Sodium Transfer

Excess sodium can be dangerous to plant metabolism and affects development and growth, unless it can be either excluded, excreted or stored out of harms way. Exclusion/excretion can be a viable strategy for unicellular plants/algae if these cells can compensate for the osmotic potential generated by high sodium externally. This is not a viable strategy for multicellular land plants. What are their options? Exclusion can be successful if the plant internal osmotic potential is constitutively low or can be adjusted rapidly but sodium will inevitably enter the plant when the stress persists long term. A better option seems to be sodium inclusion because sodium can be used as an osmoticum. In this scenario, the path of sodium through the plant must conform certain rules:

1. low sodium in the cytosol (although how low sodium must be seems to be species-specific)
2. a sodium gradient from root to shoot
3. effective storage capacity for NaCl.

It seems that HKT-like alkali ion transporters are responsible for influx, and several other transporters share responsibilities in the distribution and long-distance flux of sodium: vacuolar sodium/proton antiporters, vacuolar sodium/inositol symporters, and plasma membrane sodium/proton antiporters. We know about phosphorylation- dependent changes in the presence and activity of these transporters and the existence of supportive biochemical pathways that regulate osmolyte synthesis and water channel activity.