Abstract
Calcium ion (Ca2+) is an essential plant nutrient required for cell structure establishment, as well as a counter-cation of an anion and an intracellular messenger. Calcium is absorbed from soil by roots and delivered to shoots through the xylem. The process must be finely balanced to avoid excessive accumulation. However, the regulatory mechanisms involved in calcium homeostasis remain unclear. In this study, we identified a gain-of-function mutant of paa2, a member of the NITRATE TRANSPORTER1/PEPTIDE TRANSPORTER family (NPF), that acts as a symporter of NO3 - and other cations. Ca2+ and some other cations were over-accumulated in the apex of developing panicles in both the gain-of-function mutant paa2 and PAA2 overexpressing plants. Apical panicle abortion in the paa2 mutant was mainly caused by excessive calcium accumulation. PAA2 was preferentially expressed in various meristic tissues during panicle development. PAA2 was found in the plasma membrane, endoplasmic reticulum (ER) and prevacuolar compartment, and co-localised with the vesicle-associated membrane protein 727 (VAMP727), implying that it transported calcium ions into and out of cells. Our study revealed that the tip-orientated calcium gradient in the panicle is controlled coordinately by the PAA2-UBC45 module. These findings suggest that PAA2 is a key player in maintaining Ca2+ homeostasis during panicle development in rice.