FITNESS Acts as a Negative Regulator of Immunity and Influences the Plant Reproductive Output After Pseudomonas syringae Infection

Plants, as sessile organisms, are continuously threatened by multiple factors and therefore their profitable production depends on how they can defend themselves. We have previously reported on the characterization of fitness mutants which are more tolerant to environmental stresses due to the activation of defense mechanisms. Here, we demonstrate that in fitness mutants, which accumulate moderate levels of salicylic acid (SA) and have SA signaling activated, pathogen infection is restricted. Also, we demonstrate that NPR1 is essential in fitness mutants for SA storage and defense activation but not for SA synthesis after Pseudomonas syringae (Pst) infection. Additionally, these mutants do not appear to be metabolically impared, resulting in a higher seed set even after pathogen attack. The FITNESS transcriptional network includes defense-related transcription factors (TFs) such as ANAC072, ORA59, and ERF1 as well as jasmonic acid (JA) related genes including LIPOXYGENASE2 (LOX2), CORONATINE INSENSITIVE1 (COI1), JASMONATE ZIM-domain3 (JAZ3) and JAZ10. Induction of FITNESS expression leads to COI1 downregulation, and to JAZ3 and JAZ10 upregulation. As COI1 is an essential component of the bioactive JA perception apparatus and is required for most JA-signaling processes, elevated FITNESS expression leads to modulated JA-related responses. Taken together, FITNESS plays a crucial role during pathogen attack and allows a cost-efficient way to prevent undesirable developmental effects.

Automated summary

The study demonstrates that fitness mutants with moderate levels of salicylic acid accumulation and SA signaling activated show restricted pathogen infection and higher seed set. NPR1 is found to be essential in these mutants for SA storage and defense activation, while the FITNESS transcriptional network includes defense-related transcription factors and JA related genes, modulating JA-related responses during pathogen attack.