Abstract

ABSTRACTIn this study, zinc (Zn) deficiency caused a significant reduction in growth parameters and tissue Zn concentrations in BRRI 33 (sensitive) but not in Pokkali (tolerant). The increase of proton extrusion in both genotypes under high pH suggests that it gets triggered as a common consequence of reducing pH and solubilization of Zn. Real-time PCR showed pronounced upregulation of OsZIP4, OsDMAS1, OsNAS2 and OsPCS1 in Zn-deficient roots of Pokkali, and to a lesser extent in BRRI 33 only for OsZIP4 and OsPCS1. This suggests that OsDMAS1, OsNAS2 and OsPCS1 functions as secondary consequences leading to higher chelation and uptake of Zn under Zn deficiency in Pokkali. Further, a major increase in CAT, POD, SOD, GR and key metabolites suggests that high antioxidant defense plays a critical role in Zn deficiency tolerance in Pokkali. Further, Pokkali self-grafts and plants having Pokkali rootstock combined with BRRI 33 scion showed no significant decline in plant height, root dry matter and Zn concentration along with upregulation of Zn transporters (OsZIP4 and OsIRT1) under Zn deficiency, suggesting that signal driving mechanisms for Zn deficiency tolerance mechanisms are generated in the root and Zn-inefficient BRRI 33 is not capable of producing signals or sensing them.

Highlights

  • Zn deficiency is a well-known agricultural problem that causes leaf bronzing, growth stunting, delayed maturity and yield loss (Dobermann and Fairhurst 2000; Fageria et al 2002)

  • Real-time PCR showed pronounced upregulation of OsZIP4, OsDMAS1, OsNAS2 and OsPCS1 in Zn-deficient roots of Pokkali, and to a lesser extent in BRRI 33 only for OsZIP4 and OsPCS1. This suggests that OsDMAS1, OsNAS2 and OsPCS1 functions as secondary consequences leading to higher chelation and uptake of Zn under Zn deficiency in Pokkali

  • Pokkali selfgrafts and plants having Pokkali rootstock combined with BRRI 33 scion showed no significant decline in plant height, root dry matter and Zn concentration along with upregulation of Zn transporters (OsZIP4 and OsIRT1) under Zn deficiency, suggesting that signal driving mechanisms for Zn deficiency tolerance mechanisms are generated in the root and Zn-inefficient BRRI 33 is not capable of producing signals or sensing them

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Summary

Introduction

Zn deficiency is a well-known agricultural problem that causes leaf bronzing, growth stunting, delayed maturity and yield loss (Dobermann and Fairhurst 2000; Fageria et al 2002). Zn homeostasis in plants is tightly regulated by Zn sensors and metal chelators involved in Zn acquisition and sequestration (Clemens 2001). Genes encoding DMA and NA synthase (NAS) showed differential regulation under variable Fe and Zn status in rice, maize, Arabidopsis and barley (Inoue et al 2003; Klatte et al 2009; Johnson et al 2011). DMA in Zn-deficient rice plants are critically involved with the distribution of Zn and increase of Zn translocation (Suzuki et al 2008) and overexpression of OsNAS2 gene led a significant increase of Fe and Zn in rice endosperm (Johnson et al 2011). Phytochelatins (PCs), glutathione-derived metal-binding peptides, are involved in Zn accumulation and PC-Zn complexes formation in a few plant species but not in rice (Kobayashi and Yoshimura 2006; Chekmeneva et al 2008; Tennstedt et al 2008)

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