ABSTRACT
The hormone salicylic acid (SA) plays a crucial role in plant immunity by activating responses that arrest pathogen ingress. SA accumulation also penalizes growth, a phenomenon visible in mutants that hyperaccumulate SA, resulting in strong growth inhibition. An important question, therefore, is why healthy plants produce basal levels of this hormone when defense responses are not activated. Here, we show that basal SA levels in unchallenged plants are needed for the expression of a number of immunity-related genes and receptors, such as RECEPTOR-LIKE PROTEIN 23 (RLP23). This was shown by depleting basal SA levels in transgenic Arabidopsis lines through the overexpression of the SA-inactivating hydroxylases DOWNY MILDEW-RESISTANT 6 (DMR6) or DMR6-LIKE OXYGENASE 1. RNAseq analysis revealed that the expression of a subset of immune receptor and signaling genes is strongly reduced in the absence of SA. The biological relevance of this was shown for RLP23: In SA-depleted and SA-insensitive plants, responses to the RLP23 ligand, the microbial pattern nlp24, were strongly reduced, whereas responses to flg22 remained unchanged. We hypothesize that low basal SA levels are needed for the expression of a subset of immune system components that enable early pathogen detection and activation of immunity.
Subject(s)
Arabidopsis Proteins , Arabidopsis , Gene Expression Regulation, Plant , Plant Diseases , Plant Immunity , Salicylic Acid , Salicylic Acid/metabolism , Arabidopsis/genetics , Arabidopsis/immunology , Arabidopsis/microbiology , Plant Immunity/genetics , Arabidopsis Proteins/genetics , Arabidopsis Proteins/metabolism , Plant Diseases/microbiology , Plant Diseases/immunology , Plant Diseases/genetics , Plants, Genetically ModifiedABSTRACT
In the absence of light signals, Arabidopsis plants fail to develop the rosette habit typical for this species. Instead, plants display caulescent growth due to elongation of rosette internodes. This aspect of photomorphogenic development has been paid little attention and molecular events involved, downstream of photoreceptor signaling, remain to be identified. Using a combination of genetic and molecular approaches, we show that Arabidopsis rosette habit is a photomorphogenic trait controlled by induction of ARABIDOPSIS THALIANA HOMEOBOX GENE1 (ATH1) as downstream target of multiple photoreceptors. ATH1 induction prevents rosette internode elongation by maintaining the shoot apical meristem (SAM) rib zone area inactive and requires inactivation of photomorphogenesis inhibitors, including PHYTOCHROME INTERACTING FACTOR (PIF) proteins. ATH1 activity results in tissue-specific inhibition of PIF expression, establishing double-negative feedback-regulation at the SAM. Light-requirement for ATH1 expression can be overcome by high sugar availability to the SAM. Both sugar and light signals that induce ATH1 and, subsequently, rosette habit are mediated by TOR kinase. Collectively, our data reveal a SAM-specific, double-negative ATH1-PIF feedback loop at the basis of rosette habit. Upstream, TOR kinase functions as central hub integrating light and energy signals that control this for Arabidopsis quintessential trait.
