The analysis of an Arabidopsis triple knock-down mutant reveals functions for MBF1 genes under oxidative stress conditions
The analysis of an Arabidopsis triple knock-down mutant reveals functions for MBF1 genes under oxidative stress conditions
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DOI：
10.1016/j.jplph.2009.09.003
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发表时间：
2010-01-01
影响因子：
4.3
通讯作者：
Anahi Casalongue, Claudia
中科院分区：
文献类型：
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作者：
Pamela Arce, Debora;Veronica Godoy, Andrea;Anahi Casalongue, Claudia
多蛋白桥接因子1（MBF 1）类型的转录共激活因子属于通过连接转录因子和基础转录机制来控制基因表达的小的多基因家族。在本报告中，拟南芥MBF 1基因AtMBF 1a，AtMBF 1b和AtMBF 1c的三重敲低突变体（abc-）的产生。用过氧化氢和甲基紫精等氧化剂对突变体进行表型鉴定，结果表明突变体对氧化胁迫更敏感。三重敲低突变体，abc-也是敏感的高浓度山梨醇介导的渗透胁迫。此外，abc-表型部分或完全获救AtMBF 1c cDNA过表达（abc- +c）取决于生理和发育条件。AtMBF 1 s调节ABR 1的表达，ABR 1是乙烯反应因子家族的成员，并作为阿坝阻遏物。因此，我们认为AtMBF 1基因家族可能是乙烯、阿坝和胁迫信号通路之间的一个调控元件。此外，在abc-突变体中检测到更高水平的HSP 70 mRNA和免疫反应性HSP 70蛋白。对MBF 1c可能作为HSP基因负调控因子的参与进行了讨论。由爱思唯尔有限公司出版。
Transcriptional co-activators of the multiprotein bridging factor 1 (MBF1) type belong to a small multigenic family that controls gene expression by connecting transcription factors and the basal transcription machinery. In this report, a triple knock-down mutant (abc-) for the Arabidopsis thaliana MBF1 genes AtMBF1a, AtMBF1b and AtMBF1c was generated. The phenotypic characterization using oxidative agents Such as hydrogen peroxide and methyl viologen revealed that the abc- mutant was more sensitive to oxidative stress. The triple knock-down mutant, abc- was also sensitive to osmotic stress mediated by high concentrations of sorbitol. Furthermore, the abc- phenotype was partially or completely rescued by AtMBF1c cDNA over-expression (abc- +c) depending on physiological and developmental conditions. AtMBF1s regulate the expression of ABR1, which is a member of the ethylene-response factor family and acts as ABA repressor. Thus, we conclude that AtMBF1 gene family may function as a regulatory component of the cross-talk node between ethylene, ABA and stress signal pathways. Furthermore, higher levels of a HSP70 mRNA and an immunoreactive HSP70 protein were detected in the abc- mutant. The participation of MBF1c as a possible negative regulator of HSP genes was discussed. Published by Elsevier GmbH.