The retinoblastoma homolog RBR1 mediates localization of the repair protein RAD51 to DNA lesions inArabidopsis.
The retinoblastoma protein (Rb), which typically functions as a transcriptional repressor of E2F-regulated genes, represents a major control hub of the cell cycle. Here, we show that loss of theArabidopsisRb homolog RETINOBLASTOMA-RELATED 1 (RBR1) leads to cell death, especially upon exposure to genotoxic drugs such as the environmental toxin aluminum. While cell death can be suppressed by reduced cell-proliferation rates,rbr1mutant cells exhibit elevated levels of DNA lesions, indicating a direct role of RBR1 in the DNA-damage response (DDR). Consistent with its role as a transcriptional repressor, we find that RBR1 directly binds to and represses key DDR genes such as RADIATION SENSITIVE 51 (RAD51), leaving it unclear whyrbr1mutants are hypersensitive to DNA damage. However, we find that RBR1 is also required for RAD51 localization to DNA lesions. We further show that RBR1 is itself targeted to DNA break sites in a CDKB1 activity-dependent manner and partially co-localizes with RAD51 at damage sites. Taken together, these results implicate RBR1 in the assembly of DNA-bound repair complexes, in addition to its canonical function as a transcriptional regulator.
Department of Molecular Mechanisms of Phenotypic Plasticity, Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, Université de Strasbourg, Strasbourg, France.|Department of Developmental Biology, Biozentrum Klein Flottbek University of Hamburg, Hamburg, Germany.
Sascha
S
Biedermann
RIKEN Center for Sustainable Resource Science, Tsurumi, Yokohama, Japan.
Hirofumi
0000-0003-3370-4111
H
Harashima
Department of Developmental Biology, Biozentrum Klein Flottbek University of Hamburg, Hamburg, Germany.
Poyu
P
Chen
Department of Developmental Biology, Biozentrum Klein Flottbek University of Hamburg, Hamburg, Germany.
Maren
0000-0002-1070-9107
M
Heese
Institut de Biologie de l'Ecole Normale Supérieure, CNRS UMR 8197-INSERM U 1024, Paris, France.
Daniel
D
Bouyer
Department of Developmental Biology, Biozentrum Klein Flottbek University of Hamburg, Hamburg, Germany.
Kostika
K
Sofroni
Department of Molecular Mechanisms of Phenotypic Plasticity, Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, Université de Strasbourg, Strasbourg, France arp.schnittger@uni-hamburg.de.|Department of Developmental Biology, Biozentrum Klein Flottbek University of Hamburg, Hamburg, Germany.
Arp
0000-0001-7067-0091
A
Schnittger
D017360:Arabidopsis / Q000201:enzymology* / Q000235:genetics*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism*; D016923:Cell Death; D004260:DNA Repair; D018744:DNA, Plant / Q000378:metabolism*; D017353:Gene Deletion; D011485:Protein Binding; D051135:Rad51 Recombinase / Q000378:metabolism*
D029681:Arabidopsis Proteins; D018744:DNA, Plant; C487568:RBR1 protein, Arabidopsis; C495146:ATRAD51 protein, Arabidopsis; D051135:Rad51 Recombinase

Arabidopsis
; DNA‐damage response; RAD51; retinoblastoma