DNA replication stress threatens genome stability and affects plant growth and development. How plants resolve replication stress is poorly understood. The protein kinase WEE1-mediated cell cycle arrest is required for replication stress responses. The E3 ubiquitin ligases anaphase-promoting complex/cyclosome (APC/C) and Skp1/Cullin 1/F-box (SCF) are essential regulators of the cell cycle. Here, we show that APC/C^CDC20 mediates the degradation of SCF^FBL17 during replication stress responses in Arabidopsis thaliana. Biochemically, WEE1 interacts with and phosphorylates the APC/C co-activator APC10, which enhances the interaction between F-BOX-LIKE17 (FBL17) and CELL DIVISION CYCLE 20 (CDC20), an activator of APC/C. Both APC10 and CDC20 are required for the polyubiquitination and degradation of FBL17. Genetically, silencing CDC20 or APC10 confers plant hypersensitivity to replication stress, which is suppressed by loss of FBL17. Collectively, our study suggests that WEE1 activates APC/C to inhibit FBL17, providing insight into replication stress responses in plants.

Background: The Actinidia deliciosa cultivar ‘Guichang’ is a remarkable kiwifruit variety. The phenotypic traits of this variety are influenced by the climatic conditions in Guizhou. The flowering time, which is shaped by multiple environmental factors, has a substantial impact on both the fruit yield and quality. Objectives and Methods: This study was designed to explore the molecular mechanisms underlying the transition from bud to flowering in ‘Guichang’ through transcriptomic and proteomic analyses. Results: The transcriptomic results revealed that 6201 genes were up-regulated, while 5849 genes were down-regulated during this transition. Key genes related to hormone signaling, such as AdPIF4, AdBSK, AdBRI1, and AdCYCD3, were recognized as crucial regulators. The proteomic analysis detected a total of 10,488 proteins. Among them, AdBSK1 was regulated, while AdPIF4, AdBRI1, and AdCYCD3 showed stable expressions. A moderate positive correlation (with a Pearson correlation coefficient of 0.445) was found between the expression levels of transcriptomics and proteomics. When AdBSK1 was over-expressed in Arabidopsis, it promoted earlier flowering. This was achieved by down-regulating FLC and up-regulating FT and SOC1. Conclusions: This study clarifies the molecular mechanisms involved in the bud-to-flowering transition in ‘Guichang’. It emphasizes the intricate interactions among hormonal pathways, key genes, and proteins, which are consistent with the broader understanding of plant flowering regulation in recent research. These findings are significant for deepening our understanding of, and potentially controlling, the flowering mechanisms.

DNA double-strand breaks (DSBs) are the most toxic DNA damage for cells. Homologous recombination (HR) is a precise DSB repair mechanism as well as a basis for gene targeting using genome-editing techniques. Despite the importance of HR, the HR mechanism in plants is poorly understood. In a genetic screen for DNA Damage Response Mutants (DDRMs), we find that the Arabidopsis ddrm2 mutant is hypersensitive to DSB-inducing reagents. DDRM2 encodes a protein with four BRCA1 C-terminal (BRCT) domains and is highly conserved in plants including the earliest land plant linage, bryophytes. The plant-specific transcription factor SOG1 binds to the promoter of DDRM2 and activates its expression, suggesting that DDRM2 is a direct target of SOG1. In consistence, the expression of DDRM2 is induced by DSBs in a SOG1-dependent manner. Epistasis analysis indicates that DDRM2 functions downstream of SOG1. Similar to the sog1 mutant, the ddrm2 mutant shows dramatically reduced HR efficiency. Our study suggests that the SOG1-DDRM2 module is required for HR, providing new insights into the HR mechanisms in plants and a potential target for improving the efficiency of gene targeting. One Sentence Summary: A genetic screen in Arabidopsis reveals that the multi-BRCT domain protein DDRM2 is required for homologous recombination and is targeted by the master DNA damage response regulator SOG1.