Rice RCN1/OsABCG5 mutation alters accumulation of essential and nonessential minerals and causes a high Na/K ratio, resulting in a salt-sensitive phenotype.

Mineral balance and salt stress are major factors affecting plant growth and yield. Here, we characterized the effects of rice (Oryza sativa L.) reduced culm number1 (rcn1), encoding a G subfamily ABC transporter (OsABCG5) involved in accumulation of essential and nonessential minerals, the Na/K ratio, and salt tolerance. Reduced potassium and elevated sodium in field-grown plants were evident in rcn1 compared to original line 'Shiokari' and four independent rcn mutants, rcn2, rcn4, rcn5 and rcn6. A high Na/K ratio was evident in the shoots and roots of rcn1 under K starvation and salt stress in hydroponically cultured plants. Downregulation of SKC1/OsHKT1;5 in rcn1 shoots under salt stress demonstrated that normal function of RCN1/OsABCG5 is essential for upregulation of SKC1/OsHKT1;5 under salt stress. The accumulation of various minerals in shoots and roots was also altered in the rcn1 mutant compared to 'Shiokari' under control conditions, potassium starvation, and salt and d-sorbitol treatments. The rcn1 mutation resulted in a salt-sensitive phenotype. We concluded that RCN1/OsABCG5 is a salt tolerance factor that acts via Na/K homeostasis, at least partly by regulation of SKC1/OsHKT1;5 in shoots.