The Arabidopsis RRM domain proteins EDM3 and IBM2 coordinate the floral transition and basal immune responses.

SUMMARY: The transition from vegetative to reproductive development (floral transition) is a costly process in annual plants requiring increased investments in metabolic resources. The Arabidopsis thaliana (Arabidopsis) PHD finger protein EDM2 and RRM domain proteins EDM3 and IBM2 are known to form chromatin‐associated complexes controlling transcript processing. We are reporting that distinct splice isoforms of EDM3 and IBM2 cooperate in the coordination of the floral transition with basal immune responses. These cooperating splice isoforms, termed EDM3L and IBM2L, control the intensity of basal immunity and, via a separate pathway, the timing of the floral transition. During the developmental phase prior to the floral transition expression of EDM3L and IBM2L strongly and gradually increases, while these isoforms simultaneously down‐regulate expression of the floral suppressor gene FLC and promote the transition to reproductive growth. At the same time these accumulating EDM3 and IBM2 splice isoforms gradually suppress basal immunity against the virulent Noco2 isolate of the pathogenic oomycete Hyaloperonospora arabidopsidis and down‐regulate expression of a set of defense‐associated genes and immune receptor genes. We are providing clear evidence for a functional link between the floral transition and basal immunity in the annual plant Arabidopsis. Coordination of these two biological processes, which compete for metabolic resources, is likely critical for plant survival and reproductive success. Significance Statement: We are providing clear evidence for a dynamic mechanism coordinating in Arabidopsis two processes competing for metabolic resources, the transition from vegetative to reproductive growth and basal immunity. As Arabidopsis development approaches the transition to flowering distinct splice‐isoforms of the RRM‐domain proteins EDM3 and IBM2 accumulate and enable the floral transition by gradually down‐regulating the floral suppressor gene FLC, while, via a separate pathway, progressively limiting the extent of basal immune responses. [ABSTRACT FROM AUTHOR]