Salt tolerance in plants is mediated by Na+ extrusion from the cytosol by the plasma membrane Na+/H+ antiporter SOS1. This is activated in Arabidopsis root by the protein kinase complex SOS2–SOS3 and in Arabidopsis shoot by the protein kinase complex CBL10–SOS2, with SOS2 as a key node in the two pathways. The sos1 mutant is more sensitive than the sos2 mutant, suggesting that other partners may positively regulate SOS1 activity. Arabidopsis has 26 CIPK family proteins of which CIPK8 is the closest homolog to SOS2. It is hypothesized that CIPK8 can activate Na+ extrusion by SOS1 similarly to SOS2. The plasma membrane Na+/H+ exchange activity of transgenic yeast co-expressing CBL10, CIPK8, and SOS1 was higher than that of untransformed and SOS1 transgenic yeast, resulting in a lower Na+ accumulation and a better growth phenotype under salinity. However, CIPK8 could not interact with SOS3, and the co-expression of SOS3, CIPK8, and SOS1 in yeast did not confer a significant salt tolerance phenotype relative to SOS1 transgenic yeast. Interestingly, cipk8 displayed a slower Na+ efflux, a higher Na+ level, and a more sensitive phenotype than wild-type Arabidopsis, but grew better than sos2 under salinity stress. As expected, sos2cipk8 exhibited a more severe salt damage phenotype relative to cipk8 or sos2. Overexpression of CIPK8 in both cipk8 and sos2cipk8 attenuated the salt sensitivity phenotype. These results suggest that CIPK8-mediated activation of SOS1 is CBL10-dependent and SOS3-independent, indicating that CIPK8 and SOS2 activity in shoots is sufficient for regulating Arabidopsis salt tolerance.

Although it is well established that the Polycomb Group (PcG) complexes maintain gene repression through the incorporation of H2AK121ub and H3K27me3, little is known about the effect of these modifications on chromatin accessibility, which is fundamental to understand PcG function. Here, by integrating chromatin accessibility, histone marks and expression analyses in different Arabidopsis PcG mutants, we show that PcG function regulates chromatin accessibility. We find that H2AK121ub is associated with a less accessible but still permissive chromatin at transcriptional regulation hotspots. Accessibility is further reduced by EMF1 acting in collaboration with PRC2 activity. Consequently, H2AK121ub/H3K27me3 marks are linked to inaccessible although responsive chromatin. In contrast, only-H3K27me3-marked chromatin is less responsive, indicating that H2AK121ub-marked hotspots are required for transcriptional responses. Nevertheless, despite the loss of PcG activities leads to increased chromatin accessibility, this is not necessarily accompanied by transcriptional activation, indicating that accessible chromatin is not always predictive of gene expression.

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