The PHD finger protein EDM2 and the two RRM domain proteins EDM3 and IBM2 were shown to preferentially target genes that contain heterochromatin. In my thesis research, I found that only the longer IBM2 isoforms, IBM2L, interacts with both expressed EDM3 isoforms, EDM3S and EDM3L. These interactions positively regulate flowering time and negatively regulate basal immunity. Mutants of EDM3 and IBM2 exhibit a delay of gradually declined expression of the floral suppressor gene FLC during the progression of development. This is negatively correlated with a gradual increase of the transcript levels of the interacting EDM3 and IBM2 isoforms. Moreover, both EDM3L and IBM2L directly target certain defense-associated genes and suppress basal immunity. Lastly, these isoforms are also found to coordinate the floral transition with a gradual repression of basal immunity. Collectively, these findings suggest a functional link between basal immunity and flowering time control. Both processes are clearly coordinated by EDM3L and IBM2L. I further found that only IBM2L can co-localize with both EDM3 isoforms at the COPIA-R7 retrotransposon within the plant immune receptor gene RPP7. Consistently, only IBM2L can rescue RPP7-mediated resistance against Hyaloperonospora arabidopsidis (Hpa) Hiks1 and expression levels of the full-length RPP7-coding transcripts. Like mutants of EDM2, edm3 and ibm2 mutants also exhibit growth defects. We found that EDM2, EDM3 and IBM2 negatively regulate peroxidase activity by downregulating the expression levels of peroxidases. I further found that all three genes promote growth and negatively regulate basal immunity partly by inhibiting peroxidase activity. As growth defects in edm2, edm3 and ibm2 mutants are only partially rescued by suppression of peroxidase activity, there may exist other mechanisms coordinating immunity and growth. By crossing with the sid2-2 and pad4 mutants, which are deficient in SA-mediated immunity, and the transgenic NahG line, which cannot accumulate SA, growth defects in all three mutants are fully or partly rescued. Lastly, we also found that growth defects and enhanced basal immunity can be partly rescued by the longer IBM1 isoform, IBM1L. Collectively, my results show that EDM2, EDM3 and IBM2 have complex roles in coordinating immunity and developmental processes in Arabidopsis.