【摘要】 烟草愈伤组织的培养细胞中,当钙离子载体将Ca²⁺导入细胞时,细胞质流停止.CaM拮抗剂试验表明,高钙使细胞质流停止的效应可能与CaM无关,除W7外的多种CaM拮抗剂都明显而且可逆地抑制细胞质流。酶联免疫吸附分析（ELISA）检出培养细胞中存在有CaM。间接酶标免疫组织化学分析进一步证明CaM存在于胞质条纹中。更多还原

【Abstract】 Using the cultured cells of tobacco callusas a intact cell model, we studied the mechanismof cytoplasmic streaming. The detecting rea-gents included microfilament depolymerizingagent, cytochalasin B; microtubule depoly-merizing agent, colchicine; Ca²⁺ ionophore A23187; Ca²⁺ chelator EGTA; calmodulin（CaM）antagonists. chlopromazine, fluephenazine,Tetand W7. The experiment results indicated that cyto-plasmic streaming was reversely inhibited onlyby cytochalasin B, but not by colchicine, sug-gesting that cytoplasmic streaming was control-led by microfilament. This is a typical modelfor studying cytoplasmic streaming. When in-tracellular Ca²⁺ was increased by introduction of10～40 μmol/L A 23187,55～100% cells cytoplas-mic streaming stopped （Fig. 1）. This evidencefurther confirmed that high concentration ofCa²⁺ could negatively control cytoplasmic stre-aming. Whenever 50 μmol/L CPZ or 20 μmol/LW7 was added during or after A23187 treat-ment, the reagents had no effects on the ces-sation of streaming induced by A 23187 （Fig. 2）.This may imply that streaming cessation inducedby high concentration of cytosol Ca²⁺ had norelation with CaM. Except W7, most of theCaM antagonists （20～100 μml/L） inhibitedthe normal cytoplasmic streaming considerablyand reversely （Table 1, Fig. 3）. CaM wasdetected in the culturcd cells by enzyme linkedimmunosorbent assay （ELISA） and was furtherfound in cytoplasmic striation by indirect en-zyme linked immunocytochemical method （Fig.5）. These observations suggest that normalcytoplasmic streaming is regulated by Ca²⁺and CaM.更多还原