Plant defense responses are repressed under non-pathogenic conditions to ensure optimal plant growth and development. R (Disease Resistance) genes are central regulators mediating robust disease resistance. An R gene SNC1 is negatively regulated by an evolutionarily conserved copine gene BON1 in Arabidopsis. The loss of BON1 function leads to enhanced disease resistance but a growth defect in a SNC1 dependent manner. To understand how the R gene SNC1 is regulated, I analyzed enhancers and suppressors of bon1 mutants. The study of bon1 enhancer ebo30 reveals an effect on R gene expression by cell cycle progression. The ebo30 mutant is an overexpression allele of OSD1 (omission of second division 1). Both OSD1 gene and its homolog UVI4 are negative regulators of anaphase-promoting complex/cyclosome (APC/C), a multisubunit ubiquitin E3 ligase that regulates the progression of cell cycles. Overexpression of OSD1 or UVI4 as well as down regulation of APC10 confers enhanced resistance to a bacterial pathogen. Further, enhanced immune response induced by OSD1 overexpression is dependent on CYCB1;1 and the R gene SNC1. Together, this study suggests that mis-regulated cell cycle progression has an impact on R gene expression and plant immunity. This notion is reinforced by the study of interaction of UVI4 and OSD1 with CPR5, a gene involved in both defense and cell cycle regulation. The cpr5 mutant was reported to have reduced endoreduplication and enhanced disease resistance. These cell cycle defects of osd1 and uvi4 single and double mutants can be suppressed by cpr5 mutation. Therefore, the CPR5 gene may have a direct role in cell cycle regulation and subsequently affect plant immunity. The study of mos1, a suppressor of bon1 reveals a new transcriptional regulator for plant immunity, flowering time and endoreduplication. The mos1 mutant has compromised defense responses, is late flowering, and has enhanced endoreduplication. These phenotypes are due to the change of expression of SNC1, FLC, and potentially CYCD3;1 respectively. The function of MOS1 in modulating flowering time and cell cycle progression is dependent on SUF4, a previously known transcription factor for flowering time control. MOS1 is found to physically interact with SUF4, and may thus repress its function. The interaction of MOS1 and SUF4 might be influenced by MAD2, a component in the spindle assembly checkpoint complex. The interactions among MOS1, MAD2 with SUF4 suggest an intriguingly possibility that checkpoint machinery might have a direct impact on flowering time control. In sum, this study provides insights into complex regulation on R genes in plants, and discusses potential connections among regulations of defense, cell cycle, and flowering time.