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钙调素拮抗剂对生长素诱导伸长的影响。

Effect of calmodulin antagonists on auxin-induced elongation.

机构信息

Department of Horticulture and Landscape Architecture, Washington State University, Pullman, Washington 99164-6414.

出版信息

Plant Physiol. 1985 Sep;79(1):28-33. doi: 10.1104/pp.79.1.28.

Abstract

Coleoptile segments of oat (Avena sativa var Cayuse) and corn (Zea mays L. var Patriot) were incubated in different concentrations of calmodulin antagonists in the presence and absence of alpha-naphthaleneacetic acid. The calmodulin antgonists (chlorpromazine (CP), trifluoperazine, and fluphenazine) inhibited the auxin-induced elongation at 5 to 50 micromolar concentrations. Chlorpromazine sulfoxide, an analog of chlorpromazine, did not have significant effect on the elongation of oat and corn coleoptiles. A specific inhibitor of calmodulin N-(6-aminohexyl)5-chloro-1-naphthalenesulfonamide hydrochloride (W-7, a naphthalenesulfonamide derivative) inhibited coleoptile elongation, while its inactive analog N-(6-aminohexyl)-1-naphthalenesulfonamide hydrochloride (W-5) was ineffective at similar concentrations. During a 4-hour incubation period, coleoptile segments accumulated significant quantities of (3)H-CP. About 85 to 90% of auxin-induced growth was recovered after 4 hours of preincubation with CP or 12 hours with W-7 and transferring coleoptiles to buffer containing NAA. Leakage of amino acids from coleoptiles increased with increasing concentration of CP, showing a rapid and significant increase above 20 micromolar CP. The amount of amino acids released in the presence of W-7 and W-5 was significantly lower than the amount released in the presence of CP. Both W-5 and W-7 increased amino acid release but only W-7 inhibited auxin-induced growth. Calmodulin activity measured by phosphodiesterase activation did not differ significantly between auxin-treated and control coleoptile segments. These results suggest the possible involvement of calmodulin in auxin-induced coleoptile elongation.

摘要

燕麦(Avena sativa var Cayuse)和玉米(Zea mays L. var Patriot)的胚芽鞘在不同浓度的钙调蛋白拮抗剂存在或不存在α-萘乙酸的情况下孵育。钙调蛋白拮抗剂(氯丙嗪(CP)、三氟拉嗪和氟奋乃静)在 5 至 50 微摩尔浓度下抑制了生长素诱导的伸长。氯丙嗪亚砜,氯丙嗪的类似物,对燕麦和玉米胚芽鞘的伸长没有显著影响。钙调蛋白的一种特异性抑制剂 N-(6-氨基己基)5-氯-1-萘磺酰胺盐酸盐(W-7,一种萘磺酰胺衍生物)抑制了胚芽鞘的伸长,而其非活性类似物 N-(6-氨基己基)-1-萘磺酰胺盐酸盐(W-5)在类似浓度下无效。在 4 小时的孵育期间,胚芽鞘段积累了大量的(3)H-CP。用 CP 预处理 4 小时或用 W-7 预处理 12 小时并将胚芽鞘转移到含有 NAA 的缓冲液中后,约 85-90%的生长素诱导的生长得到恢复。随着 CP 浓度的增加,氨基酸从胚芽鞘中的渗漏增加,在 20 微摩尔 CP 以上迅速且显著增加。在 W-7 和 W-5 的存在下释放的氨基酸量明显低于 CP 存在下释放的氨基酸量。W-5 和 W-7 均增加了氨基酸的释放,但只有 W-7 抑制了生长素诱导的生长。用磷酸二酯酶激活法测量的钙调蛋白活性在生长素处理和对照胚芽鞘段之间没有显著差异。这些结果表明钙调蛋白可能参与了生长素诱导的胚芽鞘伸长。

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