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乙烯合成抑制剂可抑制蚕豆叶片表皮中生长素诱导的气孔开放。

Inhibitors of ethylene synthesis inhibit auxin-induced stomatal opening in epidermis detached from leaves of Vicia faba L.

作者信息

Merritt F, Kemper A, Tallman G

机构信息

Natural Science Division, Pepperdine University, 24255 Pacific Coast Highway, Malibu, CA 90265, USA.

出版信息

Plant Cell Physiol. 2001 Feb;42(2):223-30. doi: 10.1093/pcp/pce030.

DOI:10.1093/pcp/pce030
PMID:11230577
Abstract

Using leaf epidermis from Vicia faba, we tested whether auxin-induced stomatal opening was initiated by auxin-induced ethylene synthesis. Epidermis was dark-incubated in buffered KNO3 containing 0.1 mM alpha-napthalene acetic acid or 1 mM indole-3-acetic acid. Maximum net opening was ca. 4 micron after 6 h. Opening was reversed by 20 microM ABA, 0.1 mM CaCl2. 1-Aminocyclopropane carboxylic acid (ACC) synthase catalyzes synthesis of ACC, the immediate precursor to ethylene. Auxin-induced stomatal opening was fully inhibited by 10 microM 1-aminoethoxyvinylglycine (AVG), an ACC synthase inhibitor. In solutions containing AVG, auxin-induced opening was restored in a concentration-dependent manner by exogenous ACC, but not in control solutions lacking an auxin. ACC-mediated reversal of AVG-inhibition of stomatal opening was inhibited by alpha-aminoisobutyric acid (AIB), an inhibitor of ACC oxidase, the last enzyme in the ethylene biosynthetic pathway, by 10 microM silver thiosulfate (STS), an inhibitor of ethylene action, and by 20 microM ABA, 0.1 mM CaCl2. CoCl2, an inhibitor of ethylene synthesis, also inhibited auxin-induced opening. Both STS and CoCl2 inhibited opening induced by light or by fusicoccin, but neither light- nor fusicoccin-induced opening was inhibited by AVG. These results support the hypothesis that auxin-induced stomatal opening is mediated through auxin-induced ethylene production by guard cells.

摘要

我们使用蚕豆叶表皮来测试生长素诱导的气孔开放是否由生长素诱导的乙烯合成引发。将表皮在含有0.1 mM α-萘乙酸或1 mM吲哚-3-乙酸的缓冲硝酸钾中进行暗培养。6小时后最大净开放度约为4微米。20 microM脱落酸、0.1 mM氯化钙可使开放逆转。1-氨基环丙烷羧酸(ACC)合酶催化乙烯的直接前体ACC的合成。生长素诱导的气孔开放被10 microM 1-氨基乙氧基乙烯基甘氨酸(AVG,一种ACC合酶抑制剂)完全抑制。在含有AVG的溶液中,生长素诱导的开放可被外源ACC以浓度依赖的方式恢复,但在不含生长素的对照溶液中则不能。ACC介导的对AVG抑制气孔开放的逆转被α-氨基异丁酸(AIB,乙烯生物合成途径中的最后一种酶ACC氧化酶的抑制剂)、10 microM硫代硫酸银(STS,乙烯作用的抑制剂)、20 microM脱落酸、0.1 mM氯化钙抑制。氯化钴,一种乙烯合成抑制剂,也抑制生长素诱导的开放。STS和氯化钴都抑制由光或藤霉素诱导的开放,但AVG不抑制光或藤霉素诱导的开放。这些结果支持了这样的假设,即生长素诱导的气孔开放是通过保卫细胞中生长素诱导的乙烯产生介导的。

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