Disruption of Both AtMID1A and AtMID1B Increases The Mg²⁺-Sensitivity of Arabidopsis Plants in a Ca²⁺-Dependent Manner

Abstract

We have shown that the Arabidopsis AtMID1A gene product (AtMid1A) has a Ca²⁺-permeable, stretch-activated channel activity (2004 meeting). AtMid1A and its paralog, AtMid1B, are postulated to act as sensors of mechanical stimuli and participate in generating Ca²⁺ signals. In the last JSPP meeting, we have shown that the atmid1a/b double mutant exhibits a severe growth defect when grown on media containing high concentrations of Mg²⁺, but supplementation of CaCl₂ to the media alleviates this phenotype. We show that MgSO₄ concentrations required for the induction of the growth defect of the atmid1a/b mutant are lowered when the concentration of CaCl₂ in media is lowered. The finding suggests that the growth defect occurs when the ratio of Mg²⁺ to Ca²⁺ is higher. To explain this phenotype, we examine and discuss the following possibilities: (1) Mg²⁺ blocks Ca²⁺ channels other than AtMid1A/B and lowers [Ca²⁺]_cyt ;(2) Mg²⁺ disturbs Ca²⁺ signaling in the cytoplasm.