Abstract

The ionic form of Aluminum (Al3+) is one of the dangerous metals to the plants under acid soil condition. A principal functional tool of plant Al tolerance encompasses Al-induced stimulation of membrane transporters, which accelerates the organic acid release from the root region. The released organic acid (usually citrate, oxalate and malate) form stable and nontoxic complexes with Al in the rhizosphere. Several genes were characterized to understand the acid soil tolerance mechanisms of plants. In particular, Al-activated malate and citrate discharge from the roots are effectively involved in acid soil stress tolerance mechanisms. Based on the above mechanisms, in this present work, the cotton citrate (GhMATE1 [Multidrug and Toxic compound Extrusion]) transporters has been cloned and characterized in Cotton. Down-regulation of GhMATE1 (GhMATE1-RNAi) system increased the sensitivity to Al and proton. Moreover, plants lacking GhMATE1 released negligible amount of citrate when compared with control plants. The primary and secondary root growth of GhMATE1-RNAi-lines was significantly inhibited under Al stress conditions. Besides, Al stress responsive genes like GhALMT1 (Aluminum-activated Malate Transporter 1), GhSTOP1 (Sensitive to Proton toxicity 1) and GhALS3 (Aluminum Sensitive 3) were not affected in GhMATE1-RNAi lines. In addition, transgenic Arabidopsis plants overexpressing GhMATE1 exhibited Al tolerant phenotypes and these transgenic plants displayed accelerated root growth and enhanced citrate excretion when compared with control plants. The results pointed out that the GhMATE1 expression is Al inducible and controls the citrate-mediated Al3+ sequestration. These observations indicated that GhMATE1 is a key gene which is involved in Al induced citrate release and lateral root growth arrest.

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