2. Academic Validation
  3. Tuning of the RBR1-E2F/DP transcriptional module by the F-box protein FBL17

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

  • Sci Adv. 2026 Feb 20;12(8):eadz2439. doi: 10.1126/sciadv.adz2439.
Juliette Espanet 1,  Xiaoning He 2,  Ting Pan 3,  Naomie Gentric 1,  Thomas Potuschak 1,  Bénédicte Desvoyes 4,  Philippe Hammann 5,  Johana Chicher 5,  Rim Brik 2,  Esther Lechner 1,  David Latrasse 2,  Aladár Pettkó-Szandtner 6,  Crisanto Gutierrez 4,  Cécile Raynaud 2,  Zoltán Magyar 7,  Moussa Benhamed 2,  Shunping Yan 3,  Sandra Noir 1,  Pascal Genschik 1
Affiliations

Affiliations

  • 1 Institut de Biologie Moléculaire des Plantes, CNRS, Université de Strasbourg, 12, rue du Général Zimmer, 67084 Strasbourg, France.
  • 2 Université Paris-Saclay, CNRS, INRAE, Université Evry, Institute of Plant Sciences Paris-Saclay (IPS2), 91190 Gif-sur-Yvette, France.
  • 3 Hubei Hongshan Laboratory, Huazhong Agricultural University, 430070 Wuhan, China.
  • 4 Centro de Biologia Molecular Severo Ochoa, CSIC-UAM, 28049 Madrid, Spain.
  • 5 Plateforme Protéomique Strasbourg Esplanade du CNRS, Université de Strasbourg, 67084 Strasbourg, France.
  • 6 Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
  • 7 Institute of Plant Biology, HUN-REN Biological Research Centre, Szeged, Hungary.
PMID: 41706863 DOI: 10.1126/sciadv.adz2439
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.

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