RBR1-E2F/DP transcriptional regulation modulated by the F-box protein FBL17

ABSTRACT: In all eukaryotes, F-box proteins of SCF E3 ligase complexes have been well-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, presumably due to impaired degradation of cyclin-dependent kinase inhibitor proteins. However, the molecular mechanisms by how FBL17 operate remain poorly understood. Here we show that FBL17 interacts with different components of the RETINOBLASTOMA-RELATED1/E2F module. In particular, FBL17 directly targets the two transcription factors E2Fa and E2Fb and is involved in their protein turnover. However, it is the transcriptional repressor E2Fc, which is not a substrate of FBL17, that causes fbl17 mutant lethality. Hence, the e2fc mutation broadly suppresses cell elongation and cell proliferation defects observed in fbl17. Moreover, in the fbl17 e2fb double mutant the strong overexpression of DNA damage genes is significantly attenuated through RBR1 recruitment to its target genes. Altogether, 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.

INSTRUMENT(S):

ORGANISM(S): Arabidopsis Thaliana (mouse-ear Cress)

TISSUE(S): Seedling

SUBMITTER: Johana Chicher  

LAB HEAD: Pascal Genschik

PROVIDER: PXD063507 | Pride | 2026-02-23

REPOSITORIES: Pride