ABSTRACTCyclic Nucleotide Gated Ion Channels (CNGCs) are non-selective cation channels that are involved in regulating responses to both biotic and abiotic stresses in plants. CNGC2 has been implicated in plant immunity and Ca2+ signaling through the study of the autoimmune phenotypes exhibited by the null mutant, defense, no death1 (dnd1). However, dnd1 also shows additional phenotypes that are unique among autoimmune mutants. This suggests that CNGC2 plays multiple biological roles beyond pathogen defense. In this study, we cloned the gene that encodes the first suppressor of dnd1 (cngc2), REPRESSOR OF DEFENSE, NO DEATH1 (RDD1), which encodes an auxin biosynthesis gene, YUCCA6 (YUC6). We found that dnd1 (cngc2) is defective in auxin-mediated root growth inhibition and gravitropic responses in roots. Consistently with these auxin resistance phenotypes, we found dnd1 shows a dampened response to exogenous auxin compared to wildtype plants using the auxin inducible DR5::GUS and DII:VENUS reporter systems. Finally, auxin-induced Ca2+ influx was examined using the Förster resonance energy transfer (FRET)-based, genetically encoded Ca2+ indicator yellow cameleon (YC)-Nano65. We captured severe defects in auxin-induced Ca2+ increase in dnd1. These defects were rescued by the rdd1 mutation. Our findings highlight the unexpected involvement of CNGC2 in auxin-induced Ca2+ signaling and calls into question the current interpretation of dnd1 phenotypes in defense signaling.
TOPLESS promotes plant immunity by repressing auxin signaling and is targeted by the fungal effector Naked1