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 helicasecontaining 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.

Phosphorylation of KRP3, a KIP-related protein by MPK3 modulates rice tiller and seed number by fine-tuning cell division

“…All three studied overexpression lines of KRP3 showed a negative effect on plant height, leaf length, tiller number, seed number and seed weight. Displaying a similar effect in both overexpression as well as in mutant of any gene is not unlikely and has been observed in plenty of cases where a gene executes its function in a dose-dependent manner (Chen et al, 2023;. Considering KRP3 as a negative regulator of the cell division cycle, justifies the reduction in overall plant size and productivity in KRP3 overexpression lines.…”

The role of SMURFs in non‐cancerous diseases

“…Compared to monoubiquitination, polyubiquitin chains exert more diverse downstream signaling effects depending on the type of linkage. 5 Some of these isoform-linked ubiquitination is involved in the regulation of DNA damage repair (K6, K27, K33, and K63), 6,7 endocytosis (K63), 8 protein transport (K33), 9 proteasomal protein degradation (K48), 10 Wnt/β-linked protein signaling (K29), 11 NF-κB signaling (M1 and K63), 12 and innate immune response (M1, K33, and K63), 13 etc.…”