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首页> 外文期刊>Plant Science: An International Journal of Experimental Plant Biology >Fungal elicitor-induced cell death in Taxus chinensis suspension cells is mediated by ethylene and polyamines
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Fungal elicitor-induced cell death in Taxus chinensis suspension cells is mediated by ethylene and polyamines

机译:真菌和诱导剂诱导的红豆杉悬浮细胞死亡是由乙烯和多胺介导的

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摘要

The involvements of ethylene and polyamines in cell death induced by fungal elicitor from Asperillus niger in Taxus chinensis suspension cells were studied. Exogenous fungal elicitor stimulated cell death and enhanced ethylene production and polyamine putrescine, spermidine and spermine concentrations compared with the control. Cell death, ethylene production and putrescine concentration induced by elicitor were increased by the precursor of ethylene biosynthesis 1-aminocyclopropane-1-carboxylic acid (ACC), while were overcome by ACC together with the inhibitor of ACC synthase aminoethoxyvinylycin. In contrast, fungal elicitor-induced cell death was decreased by, and ethylene production and putrescine concentration were enhanced by the inhibitor of ethylene action silver thiosulphate. Since the biosynthetic pathways of ethylene and polyamines are linked through S-adenosylmethionine (SAM), this promoted further probation into the roles of polyamines in cell death. Exogenous polyamines putrescine, spermidine and spermine all reduced elicitor-induced ethylene production and cell death. Blocking endogenous polyamine concentrations with methylglyoxal (bis-guanylhydrazone) stimulated elicitor-induced ethylene production and cell death. These results indicated that ethylene promoted while polyamines alleviated elicitor-induced cell death
机译:研究了黑曲霉真菌引发剂在红豆杉悬浮细胞中乙烯和多胺参与细胞死亡的过程。与对照相比,外源性真菌引发剂刺激细胞死亡并增加乙烯的产生和多胺腐胺,亚精胺和亚精胺的浓度。乙烯诱导生物合成1-氨基环丙烷-1-羧酸(ACC)的前体可增加诱导物诱导的细胞死亡,乙烯生成和腐胺浓度,而ACC与ACC合酶氨基乙氧基乙烯基霉素的抑制剂可克服这些问题。相反,通过乙烯作用硫代硫酸银抑制剂,真菌引发剂诱导的细胞死亡减少,并且乙烯产生和腐胺浓度增加。由于乙烯和多胺的生物合成途径通过S-腺苷甲硫氨酸(SAM)连接,因此进一步促进了多胺在细胞死亡中的作用。外源多胺腐胺,亚精胺和亚精胺均减少了诱发剂诱导的乙烯生成和细胞死亡。用甲基乙二醛(双胍hydr)阻断内源性多胺浓度可刺激诱导物诱导的乙烯生成和细胞死亡。这些结果表明乙烯促进了而多胺减轻了诱导子诱导的细胞死亡。

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