Due to its detrimental effect on plant growth, salinity is an increasing worldwide problem for agriculture. To understand the molecular mechanisms activated in response to salt in Arabidopsis, we investigated the Catharanthus roseus Receptor like Kinase 1 Like family, containing sensors previously shown to be involved in sensing the structural integrity of the cell walls. We found that herk1the1-4 double mutants, lacking the function of HERKULES1 (HERK1) combined with a gain-of-function allele of THESEUS1 (THE1), strongly respond to salt application, resulting in an intense activation of stress responses, similarly to plants lacking FERONIA (FER) function. We report that salt triggers pectin methyl esterase (PME) activation and show its requirement for the activation of several salt-dependent responses. Because chemical inhibition of PMEs alleviates these salt-induced responses, we hypothesize a model where salt directly leads to cell wall modifications through the activation of PMEs. Responses to salt partly require the functionality of FER alone or the HERK1/THE1 combination to attenuate salt effects, highlighting the complexity of the salt sensing mechanisms that rely on the cell wall integrity.

Soil salinity is an increasing worldwide problem for agriculture, affecting plant growth and yield. In our attempt to understand the molecular mechanisms activated in response to salt in plants, we investigated the Catharanthus roseus Receptor like Kinase 1 Like (CrRLK1L) family, which contains well described sensors previously shown to be involved in maintaining and sensing the structural integrity of the cell walls. We have observed that herk1the1-4 double mutants, lacking the function of the Arabidopsis thaliana Receptor like Kinase HERKULES1 combined with a gain of function allele of THESEUS1, phenocopied the phenotypes previously reported in plants lacking FERONIA (FER) function. We report that both fer-4 and herk1the1-4 mutants respond strongly to salt application, resulting in a more intense activation of early and late stress responses. We also show that salt triggers de-methyl esterification of loosely bound pectins. These cell wall modifications might be partly responsible for the activation of the signaling pathways required to activate salt stress responses. In fact, by adding calcium chloride or by chemically inhibiting pectin methyl esterase (PME) activity we observed reduced activation of the early signaling protein Mitogen Activated Protein Kinase 6 (MPK6) as well as a reduced amplitude in salt-induced marker gene induction. We show that MPK6 is required for the full induction of the salt-induced gene expression markers we tested. However, the sodium specific root halotropism response is likely regulated by a different branch of the pathway being independent of MPK6 or calcium application but influenced by the cell wall sensors FER/HERK1/THE1-4 and PME activity. We hypothesize a model where salt-triggered modification of pectin requires the functionality of FER alone or the HERK1/THE1 combination to attenuate salt responses. Collectively, our results show the complexity of salt stress responses and salt sensing mechanisms and their connection to cell wall modifications, likely being in part responsible for the response phenotypes observed in salt treated plants.