Disruption of actin filaments induces mitochondrial Ca(2+ )release to the cytoplasm and [Ca(2+)](c )changes in Arabidopsis root hairs

BACKGROUND: Mitochondria are dynamic organelles that move along actin filaments, and serve as calcium stores in plant cells. The positioning and dynamics of mitochondria depend on membrane-cytoskeleton interactions, but it is not clear whether microfilament cytoskeleton has a direct effect on mitochondrial function and Ca(2+ )storage. Therefore, we designed a series of experiments to clarify the effects of actin filaments on mitochondrial Ca(2+ )storage, cytoplasmic Ca(2+ )concentration ([Ca(2+)](c)), and the interaction between mitochondrial Ca(2+ )and cytoplasmic Ca(2+ )in Arabidopsis root hairs. RESULTS: In this study, we found that treatments with latrunculin B (Lat-B) and jasplakinolide (Jas), which depolymerize and polymerize actin filaments respectively, decreased membrane potential and Ca(2+ )stores in the mitochondria of Arabidopsis root hairs. Simultaneously, these treatments induced an instantaneous increase of cytoplasmic Ca(2+), followed by a continuous decrease. All of these effects were inhibited by pretreatment with cyclosporin A (Cs A), a representative blocker of the mitochondrial permeability transition pore (mPTP). Moreover, we found there was a Ca(2+ )concentration gradient in mitochondria from the tip to the base of the root hair, and this gradient could be disrupted by actin-acting drugs. CONCLUSIONS: Based on these results, we concluded that the disruption of actin filaments caused by Lat-B or Jas promoted irreversible opening of the mPTP, resulting in mitochondrial Ca(2+ )release into the cytoplasm, and consequent changes in [Ca(2+)](c). We suggest that normal polymerization and depolymerization of actin filaments are essential for mitochondrial Ca(2+ )storage in root hairs.