# Tuning of the RBR1-E2F/DP transcriptional module by the F-box protein FBL17

## TL;DR

This paper shows how the FBL17 protein in Arabidopsis regulates cell cycle genes to prevent DNA damage.

## Contribution

The study reveals FBL17's role in modulating the RBR1-E2F/DP module and its impact on DNA damage response.

## Key findings

- FBL17 interacts with components of the RBR1-E2F/DP module and regulates E2Fa and E2Fb protein turnover.
- Accumulation of E2Fc, a transcriptional repressor, causes lethality in FBL17 mutants.
- FBL17 ensures proper control of cell cycle progression and prevents uncontrolled DNA damage response.

## Abstract

F-box proteins of SCF E3 ligases have been documented to control the abundance of numerous critical regulatory proteins. In Arabidopsis, one of them, F-BOX-LIKE17 (FBL17), stands out for playing a key role in DNA replication, DNA damage, and, more recently, for the control of cell size. FBL17 null mutants exhibit severe cellular defects leading to lethality. However, the molecular mechanisms by which FBL17 operate remain poorly understood. Here, we show that FBL17 interacts with different components of the RETINOBLASTOMA-RELATED1/E2F module and is involved in the protein turnover of E2Fa and E2Fb. However, mutations in E2Fa or E2Fb do not alleviate the severe fbl17 phenotype but worsen it. By contrast, it is the accumulation of the transcriptional repressor E2Fc that causes fbl17 mutant lethality. Our results highlight a key role for FBL17 in modulating the transcriptional control of E2F target genes ensuring precise control of cell cycle progression and avoiding uncontrolled DNA damage response.

FBL17 regulates the RBR1–E2F/DP transcriptional module to prevent aberrant activation of the DNA damage response in Arabidopsis.