摘要
烟草愈伤组织在含咖啡酸 ( 5mmol/L)和 /或CoCl2 ( 1 0mmol/L ,乙烯合成抑制剂 )的MS培养基上暗培养 ,同时用茉莉酸甲酯 ( 1mg/ml,简称MJ)处理愈伤组织。处理后测定乙烯、水杨酸和病程相关蛋白(PR)含量及一些抗病相关酶活性。MJ明显促进乙烯产生、增加水杨酸和PR蛋白含量 ,提高苯丙氨酸解氨酶 (PAL)、β1 ,3_葡聚糖苷酶和几丁酶的活性。咖啡酸降低MJ对乙烯和水杨酸诱导 ,CoCl2 明显降低MJ对乙烯的诱导 ,但没有明显影响MJ对水杨酸的诱导 ,两者都促进MJ诱导PAL活性而抑制MJ诱导β1 ,3_葡聚糖苷酶活性。咖啡酸明显影响MJ诱导内切几丁酶 ,几乎完全抑制对外切几丁酶的诱导 ;CoCl2 对MJ诱导内切几丁酶没有影响 ,促进对外切几丁酶的诱导。实验结果表明 ,不同的抗病相关酶活性诱导有不同的信号传递途径 ,在所测几种酶的诱导中 ,水杨酸起主要作用 ,乙烯作用较小 ,MJ的诱导作用主要是由水杨酸所转导。
The tobacco calli were cultured on MS medium contained 5 mmol/L coffeic acid (CA) and/or 10 mmol/L CoCl 2 (inhibitor of ethylene synthesis) in dark (25±2 ℃), while methyl jasmonate (MJ, about 1ml/15g FW) were sprayed to the calli. Two days after treatment, the contents of ethylene, salicylic acid (SA) and pathogen related protein (PRP), as well as the activities of phenylalanine ammonia_lyase (PAL), β1,3_glucanase and chitinase (endo_, exo_) were determined. MJ significantly increased the contents of ethylene, SA and PRP and the activities of PAL, β1,3_glucanse and chitinase. CA inhibited ethylene and salicylic acid production inducing by methyl jasmonate, CoCl 2 inhibited ethylene production , but did not inhibit SA production inducing by methyl jasmonate. Both CA and CoCl 2 have coordinate role with MJ to increase the activity of PAL, but they inhibited the role of MJ for increasing β1,3_glucanase activity. CA markedly inhibited the induced role of MJ for increasing endochitinase but almost inhibited the exochitinase activity. CoCl 2 have little effect on endochitinase activity, but increased exochitinase activity. The results show that there are different pathways of signal transduction in induced different resistance enzymes and PRP. SA plays a main role and ethylene plays a minor role in those enzymes and PRP induced by MJ. MJ may be the upper molecule of SA and ethylene in signal transduction.
出处
《植物学通报》
CAS
CSCD
北大核心
2003年第1期67-74,共8页
Chinese Bulletin of Botany
基金
广东省自然科学基金资助课题 ( 94 0 72 1 )