Abstract
Calcium (Ca2+) signals are decoded by the Ca2+-sensor protein calmodulin (CaM) and are transduced to Ca2+/CaM-binding transcription factors to directly regulate gene expression necessary for acclimation responses in plants. The molecular mechanisms of Ca2+/CaM signal transduction processes and their functional significance remains enigmatic. Here we report a novel Ca2+/CaM signal transduction mechanism that allosterically regulates DNA-binding activity of GT2-LIKE 1 (GTL1), a transrepressor of STOMATAL DENSITY AND DISTRIBUTION 1 (SDD1), to repress stomatal development in response to water stress. We demonstrated that Ca2+/CaM interaction with the 2nd helix of the GTL1 N-terminal trihelix DNA-binding domain (GTL1N) destabilizes a hydrophobic core of GTL1N and allosterically inhibits 3rd helix docking to the SDD1 promoter, leading to osmotic stress-induced Ca2+/CaM-dependent activation (de-repression) of SDD1 expression. This resulted in GTL1-dependent repression of stomatal development in response to water-deficit stress. Together, our results demonstrate that a Ca2+/CaM-regulated transcriptional switch on a trihelix transrepressor directly transduces osmotic stress to repress stomatal development to improve plant water-use efficiency as an acclimation response.
Highlights
Plants sense and respond to external stimuli to acclimate and adapt to diverse environmental niches
An in vitro CaM overlay assay using AtCaM2-conjugated with horseradish peroxidase (HRP) further confirms that the interaction of GTL1N and AtCAM2 occurred only in the presence of Ca2+ (Supplementary Fig. S2)
Hyperosmotic stress-induced Ca2+/CaM signaling requires a rapid and efficient signal transduction mechanism to modulate global transcriptional regulation to cope with water deficit during drought stress
Summary
Plants sense and respond to external stimuli to acclimate and adapt to diverse environmental niches. Hyperosmotic stress induces signaling pathways that activate or repress genes necessary for water-deficit acclimation responses[4] and transcriptional regulation is a key regulatory mechanism that governs stomatal development[5]. Hyperosmotic stress-induced Ca2+/CaM allosteric control on the GTL1 transrepressor leads to SDD1 derepression, both by inhibiting binding to and promoting release from the SDD1 promoter, leading to repression of stomatal development in response to water-deficit stress. We propose that this allosteric control of the GTL1 transcription factor by Ca2+/CaM is a transcriptional switch to modulate stomatal development, thereby conserving plant water loss as a long-term developmental adaptation during water stress
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