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The DNA of all organisms is constantly damaged by physiological processes and environmental conditions. Upon persistent damage, plant growth and cell proliferation are reduced. Based on previous findings that RBR1, the only Arabidopsis homolog of the mammalian tumor suppressor gene retinoblastoma, plays a key role in the DNA damage response in plants, we unravel here the network of RBR1 interactors under DNA stress conditions. This led to the identification of homologs of every DREAM component in Arabidopsis, including previously not recognized homologs of LIN52. Interestingly, we also discovered NAC044, a mediator of DNA damage response in plants and close homolog of the major DNA damage regulator SOG1, to directly interact with RBR1 and the DREAM component LIN37B. Consistently, not only mutants in NAC044 but also the double mutant of the two LIN37 homologs and mutants for the DREAM component E2FB showed reduced sensitivities to DNA-damaging conditions. Our work indicates the existence of multiple DREAM complexes that work in conjunction with NAC044 to mediate growth arrest after DNA damage.

Chromosome axis-associated HORMA domain proteins (HORMADs), e.g., ASY1 in Arabidopsis, are crucial for meiotic recombination. ASY1, as other HORMADs, is assembled on the axis at early meiosis and depleted when homologous chromosomes synapse. Puzzlingly, both processes are catalyzed by AAA+ ATPase PCH2 together with its cofactor COMET. Here, we show that the ASY1 remodeling complex is temporally and spatially differently assembled. While PCH2 and COMET appear to directly interact in the cytoplasm in early meiosis, PCH2 is recruited by the transverse filament protein ZYP1 and brought to the ASY1-bound COMET assuring the timely removal of ASY1 during chromosome synapsis. Since we found that the PCH2 homolog TRIP13 also binds to the ZYP1 homolog SYCP1 in mouse, we postulate that this mechanism is conserved among eukaryotes. Deleting the PCH2 binding site of ZYP1 led to a failure of ASY1 removal. Interestingly, the placement of one obligatory crossover per homologous chromosome pair, compromised by ZYP1 depletion, is largely restored in this engineered zyp1 allele suggesting that crossover assurance is promoted by synapsis. In contrast, the engineered zyp1 allele, similar to the zyp1 null mutant, showed elevated type I crossover numbers indicating that PCH2-mediated eviction of ASY1 from the axis restricts crossover formation. Competing Interest Statement The authors have declared no competing interest.

The DREAM complex is a key transcriptional regulator especially involved in the control of the cell cycle and development. Here, we characterise two novel plant- specific DREAM components, FLIC and FLAC, which we identified through tandem affinity purification experiments as interactors of conserved core DREAM constituents. We demonstrate that plants lacking both FLIC and FLAC exhibit pleiotropic phenotypes, including stunted growth and reduced fertility. Notably, flic flac double mutants show an early-flowering phenotype, an aspect that we found to be shared with mutants of the core DREAM component LIN37, with which FLIC and FLAC interact in binary protein-protein interaction assays. Performing reverse affinity purification experiments, we detected the JMJ14/NAC050/NAC052 module, known for its involvement in flowering repression, in the interactome of both FLIC and FLAC. Subsequent binary interaction studies then link the JMJ14/NAC050/NAC052 module via LIN37 to the DREAM complex providing a mechanistic framework on how flowering time could be transcriptionally controlled by the DREAM complex. This study identifies two plant-specific members of the DREAM complex, explores their roles by mutant analysis and protein interaction investigation, and links them and additional DREAM complex components to the regulation of floral transition.