Cellular mechanisms to survive salt in the halophyte Cakile maritima

We recently identified two behaviours in cultured cells of the salt accumulating halophyte Cakile maritima: one related to a sustained depolarization due to Na⁺ influx through the non-selective cation channels leading to programmed cell death of these cells, a second one related to a transient depolarization allowing cells to survive (Ben Hamed-Laouti, 2016). In this study, we considered at the cellular level mechanisms that could participate to the exclusion of Na⁺ out of the cell and thus participate in the regulation of the internal contents of Na⁺ and cell survival. Upon addition of NaCl in the culture medium of suspension cells of C. maritima, we observed a rapid influx of Na⁺ followed by an efflux dependent of the activity of plasma membrane H⁺-ATPases, in accordance with the functioning of a Na⁺/H⁺ antiporter and the ability of some cells to repolarize. The Na⁺ efflux was shown to be dependent on Na⁺-dependent on Ca²⁺ influx like the SOS1 Na⁺/H⁺ antiporter. We further could observe in response to salt addition, an early production of singlet oxygen (¹O₂) probably due to peroxidase activities. This early ¹O₂ production seemed to be a prerequisite to the Na⁺ efflux. Our findings suggest that in addition to the pathway leading to PCD (Ben Hamed-Laouti, 2016), a second pathway comprising an SOS-like system could participate to the survival of a part of the C. maritima cultured cells challenged by salt stress.