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

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 defectsleading 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 moduleand is involved in the protein turnover of E2Fa and E2Fb. However, mutations in E2Fa or E2Fb do not alleviate thesevere fbl17 phenotype but worsen it. By contrast, it is the accumulation of the transcriptional repressor E2Fc thatcauses fbl17 mutant lethality.