Abstract
Abscisic acid (ABA) signaling plays important roles in plant growth, development and adaptation to various stresses. RCAR1/PYL9 has been known as a cytoplasm and nuclear ABA receptor in Arabidopsis. To obtain further insight into the regulatory mechanism of RCAR1/PYL9, a yeast two-hybrid approach was performed to screen for RCAR1/PYL9-interacting proteins and an R2R3-type MYB transcription factor, AtMYB44, was identified. The interaction between RCAR1/PYL9 and AtMYB44 was further confirmed by glutathione S-transferase (GST) pull-down and bimolecular fluorescence complementation (BiFC) assays. Gene expression analysis showed that AtMYB44 negatively regulated the expression of ABA-responsive gene RAB18, in contrast to the opposite role reported for RCAR1/PYL9. Competitive GST pull-down assay and analysis of phosphatase activity demonstrated that AtMYB44 and ABI1 competed for binding to RCAR1/PYL9 and thereby reduced the inhibitory effect of RCAR1/PYL9 on ABI1 phosphatase activity in the presence of ABA in vitro. Furthermore, transient activation assay in protoplasts revealed AtMYB44 probably also decreased RCAR1/PYL9-mediated inhibition of ABI1 activity in vivo. Taken together, our work provides a reasonable molecular mechanism of AtMYB44 in ABA signaling.
Highlights
As sessile organisms, plants cannot escape away from, but have to face environmental stresses such as heat, cold, drought, and high-salinity stresses [1,2]
In the present study, we mainly focused our study on the interaction between RCAR1/PYL9 and AtMYB44 and the significance of their interaction in Abscisic acid (ABA) signaling based on the biochemical and molecular analysis
To understand how AtMYB44 negatively regulates the expression of ABA-responsive genes, we further focused on the interaction between AtMYB44 and RCAR1/PYL9
Summary
Plants cannot escape away from, but have to face environmental stresses such as heat, cold, drought, and high-salinity stresses [1,2]. SnRK2s directly phosphorylate transcription factors ABFs/AREBs or components of the machinery regulating stomatal aperture, leading to ABA responses [3,13]. Besides these core ABA signaling elements described above, MYB transcription factors (MYBs) are key components in ABA signaling [14]. We demonstrate that AtMYB44 interacts with the ABA receptor RCAR1/PYL9, and reduces its inhibitory effect on ABI1 activity. This finding indicates that AtMYB44 may act as a negative regulator in ABA signaling. This is the first detailed report on the molecular mechanism of how AtMYB44 is involved in ABA signaling regulation
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