Chen, P., De Winne, N., De Jaeger, G., Ito, M., Heese, M., & Schnittger, A. (2023). KNO1‐mediated autophagic degradation of the Bloom syndrome complex component RMI1 promotes homologous recombination. EMBO JOURNAL, 42. https://doi.org/10.15252/embj.2022111980
Chicago author-date
Chen, Poyu, Nancy De Winne, Geert De Jaeger, Masaki Ito, Maren Heese, and Arp Schnittger. 2023. “KNO1‐mediated Autophagic Degradation of the Bloom Syndrome Complex Component RMI1 Promotes Homologous Recombination.” EMBO JOURNAL 42. https://doi.org/10.15252/embj.2022111980.
Chicago author-date (all authors)
Chen, Poyu, Nancy De Winne, Geert De Jaeger, Masaki Ito, Maren Heese, and Arp Schnittger. 2023. “KNO1‐mediated Autophagic Degradation of the Bloom Syndrome Complex Component RMI1 Promotes Homologous Recombination.” EMBO JOURNAL 42. doi:10.15252/embj.2022111980.
Vancouver
1.
Chen P, De Winne N, De Jaeger G, Ito M, Heese M, Schnittger A. KNO1‐mediated autophagic degradation of the Bloom syndrome complex component RMI1 promotes homologous recombination. EMBO JOURNAL. 2023;42.
IEEE
[1]
P. Chen, N. De Winne, G. De Jaeger, M. Ito, M. Heese, and A. Schnittger, “KNO1‐mediated autophagic degradation of the Bloom syndrome complex component RMI1 promotes homologous recombination,” EMBO JOURNAL, vol. 42, 2023.
@article{01GWKXQYJS9DRM7RBNP7RB62SA,
  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.}},
  articleno    = {{e111980}},
  author       = {{Chen, Poyu and De Winne, Nancy and De Jaeger, Geert and Ito, Masaki and Heese, Maren and Schnittger, Arp}},
  issn         = {{0261-4189}},
  journal      = {{EMBO JOURNAL}},
  keywords     = {{General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology,General Neuroscience,autophagy,DNA damage response,homologous recombination,proteasome,ubiquitination,TOPOISOMERASE-III-ALPHA,CROSS-LINK REPAIR,DNA-DAMAGE,SYNDROME PROTEIN,UBIQUITIN,PATHWAY,KINASE,FAMILY,PHOSPHORYLATION,REPLICATION}},
  language     = {{eng}},
  pages        = {{21}},
  title        = {{KNO1‐mediated autophagic degradation of the Bloom syndrome complex component RMI1 promotes homologous recombination}},
  url          = {{http://doi.org/10.15252/embj.2022111980}},
  volume       = {{42}},
  year         = {{2023}},
}
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