Loss of HKT1;5D via a spontaneous terminal deletion elevates leaf sodium in bread wheat, but is independent of yield or salinity tolerance.

Abstract

Soil salinity is a significant constraint to global wheat production, and breeding for salinity tolerance offers a sustainable solution. MW#293 is a recently developed bread wheat line, notable for both its high salinity tolerance and unusually high leaf sodium (Na⁺) accumulation. However, the association between high Na⁺ accumulation and salinity tolerance in this line was unknown. Using genetic, genomic, physiological, and agronomic approaches, we identified and delineated a terminal deletion on chromosome 4D encompassing the major Na⁺ transporter gene TaHKT1;5D and determined this as the cause of the elevated leaf Na⁺ in MW#293. In a Mace x MW#293 segregating population, leaf Na+ and shoot growth measured under salinity were shown to be under separate genetic control. Field trials were conducted in three environments ranging from slightly to moderately saline. Despite the deletion encompassing at least 286 genes, we observed neither a positive nor a negative influence on grain yield. These results suggest that TaHKT1;5D is not a critical determinant of salinity tolerance in MW#293 and related bread wheat germplasm, but that other mechanisms are responsible.