INHIBITION OF ELONGATION GROWTH BY 2 SESQUITERPENE LACTONES ISOLATED FROM HELIANTHUS-ANNUUS L - POSSIBLE MOLECULAR MECHANISM
INHIBITION OF ELONGATION GROWTH BY 2 SESQUITERPENE LACTONES ISOLATED FROM HELIANTHUS-ANNUUS L - POSSIBLE MOLECULAR MECHANISM
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DOI：
10.1007/bf00393314
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发表时间：
1982-01-01
期刊：
影响因子：
4.3
通讯作者：
HAGER, A
中科院分区：
文献类型：
--
作者：
SPRING, O;HAGER, A
从毛蕊花的叶和茎中分离得到两个大根香叶内酯类倍半萜内酯。Annuus L.它们在植物中的形成依赖于光。两种倍半萜内酯均强烈抑制IAA诱导的燕麦伸长生长。胚芽鞘节和H. Annuus L.下胚轴裂片。两种SL都不抑制酸诱导的生长，也不抑制由梭孢菌素引发的生长。在二硫苏糖醇（DTT）存在下，SL在燕麦节段试验中的抑制作用可被完全中和。这可以归因于DTT与两个SL的结合。使用TLC，抑制剂与富含SH的化合物形成加合物，例如，半胱氨酸、谷胱甘肽、巯基乙醇和滴滴涕，其Rf值与主要物质的Rf值有显着差异。如果胚芽鞘节段首先用抑制剂处理，随后洗掉抑制剂，则可以通过添加IAA溶液诱导接近正常的伸长生长。如果同时用抑制剂和IAA处理这些片段，则在去除这两种物质并重新添加IAA后，在很长一段时间内不会开始显着的生长。Fusicoccin可立即中和诱导的生长抑制。当使用2，4-D时，发生相同的不可逆抑制。如果分别用抑制剂加2，4-D或抑制剂加3，5-二氯苯氧乙酸（3，5-D）处理胚芽鞘节段，则在去除物质后，IAA诱导的生长仅发生在先前用非生长素3，5-D加抑制剂处理的胚芽鞘中。一个可能的机制描述如何抑制剂的功能进行了讨论。生长素与生长素受体的结合使SH基团游离（可能是由于受体构象的变化）;抑制剂可以不可逆地结合（通过S键）的位点。然后，IAA-受体-受体-复合物不再能够启动伸长生长。如果生长素不存在，则抑制剂和受体之间不会发生持久的键合，因为必需的SH基团仍然被掩蔽。抑制剂可以再次被洗掉。因此，2 SL必须能够在IAA诱导的反应序列开始时进行干预，而随后的步骤保持不受影响，即，质子主动分泌到细胞壁区室中，这是由梭孢菌素直接诱导的，并引起伸长生长。
Two sesquiterpene lactones belonging to the germacranolides were isolated from the leaves and stems of H. annuus L. Their formation in the plant is light-dependent. Both sesquiterpene lactones (SL) strongly inhibit IAA-induced elongation growth of Avena sativa L. coleoptile segments and H. annuus L. hypocotyl segments. Both SL do not inhibit acid-induced growth nor growth triggered by fusicoccin. In the presence of dithiothreitol (DTT), the inhibitory effect of SL in the Avena-segment-test can be completely neutralized. This can be attributed to the binding of DTT to both SL. Using TLC the inhibitors built adducts with SH-rich compounds, e.g., cysteine, glutathione, mercapto-ethanol and DDT, whose Rf-value significanlty differs from those of the primary substances. If the coleoptile segments are first treated with an inhibitor and the inhibitor is subsequently washed out, close to normal elongation growth can be induced by adding an IAA-solution. If the segments are simultaneously treated with inhibitor and IAA, no notable growth can be initiated for an extended amount of time, after the removal of both substances and the anewed addition of IAA. Fusicoccin, can immediately neutralize the induced growth inhibition. The same irreversible inhibition occurs when 2,4-D is used. If coleoptile segments are treated with an inhibitor plus 2,4-D or an inhibitor plus 3,5-dichlorophenoxyacetic acid (3,5-D), respectively, IAA-induced growth after removal of the substances only occurs in those coleoptiles which had previously been treated with the non-auxin, 3,5-D plus an inhibitor. A possible mechanism describing how the inhibitor functions is discussed. The binding of an auxin to an auxin receptor sets a SH-group free (possibly due to a change in the conformation of the receptor); a site is given to which the inhibitor can bind irreversibly (via a S-bond). The IAA-receptor-inhibitor-complex is then no longer able to initiate elongation growth. If auxin is not present, no lasting bond between the inhibitor and the receptor can occur, since the essential SH-group remains masked. The inhibitor can be washed out again. Consequently, the 2 SL have to be able to intervene at the beginning of the IAA-induced reaction sequence, while the following steps remain uninfluenced, i.e., the active excretion of protons into the cell wall compartments, which is directly induced by fusicoccin and causes elongation growth.