Effect of Nitric Oxide on Ions Absorption in Excised Root Tips of Wheat Seedlings under Drought Stress

Abstract

Longchun 8139 is a wheat(Triticum aestivum L.) cultivar grown in Dingxi in Northwest China,which has stably tolerance characteristics to drought stress in morphology,physiology,and genetics.To explain the protection mechanism of nitric oxide to plants under drought stress,Longchun 8139 and two drought-sensitive cultivars Ganmai 8 and Dingxi 24 were used for testing the adaptation to drought stress.The excised root tips(2±0.02 cm) from the seedlings were treated with 20% polyethylene glycol(PEG)-6000 to simulate drought stress.In addition,the NO content in root tips was adjusted with 0.2 mmol L-1 sodium nitroprusside(SNP,as NO donor),and 0.3 mmol L-1 Nω-nitro-L-arginine(LNNA,a NO synthase inhibitor),and 0.4 mmol L-1 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide(PTIO,a specific NO scavenger) adding in culture medium.In the root tips of Longchun 8139,the activity of NO synthase and NO content increased remarkably,the chloride(Cl-) content decreased,whereas,the contents of calcium(Ca2+) and potassium(K+) increased,simultaneously,the activity of plasma membrane H+-ATPase was activated under drought stress.However,in the root tips of Ganmai 8 and Dingxi 24,the changing patterns of the parameters above were opposite.When applying SNP,changes of the contents of Ca2+ and K+,as well as the activity of plasma membrane H+-ATPase were observed similar to those induced by PEG in drought-tolerant cultivar,Longchun 8139.These changes in response to drought stress could be counteracted,such as,the promotion of Cl- content,the reductions of Ca2+ and K+ content,and the decrease of activity of plasma membrane H+-ATPase,if LNNA and PTIO were added in the culture medium.As to Na+ content,no obvious variations were observed among all treatments.The results indicate that NO acts as the second messenger in inducing drought resistance through influencing ions absorption,which is dependent on the increased activity of plasma membrane H+-ATPase.