Arabidopsis PLC1 Is Required for Secondary Responses to Abscisic Acid Signals
Arabidopsis PLC1 Is Required for Secondary Responses to Abscisic Acid Signals
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DOI：
10.1105/tpc.13.5.1143
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发表时间：
2001-05
期刊：
影响因子：
11.6
通讯作者：
J. Sánchez;N. Chua
中科院分区：
文献类型：
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作者：
J. Sánchez;N. Chua
1，4，5-三磷酸肌醇（Ins[1，4，5]P3）在种子萌发和成熟植物逆境响应过程中对脱落酸（阿坝）信号转导的作用尚不清楚。我们通过使用糖皮质激素诱导系统的修改版本来调节转基因表达，考虑了磷脂酶C1（由AtPLC 1编码）和Ins（1，4，5）P3 5-磷酸酶（由AtIP 5 PII编码）对阿坝信号传导的贡献。在地塞米松（Dex）诱导剂的存在下，表达AtPLC 1反义和AtIP 5 PII正义转基因的转基因株系显示阿坝对发芽和生长没有抑制作用，而在没有诱导剂的情况下，它们是敏感的。在Dex处理下，这些转基因株系在阿坝处理后积累的Ins（1，4，5）P3水平低于对照。RNA凝胶印迹分析显示，在Dex诱导的转基因植物中，ABA响应基因RD 29 a、KIN 2和RD 22的诱导减少，但COR 47没有减少。在表达诱导型AtPLC 1正义转基因的转基因株系中，AtPLC 1表达的增加不足以激活营养组织中ABA响应基因的表达。体外实验表明，当在钙存在下测定提取物时，诱导的PLC 1表达，但未检测到体内Ins（1，4，5）P3水平的增加，表明PLC 1酶是潜伏的。我们的研究结果表明，虽然增加PLC 1的活性和增加的Ins（1，4，5）P3水平是必需的最大基因诱导阿坝，AtPLC 1本身的过表达是不足以触发ABA响应基因的表达。我们建议，AtPLC 1在次生阿坝反应中发挥作用。
The role of inositol 1,4,5-trisphosphate (Ins[1,4,5]P3) in transducing the abscisic acid (ABA) signal during seed germination and in the stress responses of mature plants is poorly understood. We have considered the contributions of the phospholipase C1 (encoded by AtPLC1) and an Ins(1,4,5)P3 5-phosphatase (encoded by AtIP5PII) to ABA signaling by using a modified version of the glucocorticoid-inducible system to regulate transgene expression. In the presence of the dexamethasone (Dex) inducer, transgenic lines expressing the AtPLC1 antisense and AtIP5PII sense transgenes showed no inhibition of germination and growth by ABA, whereas in the absence of the inducer they were sensitive. In the presence of Dex, these lines accumulated lower Ins(1,4,5)P3 levels upon ABA treatment compared with that of the control transgenic lines. RNA gel blot analysis revealed a decrease in the induction of the ABA-responsive genes RD29a, KIN2, and RD22 but not COR47 in the Dex-induced transgenic plants. In transgenic lines expressing the inducible AtPLC1 sense transgene, an increase in AtPLC1 expression was not sufficient to activate the expression of ABA-responsive genes in vegetative tissues. In vitro experiments demonstrated the induced PLC1 expression when extracts were assayed in the presence of calcium, but no increase in Ins(1,4,5)P3 levels in vivo was detected, suggesting that the PLC1 enzyme was latent. Our results indicate that although an increase in PLC1 activity and increased Ins(1,4,5)P3 levels are necessary for maximal gene induction by ABA, overexpression of AtPLC1 itself is not sufficient to trigger the expression of ABA-responsive genes. We propose that AtPLC1 plays a role in secondary ABA responses.