Fig. 6.

Hypothetical model for cell wall modifications and CWI-induced signaling pathways triggered by salt stress. Salt application directly modifies the activity of pectin methyl-esterase (Fig. 4B) triggering cell wall de-methyl esterification (Fig. 3). Detection of these cell wall modifications seems to be responsible, at least in part, for the activation of salt stress responses. We show that chemicals that can inhibit PME activity (Fig. 4B) and HG methyl-esterification (Fig. 4C,D) can also alleviate the responses to salt stress (Fig. 5A-D). We hypothesize that the cell wall sensors FERONIA (FER) or HERK1/THESEUS1 attenuate most of the salt-dependent phenotypes, being required to negatively regulate the salt-dependent MPK6 activation in response to salt stress (Fig. 1C-E). However, because in control conditions these mutants already displayed minor enhanced marker gene expression as well as MPK6 activity (Fig. 1C-E, Fig. 5A-D), we speculate that their functional impairment might cause cell wall modifications, and this damage can be directly or indirectly alleviated by the presence of certain chemicals (Fig. 4B-D). We show that CaCl₂ application reduces basal gene expression levels and physiological MPK6 activity is altered in the CWI mutants (Fig. 5A,C), likely suggesting that the dual effect of MPK6 on strongly inhibiting PME activity (Fig. 4B) and/or cell wall crosslinks, might result in a faster and stronger alleviation of the salt stress phenotypes. On the other hand, treatment with chemicals (such as salt), which have an impact on the cell wall composition, lead to a stronger damage response, which correlates with a higher intensity of responses in the cell wall sensor mutants. In this scenario, one branch of the responses might depend on a direct inhibition mediated by the cell wall sensors of the downstream responses, whereas the other branch (represented by a question mark) might be uncoupled but still be dependent on their effect on the physiology of the cell walls. At the same time, the cell wall sensors seem to only mildly affect halotropism, a root-bending response that occurs independently of MPK6 and/or CaCl₂ application. It should be noted that all the cell wall analyses reported in this paper derive from whole Arabidopsis seedling extracts and the tissue or cell types in which cell wall modifications occur in response to salt remain to be determined.