The analysis of an Arabidopsis triple knock-down mutant reveals functions for MBF1 genes under oxidative stress conditions

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...

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Veröffentlicht in:Journal of plant physiology 2010-02, Vol.167 (3), p.194-200
Hauptverfasser: Pamela Arce, Débora, Verónica Godoy, Andrea, Tsuda, Kenichi, Yamazaki, Ken-ichi, Marta Valle, Estela, José Iglesias, María, Di Mauro, María Florencia, Anahí Casalongué, Claudia
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Sprache:eng
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Zusammenfassung: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.
ISSN:0176-1617
1618-1328
DOI:10.1016/j.jplph.2009.09.003