| Summary: | <p>Abstract</p> <p>Background</p> <p>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<sup>2+ </sup>storage. Therefore, we designed a series of experiments to clarify the effects of actin filaments on mitochondrial Ca<sup>2+ </sup>storage, cytoplasmic Ca<sup>2+ </sup>concentration ([Ca<sup>2+</sup>]<sub>c</sub>), and the interaction between mitochondrial Ca<sup>2+ </sup>and cytoplasmic Ca<sup>2+ </sup>in <it>Arabidopsis </it>root hairs.</p> <p>Results</p> <p>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<sup>2+ </sup>stores in the mitochondria of <it>Arabidopsis </it>root hairs. Simultaneously, these treatments induced an instantaneous increase of cytoplasmic Ca<sup>2+</sup>, 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<sup>2+ </sup>concentration gradient in mitochondria from the tip to the base of the root hair, and this gradient could be disrupted by actin-acting drugs.</p> <p>Conclusions</p> <p>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<sup>2+ </sup>release into the cytoplasm, and consequent changes in [Ca<sup>2+</sup>]<sub>c</sub>. We suggest that normal polymerization and depolymerization of actin filaments are essential for mitochondrial Ca<sup>2+ </sup>storage in root hairs.</p>
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